Prueckner S, Safar P, Kentner R, Stezoski J, Tisherman S A
Safar Center for Resuscitation Research, University of Pittsburgh, 3434 Fifth Avenue, Pittsburgh, PA 15260, USA.
J Trauma. 2001 Feb;50(2):253-62. doi: 10.1097/00005373-200102000-00010.
In previous studies, mild hypothermia (34 degrees C) during uncontrolled hemorrhagic shock (HS) increased survival. Hypothermia also increased mean arterial pressure (MAP), which may have contributed to its beneficial effect. We hypothesized that hypothermia would improve survival in a pressure-controlled HS model and that prolonged hypothermia would further improve survival.
Thirty rats were prepared under light nitrous oxide/halothane anesthesia with spontaneous breathing. The rats underwent HS with an initial blood withdrawal of 2 mL/100 g over 10 minutes and pressure-controlled HS at a MAP of 40 mm Hg over 90 minutes (without anticoagulation), followed by return of shed blood and additional lactated Ringer's solution to achieve normotension. Hemodynamic monitoring and anesthesia were continued to 1 hour, temperature control to 12 hours, and observation without anesthesia to 72 hours. After HS of 15 minutes, 10 rats each were randomized to group 1, with normothermia (38 degrees C) throughout; group 2, with brief mild hypothermia (34 degrees C during HS 15-90 minutes plus 30 minutes after reperfusion); and group 3, with prolonged mild hypothermia (same as group 2, then 35 degrees C [possible without shivering] from 30 minutes after reperfusion to 12 hours).
MAP during HS and initial resuscitation was the same in all three groups, but was higher in the hypothermia groups 2 and 3, compared with the normothermia group 1, at 45 and 60 minutes after reperfusion. Group 1 required less blood withdrawal to maintain MAP 40 mm Hg during HS and more lactated Ringer's solution for resuscitation. At end of HS, lactate levels were higher in group 1 than in groups 2 and 3 (p < 0.02). Temperatures were according to protocol. Survival to 72 hours was achieved in group 1 by 3 of 10 rats, in group 2 by 7 of 10 rats (p = 0.18 vs. group 1), and in group 3 by 9 of 10 rats (p = 0.02 vs. group 1, p = 0.58 vs. group 2). Survival time was longer in group 2 (p = 0.09) and group 3 (p = 0.007) compared with group 1.
Brief hypothermia had physiologic benefit and a trend toward improved survival. Prolonged mild hypothermia significantly increased survival after severe HS even with controlled MAP. Extending the duration of hypothermia beyond the acute phases of shock and resuscitation may be needed to ensure improved outcome after prolonged HS.
在先前的研究中，非控制性失血性休克（HS）期间轻度低温（34℃）可提高生存率。低温还可提高平均动脉压（MAP），这可能是其有益作用的原因。我们假设低温可改善压力控制的HS模型中的生存率，且长时间低温可进一步提高生存率。
30只大鼠在轻度氧化亚氮/氟烷麻醉下自主呼吸制备。大鼠先在10分钟内初始失血2 mL/100 g进行HS，然后在90分钟内将MAP控制在40 mmHg进行压力控制的HS（不进行抗凝），随后回输失血并补充额外的乳酸林格液以达到正常血压。血流动力学监测和麻醉持续1小时，体温控制持续12小时，无麻醉观察持续72小时。HS 15分钟后，每组10只大鼠随机分为：第1组，全程正常体温（38℃）；第2组，短暂轻度低温（HS 15 - 90分钟及再灌注后30分钟为34℃）；第3组，长时间轻度低温（与第2组相同，再灌注后30分钟至12小时为35℃[可能无寒战]）。
三组在HS和初始复苏期间的MAP相同，但与正常体温的第1组相比，低温的第2组和第3组在再灌注后45分钟和60分钟时MAP更高。第1组在HS期间维持MAP 40 mmHg所需的失血量更少，复苏时需要更多的乳酸林格液。HS结束时，第1组的乳酸水平高于第2组和第3组（p < 0.02）。体温符合方案设定。第1组10只大鼠中有3只存活至72小时，第2组10只大鼠中有7只存活（与第1组相比p = 0.18），第3组10只大鼠中有9只存活（与第1组相比p = 0.02，与第2组相比p = 0.58）。与第1组相比，第2组（p = 0.09）和第3组（p = 0.007）的存活时间更长。
短暂低温具有生理益处且有提高生存率的趋势。长时间轻度低温即使在MAP控制的情况下也能显著提高严重HS后的生存率。可能需要将低温持续时间延长至休克和复苏的急性期之后，以确保长时间HS后有更好的预后。
