Takasu A, Carrillo P, Stezoski S W, Safar P, Tisherman S A
Safar Center for Resuscitation Research, Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh School of Medicine, PA 15260, USA.
Crit Care Med. 1999 Aug;27(8):1557-64. doi: 10.1097/00003246-199908000-00025.
To test the hypotheses that during lethal uncontrolled hemorrhagic shock (UHS) in rats compared with normothermia and room air breathing: a) mild hypothermia would prolong survival time as well as moderate hypothermia; b) oxygen breathing would prolong survival further; and c) hypothermia and oxygen would mitigate visceral ischemia (dysoxia) during UHS.
Prospective, randomized, controlled laboratory animal study.
Animal research facility.
Male Sprague-Dawley rats.
Fifty-four rats were lightly anesthetized with halothane during spontaneous breathing. UHS was induced by blood withdrawal of 3 mL/100 g over 15 mins, followed by 75% tail amputation with topical application of heparin. Five minutes after tail cut, rats were randomly divided into nine groups (6 rats each) with three rectal temperature levels (38 degrees C [100.4 degrees F; normothermia] vs. 34 degrees C [93.2 degrees F; mild hypothermia] vs. 30 degrees C [86 degrees F; moderate hypothermia]) by surface cooling; each with 3 FIO2 levels (0.25 vs. 0.5 vs. 1.0). Rats were observed without fluid resuscitation until death (apnea and pulselessness). Visceral ischemia was monitored by observing liver and gut surface PCO2.
Mean survival time, which was 51 mins in the control group with normothermia and FIO2 of 0.25, was more than doubled with hypothermia, to 119 mins in the combined mild hypothermia groups (p < .05) and to 132 mins in the combined moderate hypothermia groups (p < .05; NS for moderate vs. mild hypothermia). FIO2 had no statistically significant effect on survival time. Increases in visceral surface PCO2 correlated with hypotension (r2 = .22 for intestine and .40 for liver). Transiently, increased FIO2, not hypothermia, mitigated visceral ischemia.
Both mild and moderate hypothermia prolonged survival time during untreated, lethal UHS in rats. Increased FIO2 had no effect on survival. The effects of hypothermia and increased FIO2 during UHS on viscera, the ability to be resuscitated, and outcome should be explored further.
验证以下假设：与正常体温和室内空气呼吸相比，在大鼠致死性失血性休克（UHS）期间：a）轻度低温与中度低温一样会延长生存时间；b）吸氧会进一步延长生存时间；c）低温和吸氧会减轻UHS期间的内脏缺血（缺氧）。
前瞻性、随机、对照实验室动物研究。
动物研究设施。
雄性Sprague-Dawley大鼠。
54只大鼠在自主呼吸期间用氟烷轻度麻醉。通过在15分钟内抽取3 mL/100 g血液诱导UHS，随后进行75%的尾部截肢并局部应用肝素。断尾后5分钟，大鼠被随机分为9组（每组6只），通过体表降温使直肠温度达到三个水平（38℃[100.4℉；正常体温]、34℃[93.2℉；轻度低温]、30℃[86℉；中度低温]）；每组再分为3个FIO2水平组（0.25、0.5、1.0）。在不进行液体复苏的情况下观察大鼠直至死亡（呼吸暂停和无脉搏）。通过观察肝脏和肠道表面PCO2监测内脏缺血情况。
在正常体温且FIO2为0.25的对照组中，平均生存时间为51分钟，低温组的平均生存时间增加了一倍多，轻度低温联合组为119分钟（p <.05），中度低温联合组为132分钟（p <.05；中度低温与轻度低温相比无显著差异）。FIO2对生存时间无统计学显著影响。内脏表面PCO2的升高与低血压相关（肠道r2 = 0.22，肝脏r2 = 0.40）。短暂地，增加FIO2而非低温减轻了内脏缺血。
在未治疗的致死性大鼠UHS期间，轻度和中度低温均延长了生存时间。增加FIO2对生存无影响。UHS期间低温和增加FIO2对内脏、复苏能力和结局的影响应进一步探讨。
