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Conduction Time (conduction + time)
Kinds of Conduction Time Selected AbstractsUsefulness of Interatrial Conduction Time to Distinguish Between Focal Atrial Tachyarrhythmias Originating from the Superior Vena Cava and the Right Superior Pulmonary VeinJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2008KUAN-CHENG CHANG M.D. Objective: Differentiation of the tachycardia originating from the superior vena cava (SVC) or the right superior pulmonary vein (RSPV) is limited by the similar surface P-wave morphology and intraatrial activation pattern during tachycardia. We sought to find a simple method to distinguish between the two tachycardias by analyzing the interatrial conduction time. Methods: Sixteen consecutive patients consisting of 8 with SVC tachycardia and the other 8 with RSPV tachycardia were studied. The interatrial conduction time from the high right atrium (HRA) to the distal coronary sinus (DCS) and the intraatrial conduction time from the HRA to the atrial electrogram at the His bundle region (HIS) were measured during the sinus beat (SR) and during the tachycardia-triggering ectopic atrial premature beat (APB). The differences of interatrial (,[HRA-DCS]SR-APB) and intraatrial (,[HRA-HIS]SR-APB) conduction time between SR and APB were then obtained. Results: The mean ,[HRA-DCS]SR-APB was 1.0 ± 5.2 ms (95% confident interval [CI],3.3,5.3 ms) in SVC tachycardia and 38.5 ± 8.8 ms (95% CI 31.1,45.9 ms) in RSPV tachycardia. The mean ,[HRA-HIS]SR-APB was 1.5 ± 5.3 ms (95% CI ,2.9,5.9 ms) in SVC tachycardia and 19.9 ± 12.0 ms (95% CI 9.9,29.9 ms) in RSPV tachycardia. The difference of ,[HRA-DCS]SR-APB between SVC and RSPV tachycardias was wider than that of ,[HRA-HIS]SR-APB (37.5 ± 9.3 ms vs. 18.4 ± 15.4 ms, P < 0.01). Conclusions: The wide difference of the interatrial conduction time ,[HRA-DCS]SR-APB between SVC and RSPV tachycardias is a useful parameter to distinguish the two tachycardias and may avoid unnecessary atrial transseptal puncture. [source] Can Simple Doppler Measurements Estimate Interatrial Conduction Time?PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003DRAGOS COZMA COZMA, D., et al.: Can Simple Doppler Measurements Estimate Interatrial Conduction Time?Prolongation of the interatrial conduction time (ia-CT) is considered an important factor in the pathophysiology of atrial fibrillation (AF) and as a criterion to perform multisite atrial pacing. Measurement of ia-CT requires an electrophysiologic study. The aim of this study was to compare echocardiographic with electrophysiologic measurements to determine if they are correlated. Methods and Results: The study included 32 consecutive patients who underwent electrophysiologic studies. We measured ia-CT between the high right atrium and the distal coronary sinus. In all patients we measured P wave duration, left atrial diameter and area, and ia-CT by Doppler echocardiography was measured as the difference in time intervals between the QRS onset and the tricuspid A wave, and the QRS onset and the mitral A wave (DT). Ia-CT was statistically correlated with DT(r = 0.79, P < 0.0001), but not with P wave duration or left atrial dimensions. Conclusions: Measurement DT may be reliable to estimate ia-CT without invasive procedure. Accordingly, DT could be used as a simple selection criterion when considering patients for atrial resynchronization therapy. (PACE 2003; 26[Pt. II]:436,439) [source] Electrophysiological determinants of hypokalaemia-induced arrhythmogenicity in the guinea-pig heartACTA PHYSIOLOGICA, Issue 4 2009O. E. Osadchii Abstract Aim:, Hypokalaemia is an independent risk factor contributing to arrhythmic death in cardiac patients. In the present study, we explored the mechanisms of hypokalaemia-induced tachyarrhythmias by measuring ventricular refractoriness, spatial repolarization gradients, and ventricular conduction time in isolated, perfused guinea-pig heart preparations. Methods:, Epicardial and endocardial monophasic action potentials from distinct left ventricular (LV) and right ventricular (RV) recording sites were monitored simultaneously with volume-conducted electrocardiogram (ECG) during steady-state pacing and following a premature extrastimulus application at progressively reducing coupling stimulation intervals in normokalaemic and hypokalaemic conditions. Results:, Hypokalaemic perfusion (2.5 mm K+ for 30 min) markedly increased the inducibility of tachyarrhythmias by programmed ventricular stimulation and rapid pacing, prolonged ventricular repolarization and shortened LV epicardial and endocardial effective refractory periods, thereby increasing the critical interval for LV re-excitation. Hypokalaemia increased the RV-to-LV transepicardial repolarization gradients but had no effect on transmural dispersion of APD90 and refractoriness across the LV wall. As determined by local activation time recordings, the LV-to-RV transepicardial conduction and the LV transmural (epicardial-to-endocardial) conduction were slowed in hypokalaemic heart preparations. This change was attributed to depressed diastolic excitability as evidenced by increased ventricular pacing thresholds. Conclusion:, These findings suggest that hypokalaemia-induced arrhythmogenicity is attributed to shortened LV refractoriness, increased critical intervals for LV re-excitation, amplified RV-to-LV transepicardial repolarization gradients and slowed ventricular conduction in the guinea-pig heart. [source] Assessment of corticodiaphragmatic pathway and pulmonary function in acute ischemic stroke patientsEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2000E. M. Khedr This study investigates the effect of stroke on the corticodiaphragmatic pathway and attempts to clarify the relationship between neurophysiological data and degree of motor disability, site of infarction in computerized tomography (CT) scan, diaphragmatic excursion, blood gases and pulmonary function in stroke patients. Using magnetic stimulation of the scalp sites and cervical roots, an assessment of corticodiaphragmatic pathway was made. The study included 34 sequentially selected patients from a total of 250 patients with acute ischemic stroke. Twenty-five (age- and sex-matched) volunteers served as controls. Sixteen patients had cortical infarction, 13 had subcortical infarction and five had both cortical and subcortical infarction. The mean according to the Scandinavian Stroke Scale was 32.2. Decreased diaphragmatic excursion was observed in 41% of the patients. Twenty-four patients (70.5%) had abnormal magnetic evoked potentials (MEPs) in the affected hemisphere. In five patients MEPs could not be elicited from the