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Rabbit Hearts (rabbit + heart)

Distribution by Scientific Domains

Medical Sciences	76%
Life Sciences	19%

Kinds of Rabbit Hearts

Langendorff-perfuse rabbit heart

Selected Abstracts

Effects of Direct Sympathetic and Vagus Nerve Stimulation on the Physiology of the Whole Heart , A Novel Model of Isolated Langendorff Perfused Rabbit Heart with Intact Dual Autonomic Innervation

EXPERIMENTAL PHYSIOLOGY, Issue 3 2001
G. André Ng
A novel isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation is described. This preparation allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. These hearts (n= 10) had baseline heart rates of 146 ± 2 beats min,1 which could be increased to 240 ±11 beats min,1 by sympathetic stimulation (15 Hz) and decreased to 74 ± 11 beats min,1 by stimulation of the vagus nerve (right vagus, 7 Hz). This model has the advantage of isolated preparations, with the absence of influence from circulating hormones and haemodynamic reflexes, and also that of in vivo preparations where direct nerve stimulation is possible without the need to use pharmacological agents. Data are presented characterising the preparation with respect to the effects of autonomic nerve stimulation on intrinsic heart rate and atrioventricular conduction at different stimulation frequencies. We show that stimulation of the right and left vagus nerve have differential effects on heart rate and atrioventricular conduction. [source]

Heterogeneity of Ventricular Fibrillation Dominant Frequency During Global Ischemia in Isolated Rabbit Hearts

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2007
Ch.B. , JANE CALDWELL M.B.
Introduction: Ventricular fibrillation (VF) studies show that ECG-dominant frequency (DF) decreases as ischemia develops. This study investigates the contribution of the principle ischemic metabolic components to this decline. Methods and Results: Rabbit hearts were Langendorff-perfused at 40 mL/min with Tyrode's solution and loaded with RH237. Epicardial optical action potentials were recorded with a photodiode array (256 sites, 15 × 15 mm). After 60 seconds of VF (induced by burst pacing), global ischemia was produced by low flow (6 mL/min), or the solution changed to impose hypoxia (95% N2/5% CO2), low pHo (6.7, 80% O2/20% CO2), or raised [K+]o (8 mM). DF of the optical signals was determined at each site. Conduction velocity (CV), action potential duration (APD90), effective refractory period (ERP), activation threshold, dV/dtmax, and membrane potential were measured in separate experiments during ventricular pacing. During VF, ischemia decreased DF in the left ventricle (LV) (to [58 ± 6]%, P < 0.001), but not the right (RV) ([93 ± 5]%). Raised [K+]o reproduced this DF pattern (LV: [67 ± 12]%, P < 0.001; RV: [95 ± 9]%). LV DF remained elevated in hypoxia or low pHo. During ventricular pacing, ischemia decreased CV in LV but not RV. Raised [K+]o did not change CV in either ventricle. Ischemia and raised [K+]o shortened APD90 without altering ERP. LV activation threshold increased in both ischemia and raised [K+]o and was associated with diastolic depolarization and decreased dV/dtmax. Conclusions: These results suggest that during VF, decreased ECG DF in global ischemia is largely due to elevated [K+]o affecting the activation thresholds in the LV rather than RV. [source]

Sex Modulates the Arrhythmogenic Substrate in Prepubertal Rabbit Hearts with Long QT 2

