Haider B, Khan M I, Burke W M, Regan T J
Am J Cardiol. 1975 Apr;35(4):504-13. doi: 10.1016/0002-9149(75)90833-4.
As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was produced in the left ventricular dysfunction. The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin. Epinephrine (0.05 mug/kg per min) elicited a significant reduction in end-diastolic pressure and increase in stroke volume. The latter was not attended by an increased incidence of ventricular fibrillation, whereas fibrillation occurred in half of the group given strophantihidin. Thus, the catecholamine was selected to study pump failure. Severe ischemic heart failure was assessed in two groups with scar from previous infarction for up to 4 hours. By 60 minutes of ischemia the increase in end-diastolic pressure and volume and decrease in stroke volume and ejection fraction were comparable in both groups. Thereafter, alternate animals received small doses of epinephrine (0.05 to 0.15 mug/kg per min) with graded increments at 60 minute intervals to counter tachyphylaxis and findings were compared with those in control dogs. Over the subsequent 3 hours, there was progressive deterioration of left anterior descending coronary artery, affecting ventricular function in the untreated group with an increase in end-diastolic pressure from 10 plus or minus 1 to 33 plus or minus 2.4 mm Hg. End-diastolic volume increased by 63 percent; stroke volume and ejection fraction decreased by 48 and 66 percent, respectively. The infusion of epinephrine was attended by a significantly lower end-diastolic pressure of 20 plus or minus 2.5 mm Hg, whereas end-diastolic volume, stroke volume and ejection fraction were restored to control levels after 4 hours of ischemia. Mortality in the untreated group was 62 percent by 4 hours; all seven animals in the treated group survived.
作为对严重缺血性心力衰竭研究的前奏，在24只接受首次急性局部缺血发作的完整麻醉犬中，测定了缺血心室对无毒剂量肾上腺素和毒毛花苷的治疗反应。在左心室功能障碍中产生了血栓性阻塞。对照犬中舒张末期压力的升高和每搏量的降低在给予毒毛花苷后没有显著改变。肾上腺素（0.05微克/千克每分钟）引起舒张末期压力显著降低和每搏量增加。后者并未伴有室颤发生率的增加，而在给予毒毛花苷的组中，有一半发生了室颤。因此，选择儿茶酚胺来研究泵衰竭。在两组有既往梗死瘢痕长达4小时的动物中评估严重缺血性心力衰竭。缺血60分钟时，两组舒张末期压力和容积的增加以及每搏量和射血分数的降低相当。此后，每隔60分钟交替给动物小剂量肾上腺素（0.05至0.15微克/千克每分钟）并逐渐增加剂量以对抗快速耐受性，并将结果与对照犬进行比较。在随后的3小时内，左前降支冠状动脉逐渐恶化，未治疗组的心室功能受到影响，舒张末期压力从10±1毫米汞柱增加到33±2.4毫米汞柱。舒张末期容积增加了63%；每搏量和射血分数分别降低了48%和66%。输注肾上腺素时，舒张末期压力显著降低至2-0±2.5毫米汞柱，而缺血4小时后舒张末期容积、每搏量和射血分数恢复到对照水平。未治疗组4小时时的死亡率为62%；治疗组的所有7只动物均存活。