affected hemisphere; the remaining 19 patients had abnormal values of both cortical latency and central conduction time (CCT). Cortical latency, CCT, amplitude of compound muscle action potentials (CMAPs) and excitability threshold of the affected hemisphere were significantly altered compared with both the unaffected hemisphere and the control group. Those patients with hemiplegia had a greater degree of hypoxia, hypocapnia and decreased serum bicarbonate level compared with the control group. Also, hemiplegic patients had different degree of respiratory dysfunction. A statistically significant association was found between neurophysiological data and disability score, diaphragmatic excursion, site of infarction in CT scan and degree of respiratory dysfunction. Central diaphragmatic impairment may occur in acute stroke and could contribute to the occurence of hypoxia in those patients. [source] Magnetically evoked motor potentials in demyelinating and axonal polyneuropathy: a comparative studyEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2000H. Takada We investigated the value of magnetically evoked motor potentials (MEPs) for the differentiation of demyelinating and axonal polyneuropathies. The study population comprised 107 patients, with polyneuropathy verified by electromyography (EMG) and nerve conduction study (NCS), who had also been examined by means of MEP. MEPs were evoked by magnetic stimulation of the cortex and the spinal roots and were recorded from three upper limb muscles and two lower limb muscles bilaterally. From the EMG/NCS results 53 patients were characterized as having primary demyelination (demyelinating patients) and 54 as having axonal involvement (axonal patients). Demyelinating patients were classified as acute (acute inflammatory demyelinating polyradiculoneuropathy: AIDP ) or chronic (chronic inflammatory demyelinating polyradiculoneuropathy: CIDP ) according to the duration of illness. A series of indices were calculated from MEP results. One demyelinating patient and two axonal patients had normal MEPs. The MEPs of the demyelinating patients showed significantly longer peripheral conduction times, larger interside differences and lower amplitudes than the axonal patients. The central conduction index and the amplitudes upon cortical stimulation were significantly higher in patients with CIDP than in those with AIDP. Peripheral conduction time prolonged by more than 85% in at least one of the 10 muscles studied or a peripheral conduction index of above 9.4 were pathognomonic for demyelination . By combining all criteria 75% of the patients could be categorized as CIDP vs. AIDP in accordance with the EMG/NCS diagnosis. Likewise, 83% were categorized correctly as demyelinating versus axonal according to the EMG/NCS data. [source] The changes in neuromuscular excitability with normobaric hyperoxia in humansEXPERIMENTAL PHYSIOLOGY, Issue 1 2010Christelle Brerro-Saby Based on previous observations in hyperbaric hyperoxia, we hypothesized that normobaric hyperoxia, often used during general anaesthesia and resuscitation, might also induce a neuromuscular excitability. In heathy volunteers, we studied the consequences of a 50 min period of pure oxygen breathing on the neuromuscular conduction time (CT), the amplitude of the compound evoked muscle potential (M-wave), the latency and amplitude of the Hoffman reflex (H reflex) and the electromyographic tonic vibratory response (TVR) of the flexor digitorum superficialis muscle to explore the proprioceptive reflex loop. Hyperoxia-induced oxidative stress was measured by the changes in blood markers of lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and antioxidant response (reduced ascorbic acid, RAA). During hyperoxia, the M-wave amplitude increased, both CT and H reflex latency were shortened, and the H reflex amplitude increased. By contrast, TVR significantly decreased. Concomitantly, an oxidative stress was assessed by increased TBARS and decreased RAA levels. This study shows the existence of dual effects of hyperoxia, which facilitates the muscle membrane excitability, nerve conduction and spinal reflexes, but reduces the gain of the proprioceptive reflex loop. The activation of the group IV muscle afferents by hyperoxia and the resulting oxidative stress might explain the TVR depression. [source] Finite element and sensitivity analysis of thermally induced flow instabilitiesINTERNATIONAL JOURNAL FOR NUMERICAL METHODS IN FLUIDS, Issue 10 2010Jean-Serge Gigučre Abstract This paper presents a finite element algorithm for the simulation of thermo-hydrodynamic instabilities causing manufacturing defects in injection molding of plastic and metal powder. Mold-filling parameters determine the flow pattern during filling, which in turn influences the quality of the final part. Insufficiently, well-controlled operating conditions may generate inhomogeneities, empty spaces or unusable parts. An understanding of the flow behavior will enable manufacturers to reduce or even eliminate defects and improve their competitiveness. This work presents a rigorous study using numerical simulation and sensitivity analysis. The problem is modeled by the Navier,Stokes equations, the energy equation and a generalized Newtonian viscosity model. The solution algorithm is applied to a simple flow in a symmetrical gate geometry. This problem exhibits both symmetrical and non-symmetrical solutions depending on the values taken by flow parameters. Under particular combinations of operating conditions, the flow was stable and symmetric, while some other combinations leading to large thermally induced viscosity gradients produce unstable and asymmetric flow. Based on the numerical results, a stability chart of the flow was established, identifying the boundaries between regions of stable and unstable flow in terms of the Graetz number (ratio of thermal conduction time to the convection time scale) and B, a dimensionless ratio indicating the sensitivity of viscosity to temperature changes. Sensitivities with respect to flow parameters are then computed using the continuous sensitivity equations method. We demonstrate that sensitivities are able to detect the transition between the stable and unstable flow regimes and correctly indicate how parameters should change in order to increase the stability of the flow. Copyright © 2009 John Wiley & Sons, Ltd. [source] Periodicity in proton conduction along a H-bonded chain.INTERNATIONAL JOURNAL OF QUANTUM CHEMISTRY, Issue 3 2008Application to biomolecules Abstract Molecular complexes are constructed to simulate proton transfer channels of the influenza A virus and of the active site of carbonic anhydrase. These