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2005
Ph.D., TONG LIU M.D.
Females have a greater susceptibility to Torsade de Pointes in congenital and drug-induced long QT syndrome (LQTS) that has been attributed to the modulation of ion channel expression by sex hormones. However, little is known regarding sex differences in pre-puberty, that is, before the surge of sexual hormones. In patients with congenital LQTS types 1 and 2, male children tend to have a greater occurrence of adverse events, especially in 10,15 year olds, than their female counterpart. To evaluate whether the rabbit model of drug-acquired LQTS exhibits similar age dependences, hearts of prepubertal rabbits were perfused, mapped optically to record action potentials (APs) and treated with an IKr blocker, E4031 to elicit LQTS2. As expected, AP durations (APD) were significantly longer in female (n = 18) than male hearts (n = 10), at long cycle length. Surprisingly, E4031 (50,250 nM) induced a greater prolongation of APDs in male than in female hearts, and in both genders reversed the direction of repolarization (apex , base to base , apex), enhancing dispersions of repolarization. Furthermore, in male hearts, E4031 (0.5 ,M) elicited early afterdepolarizations (EADs) that progressed to polymorphic ventricular tachycardia (PVT) (n = 7/10) and were interrupted by isoproterenol (40 nM) and prevented by propranolol (0.5,2.5 ,M). In female hearts, E4031 (0.5 ,M) produced marked prolongations of APDs yet few EADs with no progression to PVT (n = 16/18). Thus, sex differences are opposite in prepubertal versus adult rabbits with respect to E4031-induced APD prolongation, EADs and PVT, underscoring the fact that APD prolongation alone is insufficient to predict arrhythmia susceptibility. [source]

Heterogeneity of Ventricular Fibrillation Dominant Frequency During Global Ischemia in Isolated Rabbit Hearts

Development of an Optrode for Intramural Multisite Optical Recordings of Vm in the Heart

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2003
JONATHAN L. BYARS M.S.
Introduction: Optical mapping of transmembrane potential (Vm) is an important tool in the investigation of impulse propagation in the heart. It provides valuable information about spatiotemporal changes of Vm that cannot be obtained by other techniques, but it presently is limited to measurements from the heart surfaces. Therefore, the goal of this work was to develop a technique for intramural multisite optical measurements of Vm using fiberoptic technology. Methods and Results: An optrode, a bundle of thin optical fibers, was developed for measuring intramural optical signals at multiple sites in the heart. The optrode consisted of seven fibers with diameter of 225 ,m arranged in a hexagonal pattern that were used to deliver excitation light to the myocardium, to collect the emitted fluorescence, and to project the light onto a 16 × 16 array of photodiode detectors. Rabbit hearts were stained with the Vm -sensitive dye RH-237. Fluorescence was excited using a 100-W Hg lamp. Intramural action potentials were recorded at multiple sites separated by 2 mm inside the left ventricle. Signal-to-noise (RMS) ratio was 21.2 ± 12 (n = 7) without averaging or ratiometry and with negligible cross-talk (<1.9%) between the neighboring photodiodes. The size of the recording area for an individual fiber was estimated at approximately 0.8 mm. Conclusion: These data demonstrate feasibility of multisite transmural measurements of Vm without signal averaging and ratiometry. This technique might become useful in studies of transmural impulse conduction during arrhythmias and defibrillation. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1196-1202, November 2003) [source]

Effect of Action Potential Duration and Conduction Velocity Restitution and Their Spatial Dispersion on Alternans and the Stability of Arrhythmias

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2002
ISABELLE BANVILLE Ph.D.
Restitution and Spatial Heterogeneities vs Arrhythmias.Introduction: The slope of the action potential duration (APD) restitution curve has been used to explain wavebreaks during arrhythmia initiation and maintenance. This hypothesis remains incomplete to fully describe the experimental data. Other factors contributing to wavebreaks must be studied to further understand arrhythmia dynamics. Methods and Results: Control APDs were measured from isolated rabbit hearts using a monophasic action potential probe. APD and conduction velocity (CV) restitution were quantified over the heart surface for two drugs, diacetyl monoxime (DAM) and cytochalasin D (CytoD), using a dual camera video imaging system. For all pacing intervals: (1) control APDs were shorter than for CytoD but longer than for DAM; and (2) CV was greater for CytoD compared with DAM. APD dispersion increased as pacing interval decreased for both drugs. For DAM, increased dispersion was due to a difference in APD restitution between the right and left ventricle. For CytoD, increased dispersion was due to discordant alternans, with no significant spatial variation in restitution. Fibrillation was sustained only in the control hearts; with DAM, stable reentry was sustained with shorter APD and cycle length compared with CytoD for which only nonsustained unstable reentry occurred. Conclusion: Alternans and arrhythmia dynamics are affected by the spatial dispersion of APD restitution as well as CV restitution, not simply the slope of APD restitution. Therefore, a direct link of the APD restitution slope to alternans and arrhythmia dynamics in rabbit heart does not exist. Designing antiarrhythmic drugs to alter only the restitution slope may not be appropriate. [source]

Pharmacological studies on siculine syrup.

