Coronary Artery Occlusion in the Conscious Dog: Effects of Alterations in Heart Rate and Arterial Pressure on the Degree of Myocardial Ischemia
Coronary Artery Occlusion in the Conscious Dog: Effects of Alterations in Heart Rate and Arterial Pressure on the Degree of Myocardial Ischemia
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清醒狗的冠状动脉闭塞：心率和动脉压的变化对心肌缺血程度的影响
DOI：
10.1161/01.cir.46.2.323
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发表时间：
1972
期刊：
影响因子：
37.8
通讯作者：
S. Epstein
中科院分区：
文献类型：
--
作者：
D. Redwood;Eldonr . Smith;S. Epstein
心动过缓，伴或不伴低血压，常发生在急性心肌梗塞的早期阶段。为了确定心率和血压的变化对缺血性损伤程度的相对影响，通过给先前植入动脉周围的气球袖带充气，将闭胸意识清醒的狗的左冠状动脉前降支闭塞15分钟。通过对 12 个心肌电极记录的 S-T 升高求和来估计心肌缺血的程度。阿托品或起搏可增加心率，迷走神经电刺激可降低心率。静脉切开术产生低血压（平均血压平均下降 56 毫米汞柱）。在正常动脉压下，心率变化百分比（范围 30-215 次/分钟）与 S-T 抬高变化百分比之间呈正相关（y = 0.75 X + 30.2，r = 0.93，P < 0.01）。当低血压和心动过缓引起心肌缺血时，缺血 15 分钟时 S-T 升高总计 68 mv。当心率在存在低血压的情况下增加至对照水平时，心肌缺血期间的 ST 升高更大（平均差 29 mv，P < 0.05）。相反，当在心动过缓的情况下升高血压以控制血压时，10只狗中有7只的S-T升高低于低血压和心动过缓期间。因此，在实验性急性心肌缺血期间，出血引起的低血压会加重缺血性损伤，而心动过缓会减轻缺血性损伤。结论是，在急性心肌缺血时，即使基线心率较慢，心率也会增加；可能对心肌有害。失血性低血压引起的心肌缺血程度的改变是否与人类急性心肌梗死期间经常伴随心动过缓的低血压类型引起的改变类似，仍有待确定。
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.