complexes consist of proton donor and acceptor groups connected by a chain of water molecules. Quantum chemical calculations on the methylimidazole(H+)H2OCH3COO, model of the M2 virus channel indicate free translational motion of the water molecule between donor and acceptor, as well as concerted transfer of both H-bond protons. The proton transfer barrier does not depend on the position of the bridged water molecule and varies linearly with the difference of electrostatic potentials between the donor and acceptor. When the water chain is elongated, and with various donor and acceptor models, periodicity appears in the H-bond lengths and the progression of proton transfer in each link. This "wave" is shown to propagate along the chain, as it is driven by the displacement of a single proton. One can thereby estimate the velocity of the proton wave and proton conduction time. Computations are performed to examine the influence of immersing the system within a polarizable medium. © 2007 Wiley Periodicals, Inc. Int J Quantum Chem, 2008 [source] Ranolazine Exerts Potent Effects on Atrial Electrical Properties and Abbreviates Atrial Fibrillation Duration in the Intact Porcine HeartJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2009KAPIL KUMAR M.D. Introduction: In vitro studies and ambulatory ECG recordings from the MERLIN TIMI-36 clinical trial suggest that the novel antianginal agent ranolazine may have the potential to suppress atrial arrhythmias. However, there are no reports of effects of ranolazine on atrial electrophysiologic properties in large intact animals. Methods and Results: In 12 closed-chest anesthetized pigs, effects of intravenous ranolazine (,9 ,M plasma concentration) on multisite atrial effective refractory period (ERP), conduction time (CT), and duration and inducibility of atrial fibrillation (AF) initiated by intrapericardial acetylcholine were investigated. Ranolazine increased ERP by a median of 45 ms (interquartile range 29,50 ms; P < 0.05, n = 6) in right and left atria compared to control at pacing cycle length (PCL) of 400 ms. However, ERP increased by only 28 (24,34) ms in right ventricle (P < 0.01, n = 6). Ranolazine increased atrial CT from 89 (71,109) ms to 98 (86,121) ms (P = 0.04, n = 6) at PCL of 400 ms. Ranolazine decreased AF duration from 894 (811,1220) seconds to 621 (549,761) seconds (P = 0.03, n = 6). AF was reinducible in 1 of 6 animals after termination with ranolazine compared with all 6 animals during control period (P = 0.07). Dominant frequency (DF) of AF was reduced by ranolazine in left atrium from 11.7 (10.7,20.5) Hz to 7.6 (2.9,8.8) Hz (P = 0.02, n = 6). Conclusions: Ranolazine, at therapeutic doses, increased atrial ERP to greater extent than ventricular ERP and prolonged atrial CT in a frequency-dependent manner in the porcine heart. AF duration and DF were also reduced by ranolazine. Potential role of ranolazine in AF management merits further investigation. [source] Usefulness of Interatrial Conduction Time to Distinguish Between Focal Atrial Tachyarrhythmias Originating from the Superior Vena Cava and the Right Superior Pulmonary VeinJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2008KUAN-CHENG CHANG M.D. Objective: Differentiation of the tachycardia originating from the superior vena cava (SVC) or the right superior pulmonary vein (RSPV) is limited by the similar surface P-wave morphology and intraatrial activation pattern during tachycardia. We sought to find a simple method to distinguish between the two tachycardias by analyzing the interatrial conduction time. Methods: Sixteen consecutive patients consisting of 8 with SVC tachycardia and the other 8 with RSPV tachycardia were studied. The interatrial conduction time from the high right atrium (HRA) to the distal coronary sinus (DCS) and the intraatrial conduction time from the HRA to the atrial electrogram at the His bundle region (HIS) were measured during the sinus beat (SR) and during the tachycardia-triggering ectopic atrial premature beat (APB). The differences of interatrial (,[HRA-DCS]SR-APB) and intraatrial (,[HRA-HIS]SR-APB) conduction time between SR and APB were then obtained. Results: The mean ,[HRA-DCS]SR-APB was 1.0 ± 5.2 ms (95% confident interval [CI],3.3,5.3 ms) in SVC tachycardia and 38.5 ± 8.8 ms (95% CI 31.1,45.9 ms) in RSPV tachycardia. The mean ,[HRA-HIS]SR-APB was 1.5 ± 5.3 ms (95% CI ,2.9,5.9 ms) in SVC tachycardia and 19.9 ± 12.0 ms (95% CI 9.9,29.9 ms) in RSPV tachycardia. The difference of ,[HRA-DCS]SR-APB between SVC and RSPV tachycardias was wider than that of ,[HRA-HIS]SR-APB (37.5 ± 9.3 ms vs. 18.4 ± 15.4 ms, P < 0.01). Conclusions: The wide difference of the interatrial conduction time ,[HRA-DCS]SR-APB between SVC and RSPV tachycardias is a useful parameter to distinguish the two tachycardias and may avoid unnecessary atrial transseptal puncture. [source] Quantitative Analysis of the Duration of Slow Conduction in the Reentrant Circuit of Ventricular Tachycardia After Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2008YI-GANG LI M.D. Background: Few data are available to define the circuits in ventricular tachycardia (VT) after myocardial infarction and the conduction time (CT) through the zone of slow conduction (SCZ). This study assessed the CT of the SCZ and identified different reentrant circuits. Methods: During VTs, concealed entrainment (CE) was attempted. The SCZ was identified by a difference between postpacing interval (PPI) and VT cycle length (VTcl) ,30 ms. Since the CT in the normally conducting part of the VT circuit is constant during VT and CE, a CE site within the reentrant circuit with (S-QRS)/PPI , 50% was classified as an inner reentry in which the entire circuit was within the scar, and a CE site with (S-QRS)/PPI < 50% as a common reentry in which part of the circuit was within the scar and part out of the scar. Results: CE was achieved in 20 VTs (12 patients). Six VTs (30%) with a (S-QRS)/PPI ,50% were classified as inner reentry and 14 VTs (70%) with a (S-QRS)/PPI <50% during CE mapping as common reentry. The EG-QRS interval (308 ± 73 ms vs 109 ± 59 ms, P < 0.0001) was significantly longer and the incidence of systolic potentials higher (4/6 vs 0/12, P < 0.001) in the inner reentry group. For the 14 VTs with a common reetry, the CT of the SCZ was 348 ± 73 ms, while the CT in the normal area was 135 ± 50 ms. Conclusion: According to the proposed classification, 30% of VTs after myocardial infarction had an entire reentrant circuit within the scar. In VTs with a common reentrant circuit, the CT of the SCZ is approximately four times longer than the CT in the normal area, accounting for more than 70% of VTcl. [source] Reentrant