PHYTOTHERAPY RESEARCH, Issue 2 2009
II: effects on smooth, cardiovascular muscle preparations, skeletal
Abstract Earlier pharmacological screening showed that siculine syrup (a traditional herbal remedy purported to be useful in the prevention and treatment of sickle cell pain , crises, due to sickle cell anaemia , SCA) had antisickling and analgesic activities as well as antimicrobial and diuretic effects. SCA is an important haemoglobinopathy in Africa and many other communities/countries worldwide, with relatively high morbidity and mortality. The present study was to determine the effects of the extract on various isolated muscle preparations , smooth, skeletal and cardiovascular. Siculine (4,20 µg/mL), like acetylcholine (40,400 µg/mL), contracted the isolated rat uterus concentration dependently. Similar effects were observed with the guinea-pig ileum and rabbit jejunum (2,20 µg/mL). In contrast to these effects, the direct (muscle) and indirect (nerve) stimulations of rat phrenic nerve,diaphragm were relaxed by siculine (4 and 8 µg/mL) and d -tubocurarine (0.8 µg/mL). Siculine also concentration-dependently decreased both the rate and force of contraction of guinea-pig atria and rabbit heart and also resulted in a fall in cat blood pressure in a manner similar to those of acetylcholine. The possible therapeutic and/or toxicological consequences of these effects including the hypotensive activity is noteworthy since siculine syrup is used by the local population for the prevention and treatment of sickle cell pain crises. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Three-dimensional anatomy of the conduction system of the early embryonic rabbit heart

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2006
Florence Rothenberg
Abstract The complete embryonic cardiac conduction system is difficult to view in three dimensions, primarily because there has not been a marker of all segments of the normal system throughout all stages of development. Imaging of the conduction system components within the atria has been particularly controversial because different markers reveal different pathways that may or may not represent conduction system components. The conduction system of the adult and embryonic rabbit, however, can be labeled in its entirety with the neurofilament marker, NF-160. The conduction system of rabbit embryos at several stages of development spanning cardiac septation was therefore investigated. Optical mapping of the electrical signature of the conduction system previously revealed a close correlation between the cardiac activation patterns and the anatomy as shown by serial sections. The 3D relationship between the components of the conduction system could only be inferred from the 2D sections. The sections were consequently reconstructed using a commercial software program (AutoQuant). This is the first demonstration of the three-dimensional complete normal rabbit embryonic cardiac conduction system at several stages of development. © 2005 Wiley-Liss, Inc. [source]

Fatty acid metabolism assessed by 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume-overloaded hearts

