Cooper N, Brazier J R, McConnell D H, Buckberg G D
J Thorac Cardiovasc Surg. 1977 Feb;73(2):195-200.
This study compares (1) the effects of slowing heart rate by topical hypothermia in hearts perfused at 37 degrees C. with bradycardia produced by perfusion hypothermia (28 degrees C.) and (2) the consequences of counteracting the bardycardic effects of perfusion hypothermia by atrial pacing. Topical atrial hypothermia (myocardial temperature 37 degrees C.) produced a level of bradycardia comparable to perfusion hypothermia (82 vs. 71 beats per minute), but reduced myocardial oxygen requirements 25 per cent more than perfusion with 28 degrees C. blood. Myocardial oxygen uptake per beat did not change with topical atrial hypothermia but increased 40 per cent with perfusion hypothermia. Counteracting the bradycardic effects of perfusion hypothermia with atrial pacing (to 130 beats per minute) reduced subendocardial flow 25 per cent, caused a redistribution of flow away from the subendocardium, and produced evidence of ischemia on the intracavitary electrocardiogram. This study shows that (1) topical atrial hypothermia with systemic normothermia reduced myocardial oxygen demands as effectively as perfusion hypothermia and (2) subendocardial ischemia develops in beating empty hearts when the expected bradycardia of hypothermia does not occur.
(1)在37℃灌注的心脏中,局部低温使心率减慢的效果与灌注低温(28℃)导致的心动过缓的效果;(2)通过心房起搏抵消灌注低温的心动过缓效应的后果。局部心房低温(心肌温度37℃)产生的心动过缓程度与灌注低温相当(每分钟82次对71次),但比用28℃血液灌注多降低心肌氧需求25%。每搏心肌摄氧量在局部心房低温时未改变,但在灌注低温时增加40%。用心房起搏抵消灌注低温的心动过缓效应(至每分钟130次)使心内膜下血流减少25%,导致血流从心内膜下重新分布,并在腔内心电图上出现缺血证据。本研究表明:(1)全身正常体温下的局部心房低温与灌注低温一样有效地降低心肌氧需求;(2)在跳动的空心中,当预期的低温心动过缓未出现时,会发生心内膜下缺血。