Ventricular Tachycardia Originating from the Aortic Sinus Cusp:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2004A Case Report We report a case of idiopathic reentrant ventricular tachycardia (VT) originating from the left aortic sinus cusp. A prepotential preceding the QRS complex by 58 ms was recorded from the posterior right ventricular (RV) outflow tract. During VT entrainment observed by pacing from the midseptal RV, it initially was orthodromically captured with a long conduction time but then antidromically captured as the pacing cycle rate was increased. Pacing at that site failed to show concealed entrainment despite a postpacing interval similar to the VT cycle length. Radiofrequency catheter ablation abolished the VT in the left aortic sinus cusp where a prepotential preceding the QRS complex by 78 ms with a postpacing interval similar to the VT cycle length was recorded in addition to concealed entrainment. The findings suggest that, in this VT, a critical slow conduction zone is partially present extending from the left aortic sinus cusp to the posterior right ventricular outflow tract. The patient has remained free from VT recurrence after 5-month follow-up. [source] Aging-Related Increase to Inducible Atrial Fibrillation in the Rat ModelJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2002HIDEKI HAYASHI M.D. Aging and Atrial Fibrillation.Introduction: Aging is associated with atrial interstitial fibrosis and increased incidence of atrial fibrillation (AF). We hypothesized that aged rats are suitable for study of aging-related AF and that partial atrial cellular uncoupling induced with heptanol in young rats mimics aging-related AF. Methods and Results: Interatrial conduction time and atrial response to burst atrial pacing were evaluated in 11 young (2,3 months) and 12 old (22,24 months) male rats (Fisher 344) in the Langendorff-perfused setting. At baseline, sustained (>30 sec) atrial tachycardia (AT) and AF were induced in 10 of 12 and in 7 of 12 old rats, respectively. No such arrhythmias could be induced in the young rats. Old rats had significantly (P < 0.01) longer interatrial conduction time and P wave durations than the young rats. Burst pacing failed to induce AT and AF in all 11 young rats studied. The effects of heptanol 2 to 10 ,M were studied in both groups. Heptanol 2 to 5 ,M promoted inducible AT in all 5 young rats studied; however, when its concentration was raised to 10 ,M, AT could no longer be induced in any of the 5 young rats. No AF could be induced in any of the 5 young rats at heptanol concentrations of 2 to 10 ,M. In the old rats, AF could still be induced during perfusion of 2 ,M heptanol. However, when its concentration was raised to 5 and 10 ,M, AF could not be induced in any of the 6 old rats studied. Optical mapping using a potentiometric dye showed a periodic single wavefront of activation during AT in both groups and 2 to 4 independent wavefronts propagating in different directions during AF in the old rats. Histology revealed a significant increase in interstitial atrial fibrosis (P < 0.01), atrial cell size (P < 0.05), and heart weight in old versus young rats. Fibrosis in the old rats was highly heterogeneous. Conclusion: The rat model is suitable for study of aging-related AF. Uniform partial atrial cellular uncoupling with heptanol perfusion in the young rats, although promoting inducible AT, does not mimic aging-related AF. The results suggest that heterogeneous atrial interstitial fibrosis and atrial cell hypertrophy might contribute to the aging-related increase in atrial conduction slowing, conduction block, and inducible AF in the old rat model. [source] Altered Motor Cortex Excitability to Magnetic Stimulation in Alcohol Withdrawal SyndromeALCOHOLISM, Issue 4 2010Raffaele Nardone Background:, Alcohol addiction is a complex brain disease caused by alterations in crucial neurotransmitter systems, including gamma-aminobutyric acid (GABA) and glutamate. These disturbances could be revealed by changes in cortical excitability parameters, as assessed by transcranial magnetic stimulation (TMS). This study was aimed to further investigate the complex pathophysiology of alcohol withdrawal syndrome (AWS). Methods:, Motor cortex excitability was examined in 13 subjects with AWS in a mild predelirial state, in 12 chronic alcoholics and in 15 age-matched control subjects, using a range of TMS protocols. Central motor conduction time, resting and active motor threshold, duration of the cortical silent period, short latency intracortical inhibition (SICI), and intracortical facilitation (ICF) to paired TMS were examined. Results:, Intracortical facilitation was significantly increased in the AWS patients when compared with the chronic alcoholics and the control subjects. The other TMS parameters did not differ significantly from the controls. Administration of a single oral dose of the glutamatergic antagonist riluzole in a subgroup of 8 patients significantly reduced ICF; motor threshold and SICI were not affected by riluzole. Conclusion:, Transcranial magnetic stimulation shows a selective increase in intracortical facilitation after ethanol withdrawal. Our findings support the theory that altered glutamatergic receptor function plays an important role in the pathogenesis of human alcohol withdrawal. This study provides further physiological evidence that antiglutamatergic approaches represent an efficacious alternative for treating alcohol withdrawal symptoms. [source] Characterization of the Acute Cardiac Electrophysiologic Effects of Ethanol in DogsALCOHOLISM, Issue 9 2007Guilherme Fenelon Background: Alcohol has been related to atrial fibrillation (holiday heart syndrome), but its electrophysiologic actions remain unclear. Methods: We evaluated the effects of alcohol in 23 anesthetized dogs at baseline and after 2 cumulative intravenous doses of ethanol: first dose 1.5 ml/kg (plasma level 200 mg/dl); second dose 1.0 ml/kg (279 mg/dl). In 13 closed-chest dogs (5 with intact autonomic nervous system, 5 under combined autonomic blockade and 3 sham controls), electrophysiologic evaluation and monophasic action potential (MAP) recordings were undertaken in the right atrium and ventricle. In 5 additional dogs, open-chest biatrial epicardial mapping with 8 bipoles on Bachmann's bundle was undertaken. In the remaining 5 dogs, 2D echocardiograms and ultrastructural analysis were performed. Results: In closed-chest dogs with intact autonomic nervous system, ethanol had no effects on surface electrocardiogram and intracardiac variables. At a cycle length of 300 milliseconds, no effects were noted on atrial and ventricular refractoriness and on the right atrial