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2004
T. Miyamoto
Abstract Background, The peroxisome proliferator-activated receptor (PPAR) , is a member of the nuclear receptor superfamily and regulates gene expression of fatty acid utilization enzymes. In cardiac hypertrophy and heart failure by pressure-overload, myocardial energy utilization reverts to the fetal pattern, and metabolic substrate switches from fatty acid to glucose. However, myocardial metabolism in volume-overloaded hearts has not been rigorously studied. The aim of the present study was to examine fatty acid metabolism and protein expressions of PPAR, and fatty acid oxidation enzymes in volume-overloaded rabbit hearts. Methods, Volume-overload was induced by carotid-jugular shunt formation. Sham-operated rabbits were used as control. Chronic volume-overload increased left ventricular weight and ventricular cavity size, and relative wall thickness was decreased, indicating eccentric cardiac hypertrophy. 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) was intravenously administered, and animals were sacrificed at 5 min after injection. The 9MPA was rapidly metabolized to iodophenyl-3-methylnonanoic acid (3MNA) by ,-oxidation. Lipid extraction from the myocardium was performed by the Folch method, and radioactivity distribution of metabolites was assayed by thin-layer chromatography. The protein was extracted from the left ventricular myocardium, and levels of PPAR, and fatty acid oxidation enzymes were examined by Western blotting. Results, Myocardial distribution of 9MPA tended to be more heterogeneous in shunt than in sham rabbits (P = 0·06). In volume-overloaded hearts by shunt, the conversion from 9MPA to 3MNA by ,-oxidation was faster than the sham-control hearts (P < 0·05). However, protein levels of PPAR, and fatty acid utilization enzymes were unchanged in shunt rabbits compared with sham rabbits. Conclusions, These data suggest that myocardial fatty acid metabolism is enhanced in eccentric cardiac hypertrophy by volume-overload without changes in protein expressions of PPAR, and fatty acid utilization enzymes. Our data may provide a novel insight into the subcellular mechanisms for the pathological process of cardiac remodelling in response to mechanical stimuli. [source]

Mapping of Epicardial Activation in a Rabbit Model of Chronic Myocardial Infarction:

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2007
Endocardial, Epicardial Pacing, Response to Atrial
Introduction: This study examines the consequences of a large transmural apical infarct on the epicardial electrical activity in isolated rabbit hearts. Methods and Results: Hearts were isolated 8 weeks after coronary artery ligation. Membrane voltage from the epicardial surface of the left ventricle (LV) including the infarct was monitored using the voltage sensitive dye RH237. Optical action potentials were detected from the epicardial surface of the infarct; the signal amplitude was ,20% of those in the noninfarcted zone (NZ). Epicardial activation mapping of the LV free wall showed that during right atrial (RA) pacing, the activation sequence was not significantly different between infarcted and sham-operated groups. However, direct stimulation of the epicardium in the NZ revealed an area of slow conduction velocity (CV ,5 cm/s,1, ,10% of normal values) at the margin of the infarct zone (IZ). Within the IZ, CV was ,50% of normal. A prominent endocardial rim of myocardium in the infarct was not the source of epicardial optical signals because chemical ablation of the endocardium did not affect the epicardial activation pattern. Concluson: Therefore, remnant groups of myocytes in the mid-wall and epicardium of the infarct scar support normal electrical activation during RA pacing. Areas of delayed conduction emerge only on epicardial stimulation. [source]

Proarrhythmia as a Class Effect of Quinolones: Increased Dispersion of Repolarization and Triangulation of Action Potential Predict Torsades de Pointes

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2007
PETER MILBERG M.D.
Background: Numerous noncardiovascular drugs prolong repolarization and thereby increase the risk for patients to develop life-threatening tachyarrhythmias of the torsade de pointes (TdP) type. The development of TdP is an individual, patient-specific response to a repolarization-prolonging drug, depending on the repolarization reserve. The aim of the present study was to analyze the underlying mechanisms that discriminate hearts that will develop TdP from hearts that will not develop TdP. We therefore investigated the group of quinolone antibiotics that reduce repolarization reserve via IKr blockade in an intact heart model of proarrhythmia. Methods and Results: In 47 Langendorff-perfused, AV-blocked rabbit hearts, ciprofloxacin (n = 10), ofloxacin (n = 14), levofloxacin (n = 10), and moxifloxacin (n = 13) in concentrations from 100 ,M to 1,000 ,M were infused. Eight monophasic action potentials (MAPs) and an ECG were recorded simultaneously. After incremental pacing at cycle lengths from 900 ms to 300 ms to compare the action potential duration, potassium concentration was lowered to provoke TdP. All antibiotics led to a significant increase in QT interval and MAP duration, and exhibited reverse-use dependence. Eight simultaneously recorded MAPs demonstrated an increase in dispersion of repolarization in the presence of all antibiotics. MAP triangulation (ratio: MAP90/50) and fluctuation of consecutive action potentials were increased for all tested drugs at high concentrations. In the presence of low potassium concentration, all quinolones led to TdP: ciprofloxacin, 4 out of 10 (40%); ofloxacin, 3 out of 14 (21%); moxifloxacin, 9 out of 13 (69%); and levofloxacin, 2 out of 10 (20%). Hearts that developed TdP demonstrated a significant greater influence on dispersion of repolarization and on triangulation as compared with hearts without TdP. Conclusion: Quinolone antibiotics may be proarrhythmic due to a significant effect on myocardial repolarization. The individual response of a heart to develop TdP in this experimental model is characterized by a greater effect on dispersion of repolarization and on triangulation of action potential as compared with hearts that do not develop TdP. [source]

