Attenuation of cardiac sympathetic drive in experimental myocardial ischemia in dogs

Feola, Mario; Arbel, Emanuel R.; Glick, Gerald

doi:10.1016/s0002-8703(77)80175-0

Cited by 10 publications

(5 citation statements)

References 30 publications

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“…25 The early stages of myocardial ischemia and infarction have been examined in a variety of animal models. These paradigms suggest that cardio-cardiac reflex alterations in autonomic nerve traffic play an important role in the pathophysiology of myocardial ischemia.25-31 Afferent signals appear to arise in mechano-and/or chemoreceptors in the affected myocardium and travel through vagal fibers and sympathetic afferents to the central nervous system.…”

Section: Resultsmentioning

confidence: 99%

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Catecholamines in coronary sinus and peripheral plasma during pacing-induced angina in man.

Schwartz¹,

Sole²,

Vaughan-Neil³

et al. 1979

Circulation

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CATECHOLAMINE RESPONSE TO ANGINA/Schwartz et al. SUMMARY We measured aortic and coronary sinus dopamine (DA), epinephrine (E), and norepinephrine (NE) in eight patients with cardiac ischemia (I) and eight control subjects (C). Samples were taken at rest (73 ± 3 beats/min in C and 68 ± 3 beats/min in I) and during coronary sinus pacing to peak rates (144 ± 4 beats/min in C and 136 ± 6 beats/min in I). Arterial NE was higher in the ischemic patients at rest (254 ± 25 pg/ml in C and 324 ± 21 in I; p < 0.05). There were no differences in arterial E and DA. Neither pacing nor angina affected peripheral catecholamine concentrations. Resting myocardial NE flux was similar for both groups. With pacing, coronary sinus flow and net myocardial NE release increased significantly in both groups. The maximum relative increase in net myocardial NE release was less in the ischemic patients than in the controls (575 ± 145% in C and 255 ± 40% in I; p < 0.05). Thus, angina induced by pacing does not augment peripheral sympathetic activity. Furthermore, pacing-induced angina appears to be associated with a decrease in cardiac sympathetic tone compared with that found in paced controls.AN INCREASE IN sympathetic activity has been postulated to be a significant determinant for some of the pathophysiological events associated with angina pectoris. With a compromise in regional myocardial blood flow, an increase in circulating catecholamines, by increasing myocardial oxygen consumption, would be expected to have deleterious effects on the jeopar-

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Section: Resultsmentioning

confidence: 99%

“…Some of these afferent signals may be inhibitory, resulting in a reduction in efferent cardiac sympathetic tone. 25 28 Perhaps a similar mechanism mediates the norepinephrine response to pacing-induced angina.…”

Section: Resultsmentioning

confidence: 99%

Catecholamines in coronary sinus and peripheral plasma during pacing-induced angina in man.

Schwartz¹,

Sole²,

Vaughan-Neil³

et al. 1979

Circulation

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“…Once again, the onset latency for the heart rate decline (13 sec) was approximately one-half that for the change in the P wave of the AEG. In this example, sinus 3. Cardiovascular responses to a one-minute occlusion of the sinus node artery in an anesthetized rhesus monkey.…”

Section: Resultsmentioning

confidence: 99%

“…In addition, the effect of occlusion-induced heart rate changes on regional blood flow and contractile force was also studied to determine if these changes affect the magnitude of the ischemic insult. Methods Adult rhesus monkeys weighing [3][4][5] kg, unselected as to sex, were sedated with phencyclidine HC1 (1-2 mg/kg, i.m.) and then anesthetized with alpha-chloralose (75 mg/kg, i.v.).…”

mentioning

confidence: 99%

Etiology of the negative chronotropic responses to transient coronary artery occlusion in the anesthetized rhesus monkey.

Alter¹,

Hawkins²,

Evans³

1978

Circulation

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Etiology of the negative chronotropic response to coronary artery occlusion was studied in chloralose-anesthetized monkeys. One-minute occlusion of the circumflex (CIRC) coronary artery resulted in marked negative chronotropic responses and consistent alterations in atrial electrograms. These responses were dependent on interruption of flow to a small proximal CIRC branch, and postmortem examination revealed that it perfused the sinus node region. The negative chronotropic response was not dependent on any apparent neural reflexes because it was not affected by autonomic blockade. Coronary artery occlusion in anesthetized monkeys can result in significant decreases in heart rate and changes in atrial electrical activity when flow to the pacemaker region is interrupted. We suggest that (1) rhesus monkeys may be suitable for study of the sick sinus syndrome, and (2) atropine-resistant bradycardia and atrial arrhythmias observed in postinfarction patients may be due to sinus node artery blockade.

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“…If large enough, this increase in heart rate may add to the already substantial risk of instantaneous death after coronary occlusion. In contrast, Feola et al 26 and Corr and Gillis27 reported that bradycardia usually followed occlusion of the circumflex coronary artery in the dog and occlusion of the anterior descending coronary artery in the cat.…”

Section: Spontaneous Fibrillation During Exercisementioning

confidence: 93%

Effect of submaximal exercise on vulnerability to fibrillation in the canine ventricle.

1979

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The risk of instantaneous death due to ventricular fibrillation was compared in resting and exercised dogs. Three weeks before testing, all dogs had bipolar left ventricular stimulating electrodes implanted and a reversible snare was placed around the anterior descending coronary artery. The dogs were randomly assigned to either an exercise (13 dogs) or a control (12 dogs) group. We measured ventricular fibrillation thresholds (VFTs) in all dogs before and after inducing ischemia by tightening the snare while the dogs stood at rest. The next day, nonischemic and ischemic VFTs were redetermined for control dogs at rest and for the exercise group during a treadmill run. No statistically significant changes were noted within and between groups in nonischemic or in ischemic VFTs at rest. In five exercise dogs, spontaneous ventricular fibrillation occurred during the first 8 minutes of the ischemic run, For the eight other exercise dogs, running increased the mean drop in VFTs during coronary occlusion by 23% (p less than 0.01). These data suggest that moderate dynamic exercise may greatly enhance the risk of ventricular fibrillation and sudden death in the presence of myocardial ischemia. In the absence of ischemia, exercise does not appear to increase vulnerability to ventricular fibrillation.

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Attenuation of cardiac sympathetic drive in experimental myocardial ischemia in dogs

Cited by 10 publications

References 30 publications

Catecholamines in coronary sinus and peripheral plasma during pacing-induced angina in man.

Catecholamines in coronary sinus and peripheral plasma during pacing-induced angina in man.

Etiology of the negative chronotropic responses to transient coronary artery occlusion in the anesthetized rhesus monkey.

Effect of submaximal exercise on vulnerability to fibrillation in the canine ventricle.

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