MAP. These results were not altered by autonomic blockade. No changes occurred in sham controls. In open-chest dogs, ethanol did not affect inter-atrial conduction time, conduction velocity, and wavelength. Atrial arrhythmias were not induced in any dog, either at baseline or after ethanol. Histological and ultrastructural findings were normal but left ventricular (LV) ejection fraction decreased in treated dogs (77 vs. 73 vs. 66%; p = 0.04). Conclusion: Ethanol at medium and high doses depresses LV systolic function but has no effects on atrial electrophysiological parameters. These findings suggest that acute alcoholic intoxication does not directly promote atrial arrhythmias. [source] Sensitivity of electrophysiological tests for upper and lower motor neuron dysfunction in ALS: A six-month longitudinal studyMUSCLE AND NERVE, Issue 2 2010Mamede de Carvalho MD Abstract By following a group of amyotrophic lateral sclerosis (ALS) patients longitudinally using lower motor neuron (LMN) and upper motor neuron (UMN) markers of dysfunction it may be possible to better understand the functional relationships between these motor systems in this disease. We used neurophysiological techniques to follow UMN and LMN dysfunction in a group of 28 patients with ALS, in comparison with the ALS functional rating scale (ALS-FRS) score and the forced vital capacity (FVC). We used motor unit number estimation (MUNE), compound muscle action potential (CMAP) amplitude, and the Neurophysiological Index (NI) to quantify the LMN disorder, and transcranial motor stimulation to study cortical motor threshold, motor-evoked response amplitude, central motor conduction time, and cortical silent period (CSP). The patients were studied shortly after diagnosis and then 6 months later, using both abductor digiti minimi muscles (ADM); ADM strength was initially >MRC 3 (Medical Research Council, UK). The NI and MUNE changed more than any other variable. CSP increased by about 30%, a change more marked than the slight increase observed in the cortical motor threshold (9%). The normal increase of CSP after acute muscle fatigue was preserved during disease progression. The CSP increase correlated with the MUNE rate of decay but not to the NI reduction, perhaps because NI includes F-wave frequency in itscalculation. There was no definite correlation between UMN and LMNdysfunction or progression, but there was a link between CSP and LMN changes in ALS. The CSP may be a useful variable in following UMN dysfunction in clinical practice and in clinical trials. Muscle Nerve, 2010 [source] Clinical electrophysiological characterization of the acquired neuromyotonia phenotype of autoimmune peripheral nerve hyperexcitabilityMUSCLE AND NERVE, Issue 6 2006Paul Maddison MD Abstract Acquired autoimmune neuromyotonia is regarded as part of the spectrum of peripheral nerve hyperexcitability disorders. We aimed to use clinical neurophysiological measurements to study the extent, distribution, and characteristics of spontaneous motor unit potentials in 11 patients with acquired neuromyotonia. Investigations revealed that most spontaneous discharges recorded were motor unit, or partial motor unit potentials of normal size. Bursts of motor unit potentials arose more commonly from distal portions of the peripheral nerve and had abnormal absolute and relative refractory periods. Spontaneous discharges in some patients occurred in semirhythmic bursts in certain muscles. No patient had neurophysiological abnormalities detectable in first-order neurons of the central nervous system when using transcranial magnetic stimulation to estimate the threshold for corticomotor excitation and determine central motor conduction time. Only patients with coexistent myasthenia gravis had neurophysiologically detectable defects in neuromuscular transmission. The pathogenic region of abnormality in peripheral nerve hyperexcitability disorders therefore seems to lie within the terminal branches of peripheral motor nerves. Muscle Nerve, 2006 [source] Activation Sequence Modification During Cardiac Resynchronization by Manipulation of Left Ventricular Epicardial Pacing Stimulus StrengthPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2007USHA B. TEDROW M.D. Background: Success of cardiac resynchronization therapy (CRT) depends on altering electrical ventricular activation (VA) to achieve mechanical benefit. That increases in stimulus strength (SS) can affect VA has been demonstrated previously in cardiomyopathy patients undergoing ablation. Objective: To determine whether increasing SS can alter VA during CRT. Methods: In 71 patients with CRT devices, left ventricle (LV) pacing was performed at escalating SS. Timing from pacing stimulus to right ventricular (RV) electrogram, ECG morphology, and maximal QRS duration on 12 lead ECG were recorded. Results: Demographics: Baseline QRS duration 153 ± 25 ms, ischemic cardiomyopathy 48%, ejection fraction 24%± 7%. With increased SS, conduction time from LV to right ventricle (RV) decreased from 125 ± 56 ms to 111 ± 59 ms (P = 0.006). QRS duration decreased from 212 ± 46 ms to 194 ± 42 ms (P = 0.0002). A marked change in QRS morphology occurred in 11/71 patients (15%). The RV ring was the anode in 6, while the RV coil was the anode in 5. Sites with change in QRS morphology showed decrease in conduction time from LV to RV from 110 ± 60 ms to 64 ± 68 ms (P = 0.04). Twelve patients (16%) had diaphragmatic stimulation with increased SS. Conclusions: Increasing LV SS reduces QRS duration and conduction time from LV to RV. Recognition of significant QRS morphology change is likely clinically important during LV threshold programming to avoid unintended VA change. [source] Can Simple Doppler Measurements Estimate Interatrial Conduction Time?PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003DRAGOS COZMA COZMA, D., et al.: Can Simple Doppler Measurements Estimate Interatrial Conduction Time?Prolongation of the interatrial conduction time (ia-CT) is considered an important factor in the pathophysiology of atrial fibrillation (AF) and as a criterion to perform multisite atrial pacing. Measurement of ia-CT requires an electrophysiologic study. The aim of this study was to compare echocardiographic with electrophysiologic measurements to determine if they are correlated. Methods and Results: The study included 32 consecutive patients who underwent electrophysiologic studies. We measured ia-CT between the high right atrium and the distal coronary sinus. In all patients we measured P wave duration, left atrial diameter and area, and ia-CT by Doppler echocardiography was measured as the difference in time intervals between the QRS onset and the tricuspid A