Ventricular Fibrillation Induced by Stretch Pulse: Implications for Sudden Death Due to Commotio Cordis

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2006
FRANK BODE M.D.
Introduction: Nonpenetrating chest wall impact (commotio cordis) may lead to sudden cardiac death due to the acute initiation of ventricular fibrillation (VF). VF may result from sudden stretch during a vulnerable window, which is determined by repolarization inhomogeneity. Methods: We examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). In six Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains. Results: Sudden balloon inflation induced VF when pressure pulses of 208,289 mmHg were applied within a window of 35,88 msec after MAP upstroke, a period of intrinsic increase in repolarization dispersion. During the pressure pulse, MAPs revealed an additional increase in repolarization dispersion (time domain) by 9 ± 6 msec (P < 0.01). The maximal difference in repolarization levels (voltage domain) between sites increased from 19 ± 3% to 26 ± 3% (P < 0.05). Earliest stretch-induced activation was observed near a site with early repolarization, while sites with late repolarization showed delayed activation. Conclusions: Sudden myocardial stretch can elicit VF when it occurs during a vulnerable window that is based on repolarization inhomogeneity. Stretch pulses applied during this vulnerable window can lead to nonuniform activation. Repolarization dispersion might play a crucial role in the occurrence of fatal tachyarrhythmias during commotio cordis. [source]

Improvement of Defibrillation Efficacy with Preshock Synchronized Pacing

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2004
HUI-NAM PAK M.D., Ph.D.
Introduction: We previously demonstrated that wavefront synchronization by spatiotemporal excitable gap pacing (Sync P) is effective at facilitating spontaneous termination of ventricular fibrillation (VF). Therefore, we hypothesized that a spatiotemporally controlled defibrillation (STCD) strategy using defibrillation shocks preceded by Sync P can improve defibrillation efficacy. Method and Results: We explored the STCD effects in 13 isolated rabbit hearts. During VF, a low-voltage gradient (LVG) area was synchronized by Sync P for 0.92 second. For Sync P, optical action potentials (OAPs) adjacent to four pacing electrodes (10 mm apart) were monitored. When one of the electrodes was in the excitable gap, a 5-mA current was administered from all electrodes. A shock was delivered 23 ms after the excitable gap when the LVG area was unexcitable. The effects of STCD was compared to random shocks (C) by evaluating the defibrillation threshold 50% (DFT50; n = 35 for each) and preshock coupling intervals (n = 208 for STCD, n = 172 for C). Results were as follows. (1) Sync P caused wavefront synchronization as indicated by a decreased number of phase singularity points (P < 0.0001) and reduced spatial dispersion of VF cycle length (P < 0.01). (2) STCD decreased DFT50 by 10.3% (P < 0.05). (3) The successful shocks showed shorter preshock coupling intervals (CI; P < 0.05) and a higher proportion of unexcitable shock at the LVG area (P < 0.001) than failed shocks. STCD showed shorter CIs (P < 0.05) and a higher unexcitable shock rate at LVG area (P < 0.05) than C. Conclusion: STCD improves defibrillation efficacy by synchronizing VF activations and increasing probability of shock delivery to the unexcitable LVG area. (J Cardiovasc Electrophysiol, Vol. 15, pp. 581-587, May 2004) [source]

