Coronary Artery Occlusion in the Conscious Dog
Effects of Alterations in Heart Rate and Arterial Pressure on the Degree of Myocardial Ischemia
Bradycardia, with or without hypotension, frequently occurs in the early phases of acute myocardial infarction. To determine the relative effects of alterations in heart rate and blood pressure on the degree of ischemic injury, the left anterior descending coronary artery was occluded for 15-min periods in closed-chest conscious dogs by inflating a balloon cuff previously implanted around the artery. The degree of myocardial ischemia was estimated by summating the S-T elevation recorded from 12 myocardial electrodes. Heart rate was increased by atropine or pacing and decreased by electrical stimulation of the vagus nerve. Hypotension was produced by venesection (average decrease in mean BP, 56 mm Hg). At normal arterial pressures there was a positive correlation between percent change in heart rate (range 30-215 beats/min) and percent change in S-T elevation (y = 0.75 X + 30.2, r = 0.93, P < 0.01). When myocardial ischemia was induced during hypotension and bradycardia, S-T elevation totaled 68 mv at 15 min of ischemia. When heart rate was increased to control levels in the presence of hypotension S-T elevation during myocardial ischemia was greater (mean difference 29 mv, P < 0.05). In contrast, when blood pressure was increased to control in the presence of bradycardia, S-T elevation in seven of 10 dogs was less than during hypotension and bradycardia. Thus, during experimental acute myocardial ischemia, hypotension induced by hemorrhage increases ischemic injury, and bradycardia reduces it. It is concluded that in acute myocardial ischemia increases in heart rate, even from slow baseline rates; may be deleterious to the myocardium. It remains to be determined whether alterations in the degree of myocardial ischemia induced by hemorrhagic-hypotension are analogous to those caused by the type of hypotension that often accompanies bradycardia occurring during acute myocardial infarction in man.
- Received January 25, 1972.
- Accepted March 27, 1972.
- © 1972 American Heart Association, Inc.