DELAY IN COOLING NEGATES THE BENEFICIAL EFFECT OF MILD RESUSCITATIVE CEREBRAL HYPOTHERMIA AFTER CARDIAC-ARREST IN DOGS - A PROSPECTIVE, RANDOMIZED STUDY
DELAY IN COOLING NEGATES THE BENEFICIAL EFFECT OF MILD RESUSCITATIVE CEREBRAL HYPOTHERMIA AFTER CARDIAC-ARREST IN DOGS - A PROSPECTIVE, RANDOMIZED STUDY
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DOI：
10.1097/00003246-199309000-00019
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发表时间：
1993-09-01
影响因子：
8.8
通讯作者：
ALEXANDER, H
中科院分区：
文献类型：
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作者：
KUBOYAMA, K;SAFAR, P;ALEXANDER, H
objective.以前，我们记录了轻度低温（34摄氏度）诱导心室颤动心脏骤停后立即再灌注改善功能和形态的大脑结果。本研究的目的是测试的假设，即15分钟的延迟开始冷却后再灌注将抵消这种有益的effect.Design：前瞻性，随机，对照study.Setting.动物重症监护室。受试者。共22个定制繁殖coonhounds.Interventions：18只狗进行常温室颤停搏（无血流）12.5分钟，再灌注与简短的心肺转流，除颤5分钟内，间歇性正压通气20小时，重症监护96小时。研究了三组，每组六只狗：第1组，常温对照;第2组，从再灌注到1小时的核心温度为34 ℃;第3组，延迟开始冷却直到常温再灌注后15分钟，以及心脏停搏后15分钟到1小时15分钟的34 ℃。在再灌注后6 +/-3（SD）min，组2的鼓膜温度（代表脑温度）达到34 ℃;在再灌注后29 +/-1 min，组3的鼓膜温度达到34 ℃。与第1组相比，第2组获得的最佳总体性能类别（1，正常; 5，脑死亡）更好（p <0.05），但第3组（NS）没有。最佳神经功能缺损评分也发现了类似的结果（0%，正常; 100%，脑死亡），即，第1组为44 +/-4%，第2组为19 +/-15%（p <.01），第3组为38 +/-9%（NS）。脑组织学损伤总评分（<30例轻微损伤;> 100例严重损伤），然而，第1组为150 +/-32，第2组为81 +/-13（与第1组相比p <.001），第3组为107 +/-17（p <0.05，与第1组相比）。心脏骤停后立即诱导轻度复苏性脑低温并再灌注可改善脑功能和形态学结局，而在再灌注后延迟15分钟开始冷却可能不会改善功能结果，尽管它可能稍微减少组织损伤。
Objective. 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.Design: Prospective, randomized, controlled study.Setting. Animal intensive care unit.Subjects. A total of 22 custom-bred coonhounds.Interventions: 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.Measurements and Main Results: 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 < .05) 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).Conclusions: 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.