Spatiotemporal Correlation Between Phase Singularities and Wavebreaks During Ventricular Fibrillation

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2003
YEN-BIN LIU M.D.
Introduction: Phase maps and the detection of phase singularities (PSs) have become a well-developed method for characterizing the organization of ventricular fibrillation (VF). How precisely PS colocalizes with wavebreak (WB) during VF, however, is unknown. Methods and Results: We performed optical mapping of 27 episodes of VF in nine Langendorff-perfused rabbit hearts. A WB is a point where the activation wavefront and the repolarization waveback meet. A PS is a site where its phase is ambiguous and its neighboring pixels exhibit a continuous phase progression from ,, to +,. The correlation coefficient between the number of WBs and PSs was 0.78 ± 0.09 for each heart and 0.81 for all VF episodes (P < 0.001), indicating a significant temporal correlation. We then superimposed the WBs and PSs for every 100 frames of each episode. These maps showed a high degree of spatial colocalization. To quantify spatial colocalization, the spatial shifts between the cumulative maps of WBs and PSs in corresponding frames were calculated by automatic alignment to obtain maximum overlap between these two maps. The spatial shifts were 0.04 ± 0.31 mm on the x-axis and 0.06 ± 0.27 mm on the y-axis over a 20 × 20 mm2 mapped field, indicating highly significant spatial correlation. Conclusion: Phase mapping provides a convenient and robust approach to quantitatively describe wave propagation and organization during VF. The close spatiotemporal correlation between PSs and WBs establishes that PSs are a valid alternate representation of WB during VF and further validated the use of phase mapping in the study of VF dynamics. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1103-1109, October 2003) [source]

Effect of Action Potential Duration and Conduction Velocity Restitution and Their Spatial Dispersion on Alternans and the Stability of Arrhythmias

Electrophysiologic Deterioration After One-Minute Fibrillation Increases Relative Biphasic Defibrillation Efficacy

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000
OSCAR H. TOVAR M.D.
Biphasic Shocks and One-Minute Fibrillation. Introduction: The probability of survival decreases to 70% after 2 minutes of ventricular fibriltation. Bipliasic shocks are more effective than monophasic shocks in terminating short-duration (<30 sec) ventricular fibrillation. We tested the hypotheses that developing ischemia changes the electrophysiologic characteristics of fibrillation and that the relative efficacy of biphasic shocks increases as electrophysiologic characteristics deteriorate. Methods and Results: Monophasic (12 msec) and biphasic (6/6 msec) shocks (1 to 4 A) were tested in random order in isolated rabbit hearts after 1-minute ischemic fibrillation. Monophasic action potentials showed only a sporadic occurrence of electrical diastole after 5 seconds of fibrillation (24% of action potentials in the right ventricle and 18% in the left ventricle). After 60 seconds of fibrillation, diastole (17.83 ± 1.14 msec in the right ventricle and 21.52 ± 1.16 msec in the left ventricle) appeared after almost every action potential (P < 0.0001 compared with 5 sec), despite a lack of change in fibrillation cycle length and dominant frequency. Monophasie I50 was 2.89 A, and biphasic I50 was 1.4 A (77% reduction in energy). Normalized curve width decreased 28%. Retrospective analysis showed that shocks delivered early in the fibrillation action potential bad a greater probability of succeeding (89%) than shocks delivered late (30%; P < 0.001). Conclusion: After l-minute ischemic fibrillation, diastolic intervals occur during fibrillation. Therefore, defibrillation shocks have an approximately 29% probability of interacting with the fibrillation action potential during diastole. At this time, biphasic shocks produced a more deterministic defibrillation threshold and became even more efficacious (I50B/M = 0.48) than at short fibrillation durations (I50 B/M = 0.7). [source]

Mapping of Atrial Activation Patterns After Inducing Contiguous Radiofrequency Lesions: An Experimental Study

