Effect of autonomic neural influences on the cardiovascular changes induced by coronary occlusion.
The influence of vagal stimulation and/or beta-adrenergic receptor blockade on the heart rate, blood pressure, contractile force, and cardiac rhythm was evaluated in chloralose-anesthetized cats subjected to occlusion of the anterior descending coronary artery. Occlusion performed in 25 control animals produced significant decreases in heart rate (minus 22.9 plus or minus 4.4 beats per minute), blood pressure (minus 19.2 plus or minus 2.4 mm. Hg), and contractile force (minus 21.6 plus or minus 6.3 per cent). Death due to ventricular fibrillation occurred in five out of 25 animals. Coronary occlusion performed in the presence of vagal nerve stimulation resulted in similar decreases in blood pressure, whereas the decreases in contractile force were significantly greater than in control animals. In addition, the time to onset of the arrhythmias occurring in the vagus-stimulated group was increased. Death due to ventricular fibrillation was similar to control animals (i.e., two of seven, or 28 per cent). Blockade of beta-adrenergic receptors with propranol (0.75 mg. per kilogram) resulted in the usual decreases in rate, pressure, and force with occlusion but the duration of arrhythmias was shortened. The incidence of ventricular fibrillation was not different from that of the control animals. The combination of propranolol and vagal stimulation also failed to confer protection against ventricular fibrillation. Propranolol was observed to prevent the large decrease in contractile force seen with vagal stimulation. These results suggest that: (1) increasing vagal tone above the level existing after acute myocardial infarction does not decrease mortality, (2) propranolol pretreatment does not affect the incidence of ventricular fibrillation induced by coronary occlusion, (3) the duration of the arrhythmia after coronary occlusion is effectively shortened with propranolol, and (4) cardiac beta-adrenergic receptors do not appear to be involved in the decreases in heart rate, blood pressure, and contractile force seen with coronary occlusion.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D004558:Electric Stimulation; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000503:physiopathology*; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic; D013997:Time Factors; D014630:Vagus Nerve / Q000503:physiopathology
D011941:Receptors, Adrenergic; D011433:Propranolol