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Anesthetized Dogs (anesthetized + dog)
Selected AbstractsChanges in Left Ventricular Repolarization and Ion Channel Currents Following a Transient Rate Increase Superimposed on Bradycardia in Anesthetized DogsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000MICHAEL RUBART M.D. Electrical Remodeling of the Heart due to Rate. Introduction: We previously demonstrated in dogs that a transient rate increase superimposed on bradycardia causes prolongation of ventricular refractoriness that persists for hours after resumption of bradycardia. In this study, we examined changes in membrane currents that are associated with this phenomenon. Methods and Results: The whole cell, patch clamp technique was used to record transmembrane voltages and currents, respectively, in single mid-myocardial left ventricular myocytes from dogs with 1 week of complete AV block; dogs either underwent 1 hour of left ventricular pacing at 120 beats/min or did not undergo pacing. Pacing significantly heightened mean phase 1 and peak plateau amplitudes by ,6 and ,3 mV, respectively (P < 0.02). and prolonged action potential duration at 90% repolarization from 235 ± 8 msec to 278 ± 8 msec (1 Hz; P = 0.02). Rapid pacing-induced changes in transmembrane ionic currents included (1) a more pronounced cumulative inactivation of the 4-aminopyridine-sensitive transient outward K+ current, I to over the range of physiologic frequencies, resulting from a ,30% decrease in the population of quickly reactivating channels; (2) increases in peak density of L-type Ca2+ currents, Ica.I.' by 15% to 35% between +10 and +60 mV; and (3) increases in peak density of the Ca2+ -activated chloride current, ICl.Ca' by 30% to 120% between +30 and +50 mV. Conclusion: Frequency-dependent reduction in Ito combined with enhanced ICa.I. causes an increase in net inward current that may he responsible for the observed changes in ventricular repolarization. This augmentation of net cation influx is partially antagonized by an increase in outward ICa.Cl. [source] Pharmacology of the Selective 5-HT1B/1D Agonist FrovatriptanHEADACHE, Issue 2002M.B. Comer BSc Objective.,To determine the pharmacological profile of frovatriptan. Background.,Frovatriptan is a new 5-HT1B/1D agonist developed for the treatment of migraine. Methods.,Pharmacological studies were performed using in vitro and in vivo techniques. Results.,Radioligand-binding studies showed that frovatriptan has a high affinity for 5-HT1B and 5-HT1D receptors, and moderate affinity for 5-HT1A, 5-HT1F, and 5-HT7 receptors. In vitro, frovatriptan acts as a potent full agonist at human cloned 5-HT1B and 5-HT1D receptors, and as a moderately potent full agonist at 5-HT7 receptors. Studies of frovatriptan in isolated human arteries demonstrated a lower threshold for constriction of cerebral than coronary vasculature and a bell-shaped dose-response curve was apparent in the coronary arteries. In anesthetized dogs, frovatriptan administration produced no measurable effect on cardiac function or on blood pressure. Frovatriptan had no effects on coronary blood flow following transient coronary artery occlusion, whereas sumatriptan produced a prolonged and significant decrease in coronary blood flow. Conclusion.,The pharmacology of frovatriptan suggests that it should be an effective agent for the acute treatment of migraine, with a low potential for undesirable peripheral effects. [source] Anatomy and Physiology of the Right Interganglionic Nerve: Implications for the Pathophysiology of Inappropriate Sinus TachycardiaJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2008JING ZHOU M.D. Objective: To simulate inappropriate sinus tachycardia (IST) in experimental animals. Background: We recently found that epinephrine injected into the anterior right ganglionated plexi (ARGP) adjacent to the sinoatrial (SA) node induced an arrhythmia simulating IST. Methods: In 19 anesthetized dogs, via a right thoracotomy, the course of the interganglionic nerve (IGN) from the right stellate ganglion along the superior vena cava to the heart was delineated. High-frequency stimulation (HFS; 0.1 msec duration, 20 Hz, 4.5,9.3 V) was applied to IGN at the junction of innominate vein and SVC. Results: HFS of the IGN significantly increased the sinus rate (SR) (baseline: 156 ± 19 beats/minutes [bpm], 4.5 V: 191 ± 28 bpm*, 8.0 V: 207 ± 23 bpm*, 9.3 V: 216 ± 18 bpm*; *P < 0.01 compared to baseline) without significant changes in A-H interval or blood pressure. P-wave morphology, ice mapping, and noncontact