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2001
FRANCISCO J. CHORRO
CHORRO, F.J., et al.: Mapping of Atrial Activation Patterns After Inducing Contiguous Radiofrequency Lesions: An Experimental Study. High resolution mapping techniques are used to analyze the changes in atrial activation patterns produced by contiguous RF induced lesions. In 12 Langendorff-perfused rabbit hearts, left atrial activation maps were obtained before and after RF induction of epicardial lesions following a triple-phase sequential protocol: (phase 1) three separate lesions positioned vertically in the central zone of the left atrial wall; (phase 2) the addition of two lesions located between the central lesion and the upper and lower lesions; and (phase 3) the placement of four additional lesions between those induced in the previous phases. In six additional experiments a pathological analysis of the individual RF lesions was performed. In phase 1 (lesion diameter = 2.8 ± 0.2 mm, gap between lesions = 3 ± 0.8 mm), the activation process bordered the lesions line in two (2.0-ms cycles) and four experiments (1.0-ms cycles). In phase 2, activation bordered the lesions line in eight (2.0-ms cycles, P < 0.01 vs control) and nine experiments (1.0-ms cycles, P < 0.001), and in phase 3 this occurred in all experiments except one (both cycles, P < 0.001 vs control). In the experiments with conduction block, the increment of the interval between activation times proximal and distal to the lesions showed a significant correlation to the length of the lesions (r = 0.68, P < 0.05, 100-ms cycle). In two (17%) experiments, sustained regular tachycardias were induced with reentrant activation patterns around the lesions line. In conclusion, in this acute model, atrial RF lesions with intact tissue gaps of 3 mm between them interrupt conduction occasionally, and conduction block may be frequency dependent. Lesion overlap is required to achieve complete conduction block lines. Tachycardias with reentrant activation patterns around a lesions line may be induced. [source]

Opposite Effects of Myocardial Stretch and Verapamil on the Complexity of the Ventricular Fibrillatory Pattern: An Experimental Study

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2000
FRANCISCO J. CHORRO
CHORRO, F.J., et al.: Opposite Effects of Myocardial Stretch And Verapamil on The Complexity of The Ventricular Fibrillatory Pattern: An Experimental Study. An experimental model is used to analyze the effects of ventricular stretching and verapamil on the activation patterns during VF. Ten Langendorff-perfused rabbit hearts were used to record VF activity with an epicardial multiple electrode before, during, and after stretching with an intraventricular balloon, under both control conditions and during verapamil (Vp) infusion (0.4,0.8 ,mol). The analyzed parameters were dominant frequency (FrD) spectral analysis, the median (MN) of the VF intervals, and the type of activation maps during VF (I = one wavelet without block lines, II = two simultaneous wavelets with block lines, III = three or more wavelets with block lines). Stretch accelerates VF (FrD: 22.8 ± 6.4 vs 15.2 ± 1.0 Hz, P < 0.01; MN: 48 ± 13 vs 68 ± 6 ms, P < 0.01). On fitting the FrD time changes to an exponential model after applying and suppressing stretch, the time constants (stretch: 101.2 ± 19.6 s; stretch suppression: 97.8 ± 33.2 s) do not differ significantly. Stretching induces a significant variation in the complexity of the VF activation maps with type III increments and type I and II decrements (control: I = 17.5%, II = 50.5%, III = 32%; stretch: I = 7%, II = 36.5%, III = 56.5%, P < 0.001). Vp accelerates VF (FrD: 20.9 ± 1.9 Hz, P < 0.001 vs control; MN: 50 ± 5 ms, P < 0.001 vs control) and diminishes activation maps complexity (I = 25.5%, II = 60.5%, III = 14%, P < 0.001 vs control). On applying stretch during Vp perfusion, the fibrillatory process is not accelerated to any greater degree. However, type I and II map decrements and type III increments are recorded, though reaching percentages similar to control (I = 16.5%, II = 53%, III = 30.5%, NS vs control). The following conclusions were found: (1) myocardial stretching accelerates VF and increases the complexity of the VF activation pattern; (2) time changes in the FrD of VF during and upon suppressing stretch fit an exponential model with similar time constants; and (3) although stretching and verapamil accelerate the VF process, they exert opposite effects upon the complexity of the fibrillatory pattern. [source]

