Boyer N H, Gerstein M M
J Thorac Cardiovasc Surg. 1977 Aug;74(2):286-94.
Acute myocardial infarction with shock (AMI/S) was produced in 46 anesthetized "closed-chest" dogs by catheter injection of metallic mercury into the circumflex coronary artery. Twenty-four dogs were kept normothermic and 22 were maintained at 32 degrees C. Nine of the latter were rewarmed to 37 degrees C. and the experiments then were terminated, so that true survival time was arbitrarily shortened. Including these dogs, the survival time was three times longer than in the normothermic series (p less than 0.001). Hypothermia reduced heart rate (HR) by 34 percent, oxygen consumption by 38 percent, and myocardial oxygen consumption by an estimated 30 to 40 percent, while cardiac output (CO), stroke volume, and stroke work were unchanged. Left ventricular end-diastolic pressure (LVEDP) was reduced by 40 percent during hypothermia (p less than 0.05) and increased by 60 percent on rewarming. HR during rewarming increased substantially more than CO and thereby significantly reduced stroke volume.
通过向46只麻醉的“闭胸”犬的左旋冠状动脉内导管注射金属汞，制造出急性心肌梗死伴休克（AMI/S）模型。24只犬保持正常体温，22只犬维持在32摄氏度。后一组中有9只犬复温至37摄氏度，然后实验终止，这样实际存活时间被人为缩短。包括这些犬在内，低温组的存活时间比正常体温组延长了两倍（p<0.001）。低温使心率（HR）降低34%，耗氧量降低38%，心肌耗氧量估计降低30%至40%，而心输出量（CO）、每搏量和每搏功不变。低温期间左心室舒张末期压力（LVEDP）降低40%（p<0.05），复温时升高60%。复温期间心率增加幅度明显大于心输出量，从而显著降低每搏量。