mapping indicated that this tachycardia was sinus tachycardia. In 8 of 19 dogs, injecting hexamethonium (5 mg), a ganglionic blocker, into the ARGP attenuated the response elicited by IGN stimulation (baseline: 160 ± 21 bpm, 4.5 V: 172 ± 32 bpm, 8.0 V: 197 ± 32 bpm*, 9.3 V: 206 ± 26 bpm*; *P < 0.05 compared to baseline). In 19 of 19 animals, after formaldehyde injection into the ARGP, SR acceleration induced by IGN stimulation was markedly attenuated (baseline: 149 ± 17 bpm, 4.5 V: 151 ± 21 bpm, 8.0 V: 155 ± 23 bpm, 9.3 V: 167 ± 24 bpm*; *P < 0.05 compared to baseline). Conclusions: HFS of the IGN caused a selective and significant acceleration of the SR. A significant portion of IGN traverses the ARGP or synapses with the autonomic ganglia in the ARGP before en route to the SA node. Dysautonomia involving the IGN and/or ARGP may play an important role in IST. [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] Measurements of microvascular perfusion in healthy anesthetized dogs using orthogonal polarization spectral imagingJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2010DACVECC, Deborah C. Silverstein DVM No abstract is available for this article. [source] High Incidence of Thrombus Formation Without Impedance Rise During Radiofrequency Ablation Using Electrode Temperature ControlPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2003KAGARI MATSUDAIRA The authors hypothesized that during RF ablation, the electrode to tissue interface temperature may significantly exceed electrode temperature in the presence of cooling blood flow and produce thrombus. In 12 anesthetized dogs, the skin over the thigh muscle was incised and raised to form a cradle that was superfused with heparinized canine blood(ACT > 350 s)at 37°C. A 7 Fr, 4-mm or 8-mm ablation electrode containing a thermocouple was held perpendicular to the thigh muscle at 10-g contact weight. Interface temperature was measured at opposite sides of the electrode using tiny optical probes. RF applications(n = 157)were delivered at an electrode temperature of 45°C, 55°C, 65°C, and 75°C for 60 seconds, with or without pulsatile blood flow (150 mL/min). Without blood flow, the interface temperature was similar to the electrode temperature. With blood flow, the interface temperature (side opposite blood flow) was up to 36°C and 57°C higher than the electrode temperature using the 4- and 8-mm electrodes, respectively. After each RF, the cradle was emptied and the electrode and interface were examined. Thrombus developed without impedance rise at an interface temperature as low as 73°C without blood flow and 80°C with blood flow (11/16 RFs at 65°C electrode temperature using 4 mm and 13/13 RFs at an electrode temperature of 55°C using an 8-mm electrode with blood flow). With blood flow, interface temperature markedly exceeded the electrode temperature and the difference was greater with an 8-mm electrode (due to greater electrode cooling). In the presence of blood flow, thrombus occurred without an impedance rise at an electrode temperature as low as 65°C with a 4-mm electrode and 55°C with an 8-mm electrode. (PACE 2003; 26:1227,1237) [source] Temporal Changes in the Endocardial ST Segment During the Evolution of Myocardial Infarction in DogsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2002JONATHAN LESSICK LESSICK, J., et al.: Temporal Changes in the Endocardial ST Segment During the Evolution of Myocardial Infarction in Dogs. Acute coronary occlusion causes ST-segment elevation on the body surface ECG and on the epicardial electrogram in the territory supplied by that artery. The occurrence and significance of endocardial ST changes have not been studied. The NOGA electromechanical mapping was performed on eight anesthetized dogs at baseline, immediately after occlusion of the LAD, and again at 5 hours to assess regional changes in the ST segment. At 3 days and 4 weeks the ventricles were remapped for comparison. Regional unipolar ST-segment elevation was measured for each zone from NOGA maps at 0, 80, and 120 ms after the J point. ST segments rose immediately in the infarct zones, as demarcated by echocardiography, compared to remote zones, but by 3 days had dropped below, and at 4 weeks returned to baseline values. Immediately postocclusion, ST elevation at 120 ms best differentiated between normal versus abnormal echo scores (concordance = 0.80), probably by correcting for pressure induced ST elevation. In conclusion, acute endocardial ST-segment changes occur in the infarct zone in the dog, showing a distinctive temporal evolution. [source] | ||||||||||