Proteomics of ischemia/reperfusion injury in rabbit myocardium reveals alterations to proteins of essential functional systems

PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 5 2005
Melanie Y. White
Abstract Brief periods of myocardial ischemia prior to timely reperfusion result in prolonged, yet reversible, contractile dysfunction of the myocardium, or "myocardial stunning". It has been hypothesized that the delayed recovery of contractile function in stunned myocardium reflects damage to one or a few key sarcomeric proteins. However, damage to such proteins does not explain observed physiological alterations to myocardial oxygen consumption and ATP requirements observed following myocardial stunning, and therefore the impact of alterations to additional functional groups is unresolved. We utilized two-dimensional gel electrophoresis and mass spectrometry to identify changes to the protein profiles in whole cell, cytosolic- and myofilament-enriched subcellular fractions from isolated, perfused rabbit hearts following 15 min or 60 min low-flow (1 mL/min) ischemia. Comparative gel analysis revealed 53 protein spot differences (> 1.5-fold difference in visible abundance) in reperfused myocardium. The majority of changes were observed to proteins from four functional groups: (i) the sarcomere and cytoskeleton, notably myosin light chain-2 and troponin C; (ii) redox regulation, in particular several components of the NADH ubiquinone oxidoreductase complex; (iii) energy metabolism, encompassing creatine kinase; and (iv) the stress response. Protein differences appeared to be the result of isoelectric point shifts most probably resulting from chemical modifications, and molecular mass shifts resulting from proteolytic or physical fragmentation. This is consistent with our hypothesis that the time course for the onset of injury associated with myocardial stunning is too brief to be mediated by large changes to gene/protein expression, but rather that more subtle, rapid and potentially transient changes are occurring to the proteome. The physical manifestation of stunned myocardium is therefore the likely result of the summed functional impairment resulting from these multiple changes, rather than a result of damage to a single key protein. [source]

Remodelling of action potential and intracellular calcium cycling dynamics during subacute myocardial infarction promotes ventricular arrhythmias in Langendorff-perfused rabbit hearts

THE JOURNAL OF PHYSIOLOGY, Issue 3 2007
Chung-Chuan Chou
We hypothesize that remodelling of action potential and intracellular calcium (Cai) dynamics in the peri-infarct zone contributes to ventricular arrhythmogenesis in the postmyocardial infarction setting. To test this hypothesis, we performed simultaneous optical mapping of Cai and membrane potential (Vm) in the left ventricle in 15 rabbit hearts with myocardial infarction for 1 week. Ventricular premature beats frequently originated from the peri-infarct zone, and 37% showed elevation of Cai prior to Vm depolarization, suggesting reverse excitation,contraction coupling as their aetiology. During electrically induced ventricular fibrillation, the highest dominant frequency was in the peri-infarct zone in 61 of 70 episodes. The site of highest dominant frequency had steeper action potential duration restitution and was more susceptible to pacing-induced Cai alternans than sites remote from infarct. Wavebreaks during ventricular fibrillation tended to occur at sites of persistently elevated Cai. Infusion of propranolol flattened action potential duration restitution, reduced wavebreaks and converted ventricular fibrillation to ventricular tachycardia. We conclude that in the subacute phase of myocardial infarction, the peri-infarct zone exhibits regions with steep action potential duration restitution slope and unstable Cai dynamics. These changes may promote ventricular extrasystoles and increase the incidence of wavebreaks during ventricular fibrillation. Whereas increased tissue heterogeneity after subacute myocardial infarction creates a highly arrhythmogenic substrate, dynamic action potential and Cai cycling remodelling also contribute to the initiation and maintenance of ventricular fibrillation in this setting. [source]