wave, and the QRS onset and the mitral A wave (DT). Ia-CT was statistically correlated with DT(r = 0.79, P < 0.0001), but not with P wave duration or left atrial dimensions. Conclusions: Measurement DT may be reliable to estimate ia-CT without invasive procedure. Accordingly, DT could be used as a simple selection criterion when considering patients for atrial resynchronization therapy. (PACE 2003; 26[Pt. II]:436,439) [source] Clinical Significance of the Atrial Fibrillation Threshold in Patients with Paroxysmal Atrial FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2001KEIJI INOUE INOUE, K., et al.: Clinical Significance of the Atrial Fibrillation Threshold in Patients with Paroxysmal Atrial Fibrillation. AF threshold and the other electrophysiological parameters were measured to quantify atrial vulnerability in patients with paroxysmal atrial fibrillation (PAF, n = 47), and those without AF (non-PAF, n = 25). Stimulations were delivered at the right atrial appendage with a basic cycle length of 500 ms. The PAF group had a significantly larger percentage of maximum atrial fragmentation (%MAF, non-PAF: mean ± SD = 149 ± 19%, PAF: 166 ± 26%, P = 0.009), fragmented atrial activity zone (FAZ, non-PAF: median 0 ms, interquartile range 0,20 ms, PAF: 20 ms, 10,40 ms, P = 0.008). Atrial fibrillation threshold (AF threshold, non-PAF: median 11 mA, interquartile range 6,21 mA, PAF: 5 mA, 3,6 mA, P < 0.001) was smaller in the PAF group than in the non-PAF group. Sensitivity, specificity, and positive predictive value of electrophysiological parameters were as follows, respectively: %MAF (cut off at 150%, 78%, 52%, 76%), FAZ (cut off at 20 ms, 47%, 84%, 85%), AF threshold (cut off at 10 mA, 94%, 60%, 81%). There were no statistically significant differences between the non-PAF and PAF groups in the other parameters (effective refractory period, interatrial conduction time, maximum conduction delay, conduction delay zone, repetitive atrial firing zone, wavelength index), that were not specific for PAF. In conclusion, the AF threshold could be a useful indicator to evaluate atrial vulnerability in patients with AF. [source] Prevention of the Initiation of Atrial Fibrillation: Mechanism and Efficacy of Different Atrial Pacing ModesPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2000WEN-CHUNG YU Several atrial pacing modes have been reported to be effective in the prevention of atrial fibrillation (AF); they included biatrial pacing, dual site right atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus pacing. However, the relative efficacy and electrophysiological mechanisms of these pacing modes in the prevention of AF are not clear. In 15 patients (age 54 ± 14 years) with paroxysmal AF, P wave duration, effective refractory period, and atrial conduction time were determined with six different atrial drive pacings, that were right atrial appendage (RAA), BB, right posterior interatrial septum (RPS), distal coronary sinus (DCS), RAA plus RPS simultaneously (DSA), and RAA plus DCS simultaneously (BiA). All these patients consistently had AF induced with early RAA extrastimulation coupling to RAA drive pacing. No patient had AF induced with RAA extrastimulation coupled to BB, RPS, or DCS drive pacing, but seven and eight patients had AF induced with RAA extrastimulation coupled to DSA and BiA drive pacing, respectively. The P wave duration was longest during RAA pacing, and became shorter during other atrial pacing modes. Analysis of electrophysiological change showed that early RAA extrastimulation coupled to RAA drive pacing caused the longest atrial conduction delay among these atrial pacing modes; BB, RPS, and DCS drive pacing caused a greater reduction of this conduction delay than DSA and BiA drive pacing. In addition, the effective refractory periods of RAA determined with BB, RPS, and DCS drive pacing were similar and longer than that determined with DSA and BiA drive pacing. In patients with paroxysmal AF, this arrhythmia was readily induced with RAA extrastimuli coupled to RAA drive pacing. BB, RPS, and DCS pacing were similar and more effective than DSA and BiA pacing in preventing AF. [source] Preserving Normal Ventricular Activation Versus Atrioventricular Delay Optimization During Pacing: The Role of Intrinsic Atrioventricular Conduction and Pacing RatePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2000IVAN ILIEV ILIEV The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 ± 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal A V delay in the DDD mode and comparison between AAI and DDD with optimal A V delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (AHI) was 282 ± 68 ms for rate 70/min and 330 ± 98 ms for rate 90/min (P < 0.01). The optimal A V delay was 159 ± 22 ms, A V delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16%± 9%. At rate 70/min the patients with ARI , 270 ms had higher AFTVI in AAI than in DDD (0.214 ± 0.05 m vs 0.196 ± 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI(0.192 ± 0.03 m vs 0.166 ± 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 ± 0.03 m vs 0.162 ± 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 ± 0.05 m vs 0.173 ± 0.05 mP < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 ± 0.05 m vs 0.158 ± 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate. [source] P-Wave Dispersion: A Novel Predictor of Paroxysmal Atrial FibrillationANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2001Polychronis E. Dilaveris M.D. Background: The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (AF). Previous studies have demonstrated that individuals with a clinical history of paroxysmal AF show a significantly increased P-wave duration in 12-lead surface electrocardiograms (ECG) and signal-averaged ECG recordings. Methods: The inhomogeneous and discontinuous atrial conduction in patients with paroxysmal AF has recently been studied with a new ECG index, P-wave dispersion. P-wave dispersion is defined as the difference between the longest and the shortest P-wave duration recorded from multiple different surface ECG leads. Up to now the most extensive clinical evaluation of P-wave dispersion has been performed in the assessment of the risk for AF in patients without apparent heart disease, in hypertensives, in patients with coronary artery disease and in patients undergoing coronary artery bypass surgery. P-wave dispersion has proven to be a sensitive and specific ECG predictor of AF in the various clinical settings. However, no electrophysiologic study has proven up to now the suspected relationship between the dispersion in the atrial conduction times and P-wave dispersion. The methodology used for the calculation of P-wave dispersion