Kuboyama K, Safar P, Radovsky A, Tisherman S A, Stezoski S W, Alexander H
International Resuscitation Research Center (IRRC), University of Pittsburgh School of Medicine, PA.
Crit Care Med. 1993 Sep;21(9):1348-58. doi: 10.1097/00003246-199309000-00019.
Previously, we documented that mild hypothermia (34 degrees C) induced immediately with reperfusion after ventricular fibrillation cardiac arrest in dogs improves functional and morphologic cerebral outcome. This study was designed to test the hypothesis that a 15-min delay in the initiation of cooling after reperfusion would offset this beneficial effect.
Prospective, randomized, controlled study.
Animal intensive care unit.
A total of 22 custom-bred coonhounds.
Eighteen dogs underwent normothermic ventricular fibrillation arrest (no blood flow) of 12.5 mins, reperfusion with brief cardiopulmonary bypass, defibrillation within 5 mins, intermittent positive-pressure ventilation to 20 hrs, and intensive care to 96 hrs. Three groups of six dogs each were studied: group 1, normothermic controls; group 2, core temperature 34 degrees C from reperfusion to 1 hr; and group 3, delayed initiation of cooling until 15 mins after normothermic reperfusion, and 34 degrees C from 15 mins to 1 hr 15 mins after cardiac arrest.
Tympanic membrane temperature (which represented brain temperature) in group 2 reached 34 degrees C at 6 +/- 3 (SD) mins after reperfusion; and in group 3 at 29 +/- 1 mins after reperfusion. Best overall performance categories achieved (1, normal; 5, brain death) compared with group 1, were better in group 2 (p < 0.5) but not in group 3 (NS). Similar results were found with best neurologic deficit scores (0%, normal; 100%, brain death), i.e., 44 +/- 4% in group 1, 19 +/- 15% in group 2 (p < .01), and 38 +/- 9% in group 3 (NS). Total brain histologic damage scores (< 30 minimal damage; > 100 severe damage), however, were 150 +/- 32 in group 1, 81 +/- 13 in group 2 (p < .001 vs. group 1), and 107 +/- 17 in group 3 (p < .05 vs. group 1).
Mild, resuscitative cerebral hypothermia induced immediately with reperfusion after cardiac arrest improves cerebral functional and morphologic outcome, whereas a delay of 15 mins in initiation of cooling after reperfusion may not improve functional outcome, although it may slightly decrease tissue damage.
此前，我们记录到犬心室颤动心脏骤停后再灌注时立即诱导轻度低温（34摄氏度）可改善脑功能和形态学转归。本研究旨在验证以下假设：再灌注后延迟15分钟开始降温会抵消这种有益效果。
前瞻性、随机、对照研究。
动物重症监护病房。
共22只定制繁育的猎浣熊犬。
18只犬经历12.5分钟的常温心室颤动骤停（无血流），短暂体外循环再灌注，5分钟内除颤，间歇性正压通气20小时，重症监护96小时。每组6只犬，共三组：第1组，常温对照组；第2组，从再灌注至1小时核心体温为34摄氏度；第3组，延迟开始降温直至常温再灌注后15分钟，心脏骤停后15分钟至1小时15分钟核心体温为34摄氏度。
第2组鼓膜温度（代表脑温）在再灌注后6±3（标准差）分钟达到34摄氏度；第3组在再灌注后29±1分钟达到。与第1组相比，最佳总体表现类别（1，正常；5，脑死亡）在第2组更好（p<0.5），但第3组无差异（无统计学意义）。最佳神经功能缺损评分（0%，正常；100%，脑死亡）也有类似结果，即第1组为44±4%，第2组为19±15%（p<0.01），第3组为38±9%（无统计学意义）。然而，全脑组织学损伤评分（<30为轻度损伤；>100为重度损伤），第1组为150±32，第2组为81±13（与第1组相比p<0.001），第3组为107±17（与第1组相比p<0.05）。
心脏骤停后再灌注时立即诱导轻度复苏性脑低温可改善脑功能和形态学转归，而再灌注后延迟15分钟开始降温可能无法改善功能转归，尽管可能会轻微减少组织损伤。
