Davis R F, DeBoer L W, Rude R E, Lowenstein E, Maroko P R
Anesthesiology. 1983 Nov;59(5):402-11. doi: 10.1097/00000542-198311000-00007.
The effect of halothane anesthesia on myocardial necrosis resulting from coronary artery ligation was examined in 28 anesthetized mongrel dogs. In 18 dogs, the left anterior descending coronary artery (LAD) was ligated immediately proximal to the first apical diagonal branch, and 1 h later the dogs were assigned randomly either to receive halothane, 0.5-1.0% inspired in room air for 12 h (n = 10) or to awaken without further intervention (control, n = 8). Infarct size was measured by staining the myocardium with triphenyl tetrazolium chloride 24 h after LAD ligation. Infarct size in halothane-treated dogs was 17.8 +/- 2.0% of the left ventricle, compared with 27.3 +/- 3.3% in control dogs (P less than 0.05). Myocardial salvage was present transmurally but was greatest in epicardial regions. In 10 additional dogs, hemodynamic variables (heart rate, arterial pressure, left ventricular end-diastolic pressure, peak left ventricular dP/dt, tension-time index, and rate-pressure product) were measured or calculated, and radionuclide-labeled microspheres were injected for measurement of cardiac output and regional myocardial blood flow (RMBF). Thirty minutes after LAD ligation and after initial hemodynamic measurements and microsphere injection, these dogs were assigned randomly to receive either halothane, 1.0%, inspired in room air (n = 5) or no intervention (control, n = 5). After 15 min of halothane inhalation (45 min after LAD ligation in control dogs), measurements were repeated. Halothane inhalation reduced heart rate, arterial pressure, and indexes of left ventricular contractile and pump performance. During halothane treatment, RMBF declined in normal myocardium but not in ischemic regions, while neither normal nor ischemic zone RMBF changed in control dogs. Systemic vascular resistance was unchanged in either group. Thus, halothane was associated with a 35% smaller myocardial infarct, transmural myocardial salvage, reduced heart rate, reduced left ventricular contractile and pump performance, reduced RMBF to nonischemic regions, and unchanged RMBF in the ischemic myocardium.
在28只麻醉的杂种犬中研究了氟烷麻醉对冠状动脉结扎所致心肌坏死的影响。18只犬，在第一支心尖对角支近端立即结扎左前降支冠状动脉（LAD），1小时后，将犬随机分为两组，一组吸入含0.5 - 1.0%氟烷的室内空气12小时（n = 10），另一组不做进一步干预使其苏醒（对照组，n = 8）。在LAD结扎24小时后，用氯化三苯基四氮唑对心肌进行染色来测量梗死面积。氟烷处理组犬的梗死面积为左心室的17.8±2.0%，而对照组犬为27.3±3.3%（P＜0.05）。心肌挽救呈透壁性，但在心外膜区域最为明显。另外10只犬，测量或计算血流动力学变量（心率、动脉压、左心室舒张末期压力、左心室dp/dt峰值、张力 - 时间指数和速率 - 压力乘积），并注射放射性核素标记的微球以测量心输出量和局部心肌血流量（RMBF）。在LAD结扎30分钟后以及进行初始血流动力学测量和微球注射后，将这些犬随机分为两组，一组吸入含1.0%氟烷的室内空气（n = 5），另一组不做干预（对照组，n = 5）。吸入氟烷15分钟后（对照组在LAD结扎45分钟后），重复测量。吸入氟烷可降低心率、动脉压以及左心室收缩和泵功能指标。在氟烷治疗期间，正常心肌区域的RMBF下降，但缺血区域未下降，而对照组犬的正常和缺血区域的RMBF均未改变。两组的全身血管阻力均未改变。因此，氟烷与心肌梗死面积减小35%、透壁性心肌挽救、心率降低、左心室收缩和泵功能降低、非缺血区域的RMBF降低以及缺血心肌的RMBF不变有关。