is not standardized and more efforts to improve the reliability and reproducibility of P-wave dispersion measurements are needed. Conclusions: P-wave dispersion constitutes a recent contribution to the field of noninvasive electrocardiology and seems to be quite promising in the field of AF prediction. A.N.E. 2001;6(2):159,165 [source] A Review of HNS-32: A Novel Azulene-l-Carboxamidine Derivative with Multiple Cardiovascular Protective ActionsCARDIOVASCULAR THERAPEUTICS, Issue 4 2001Yoshio Tanaka ABSTRACT HNS-32 [N1,N1 -dimethyl- N2 -(2-pyridylmethyl)-5-isopropyl-3,8-dimethylazulene-1-carboxamidine] (CAS Registry Number: 186086-10-2) is a newly synthesized azulene derivative. Computer simulation showed that its three dimensional structure is similar to that of the class Ib antiarrhythmic drugs, e.g., lidocaine or mexiletine. HNS-32 potently suppressed ventricular arrhythmias induced by ischemia due to coronary ligation and/or ischemia-reperfusion in dogs and rats. In the isolated dog and guinea pig cardiac tissues, HNS-32 had negative inotropic and chronotropic actions, prolonged atrial-His and His-ventricular conduction time and increased coronary blood flow. In the isolated guinea pig ventricular papillary muscle, HNS-32 decreased maximal rate of action potential upstroke (V,max) and shortened action potential duration (APD). These findings suggest that HNS-32 inhibits inward Na+ and Ca2+ channel currents. In the isolated pig coronary and rabbit conduit arteries, HNS-32 inhibited both Ca2+ channel-dependent and -independent contractions induced by a wide variety of chemical stimuli. HNS-32 is a potent inhibitor of protein kinase C (PKC)-mediated constriction of cerebral arteries. It is likely to block both, Na+ and Ca2+ channels expressed in cardiac and vascular smooth muscles. These multiple ion channel blocking effects are largely responsible for the antiarrhythmic and vasorelaxant actions of HNS-32. This drug may represent a novel approach to the treatment of arrhythmias. [source] Development of the corticospinal system and hand motor function: central conduction times and motor performance testsDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 4 2000U M Fietzek Maturation of the corticospinal (CS) tract and hand motor function provide paradigms for central nervous system development. In this study, involving 112 participants (aged from 0.2 to 30 years), we evaluated central motor conduction times (CMCT) obtained with transcranial magnetic stimulation (TMS) during preinnervation conditions of facilitation and relaxation. Auditory reaction time, velocity of a ballistic movement of the arm, finger tapping, diadochokinesis, and fine motor visuomanual tracking were also examined. The maturation profiles for every parameter were calculated. CMCTs for the different preinnervation conditions reached adult values at different times and this could be explained by maturation of excitability at the cortical and spinal level. A stable phase for CMCTs and reaction time was reached during childhood. Parameters which measured motor speed and skill indicated that the development of these continued into adulthood. The maturation of the fast CS tract seems to be completed before the acquisition of the related motor performance has been accomplished. In conclusion, we could demonstrate that data from several neurophysiological methods can be combined and used to study the maturation of the function of the nervous system. This approach could allow appraisal of pathological conditions that show parallels with omissions or lack of developmental progress. [source] Magnetically evoked motor potentials in demyelinating and axonal polyneuropathy: a comparative studyEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2000H. Takada We investigated the value of magnetically evoked motor potentials (MEPs) for the differentiation of demyelinating and axonal polyneuropathies. The study population comprised 107 patients, with polyneuropathy verified by electromyography (EMG) and nerve conduction study (NCS), who had also been examined by means of MEP. MEPs were evoked by magnetic stimulation of the cortex and the spinal roots and were recorded from three upper limb muscles and two lower limb muscles bilaterally. From the EMG/NCS results 53 patients were characterized as having primary demyelination (demyelinating patients) and 54 as having axonal involvement (axonal patients). Demyelinating patients were classified as acute (acute inflammatory demyelinating polyradiculoneuropathy: AIDP ) or chronic (chronic inflammatory demyelinating polyradiculoneuropathy: CIDP ) according to the duration of illness. A series of indices were calculated from MEP results. One demyelinating patient and two axonal patients had normal MEPs. The MEPs of the demyelinating patients showed significantly longer peripheral conduction times, larger interside differences and lower amplitudes than the axonal patients. The central conduction index and the amplitudes upon cortical stimulation were significantly higher in patients with CIDP than in those with AIDP. Peripheral conduction time prolonged by more than 85% in at least one of the 10 muscles studied or a peripheral conduction index of above 9.4 were pathognomonic for demyelination . By combining all criteria 75% of the patients could be categorized as CIDP vs. AIDP in accordance with the EMG/NCS diagnosis. Likewise, 83% were categorized correctly as demyelinating versus axonal according to the EMG/NCS data. [source] Sympathetic control of short-term heart rate variability and its pharmacological modulationFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2007Jean-Luc Elghozi Abstract The static relationship between heart rate (HR) and the activity of either vagal or sympathetic nerves is roughly linear within the physiological range of HR variations. The dynamic control of HR by autonomic nerves is characterized by a fixed time delay between the onset of changes in nerve activity and the onset of changes in HR. This delay is much longer for sympathetically than for vagally mediated changes in HR. In addition, the kinetics of the HR responses shows the properties of a low-pass filter with short (vagal) and long (sympathetic) time constants. These differences might be secondary to differences in nervous conduction times, width of synaptic cleft, kinetics of receptor activation and post-receptor events. Because of the accentuated low-pass filter characteristics of the HR response to sympathetic modulation, sympathetic influences are almost restricted to the very-low-frequency component of HR variability, but the chronotropic effects of vagal stimulation usually predominate over those of sympathetic stimulation in this frequency band. Oscillations in cardiac sympathetic nerve activity are not involved in respiratory sinus arrhythmia (high-frequency component) and make a minor contribution to HR oscillations of approximately 10-s period (low-frequency component of approximately 0.1 Hz), at least in the supine position. In the latter case, HR oscillations are derived mainly from a baroreflex, vagally mediated response to blood pressure Mayer waves. Beta-blockers and centrally acting sympathoinhibitory drugs share the ability to improve the baroreflex control of HR, possibly through vagal facilitation, which might be beneficial in several cardiovascular diseases. [source] Increased Right Ventricular Repolarization Gradients Promote Arrhythmogenesis in a Murine Model of Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2010CLAIRE A. MARTIN M.R.C.P. Repolarization Gradients in Brugada Syndrome.,,Introduction: Brugada syndrome (BrS) is associated with loss of Na+ channel function and increased risks of a ventricular tachycardia exacerbated by flecainide but reduced by quinidine. Previous studies in nongenetic models have implicated both altered conduction times and repolarization gradients in this arrhythmogenicity. We compared activation latencies and spatial differences in action potential recovery between different ventricular regions in a murine Scn5a+/, BrS model, and investigated the effect of flecainide and quinidine upon these. Methods and Results: Langendorff-perfused wild-type and Scn5a+/, hearts were subjected to regular pacing and a combination of programmed electrical stimulation techniques. Monophasic action potentials were recorded from the right (RV) and left ventricular (LV) epicardium and endocardium before and following flecainide (10 ,M) or quinidine (5 ,M) treatment, and activation latencies measured. Transmural repolarization gradients were then calculated from the difference between neighboring endocardial and epicardial action potential durations (APDs). Scn5a+/, hearts showed decreased RV epicardial APDs, accentuating RV, but not LV, transmural gradients. This correlated with increased arrhythmic tendencies compared with wild-type. Flecainide increased RV transmural gradients, while quinidine decreased them, in line with their respective pro- and antiarrhythmic effects. In contrast, Scna5+/, hearts showed slowed conduction times in both RV and LV, exacerbated not only by flecainide but also by quinidine, in contrast to their differing effects on arrhythmogenesis. Conclusion: We use a murine genetic model of BrS to systematically analyze LV and RV action potential kinetics for the first time. This establishes a key role for accentuated transmural gradients, specifically in the RV, in its arrhythmogenicity. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1153-1159) [source] Autonomic Blockade Unmasks Maturational Differences in Rate-Dependent Atrioventricular Nodal Conduction and Facilitation in the MouseJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2003SAMIR SABA M.D. Maturational Differences in Murine AVN Conduction. Introduction: In large animals, rate-dependent AV nodal (AVN) properties of conduction are modulated by autonomic inputs. In this study, we investigated whether the properties of AVN conduction and facilitation are altered by autonomic blockade in the mouse and whether this effect is age dependent. Methods and Results: Young (age 4,6 weeks; n = 11) and adult (age 8,9 months; n = 11) female mice underwent in vivo electrophysiologic testing, before and after autonomic blockade. After autonomic blockade, the adult mice had significantly longer AVN effective refractory period (AVNERP; 67 ± 14 msec vs 56 ± 4 msec, P = 0.05) and functional refractory period (AVNFRP; 81 ± 10 msec vs 72 ± 4 msec, P = 0.05). With autonomic blockade, the increase from baseline of AVN Wenckebach cycle length (,AVW; 1.8 ± 8.1 msec vs 8.8 ± 3.3 msec, P = 0.04), as well as of AVNERP (,AVNERP; 3.5 ± 3.5 msec vs 21.4 ± 12.6 msec, P = 0.002) and AVNFRP (,AVNFRP; 2.3 ± 3.2 msec vs 12.8 ± 9.0 msec, P = 0.008), was significantly larger in adult than in young mice. Compared with young mice, adult mice were less likely to exhibit AVN facilitation (44% vs 90%, P = 0.03) and had smaller maximal shortening of AVN conduction times after the "test beat" for any coupling of the "facilitating beat" (4 ± 4 msec vs 7 ± 3 msec, P = 0.05). Conclusion: Complete autonomic blockade significantly increases AVN conduction times and refractory periods in adult but not in young mice. Adult mice also exhibit less AVN facilitation. Our results confirm that, like in larger animals, rate-dependent murine AVN properties of conduction are under autonomic regulation. Adult mice have higher sympathetic AVN inputs at baseline, leading to slower conduction after autonomic blockade. (J Cardiovasc Electrophysiol, Vol. 14, pp. 191-195, February 2003) [source] Mild carbon monoxide exposure and auditory function in the developing ratJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2003Janet E. Stockard-Sullivan Abstract We have examined the influence of chronic mild exposure to carbon monoxide (CO) on cognitive (learning) and auditory function in the developing rat. We have demonstrated that the auditory pathway is compromised at exposures less than 50 ppm, whereas learning was not influenced at 100 ppm. Artificially reared rat pups were exposed to CO during the brain growth spurt and onset of myelination. Spatial learning was assessed using the Morris Water Maze and three tests of auditory function: (1) auditory brainstem conduction times; (2) the amplitude of the eighth nerve's action potential; and (3) otoacoustic emissions carried out on rat pups (age 22, 24 days). The pups were gastrostomy-reared on a rat milk substitute and chronically exposed to CO at discrete concentrations in the range of 12,100 ppm from 6 days of age to post-weaning at 21,23 days of age. We found no difference in auditory brainstem conduction times at all CO concentrations in comparison to non-exposed controls. There was a difference in otoacoustic emissions for test and controls at CO concentrations of 50 ppm but not at lower concentrations. There was a consistent attenuation of the amplitude of the eighth nerve's action potential, even at the lowest CO exposure examined. The attenuation of the amplitude of the action potential of the eighth nerve at 50 ppm carbon monoxide exposure did not completely recover by 73 days of age. We conclude that prolonged mild exposure to carbon monoxide during development causes measurable functional changes at the level of the eighth cranial nerve. © 2003 Wiley-Liss, Inc. [source] | |||||||||||||||||||||||||||||||