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首页> 外文期刊>The Journal of trauma >Therapeutic mild hypothermia: effects on coagulopathy and survival in a rat hemorrhagic shock model.
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Therapeutic mild hypothermia: effects on coagulopathy and survival in a rat hemorrhagic shock model.

机译:亚低温治疗:对大鼠失血性休克模型的凝血功能和存活率的影响。

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OBJECTIVE:: To determine the effects of therapeutic hypothermia on coagulation parameters during hemorrhagic shock (HS) and fluid resuscitation and on survival, in a rat HS model. METHODS:: Under light anesthesia and spontaneous breathing, 24 rats underwent HS (phase I) for 90 minutes, during which 2.5 mL/100 g blood was withdrawn over 15 minutes; fluid resuscitation (phase II) for 60 minutes, during which no blood was reinfused but 5.0 mL/100 g lactated Ringer's solution was infused over 30 minutes; and an observation (phase III) without anesthesia until 72 hour. After the volume-controlled hemorrhage, rats were randomized into a hypothermia group (n = 12, 33 degrees C) or a normothermia group (n = 12, 38 degrees C). The rectal temperature in each group was maintained during phases I and II. Whole blood coagulopathy was assessed by Sonoclot analysis (SA) at baseline and the end of phases I and II. Fibrinolysis parameters of thrombin-antithrombin III complex and plasma-alpha-2-plasmin inhibitor complex were also monitored. RESULTS:: At 72 hour, 10 of 12 hypothermia group rats, and 5 of 12 normothermia group rats remained alive (p < 0.05). Fluid resuscitation significantly decreased hematocrit (20% +/- 5%) compared with baseline (33% +/- 5%; p < 0.05) in all rats. SA showed no significant differences between groups at the end of phase I. However, at the end of phase of II, SA revealed a decreased clot rate clot signal/min vs. 34 clot signal/min +/- 14 clot signal/min; p < 0.05) and a prolonged "time to peak" in hypothermia (15 minutes +/- 5 minutes versus 6 minutes +/- 2 minutes; p < 0.05). No differences in thrombin-antithrombin III complex and plasma-alpha-2-plasmin inhibitor complex values were seen between groups throughout the experiment. CONCLUSIONS:: Therapeutic mild hypothermia of 33 degrees C did not cause coagulopathy during HS, but did impair SA coagulation parameters during fluid resuscitation, probably because of dilution. Hypothermia also prolonged survival after HS. Impairments to coagulation parameters did not worsen outcomes in the rat HS model.
机译:目的:在大鼠HS模型中,确定治疗性低温对失血性休克(HS)和液体复苏期间凝血参数的影响以及对存活率的影响。方法:在轻度麻醉和自发呼吸下,对24只大鼠进行HS(I期)90分钟,在此期间15分钟内抽取2.5 mL / 100 g血液。进行液体复苏(II期)60分钟,在此期间未再注入血液,但在30分钟内注入了5.0 mL / 100 g乳酸林格氏液;并观察(III期)直到72小时才麻醉。体积控制性出血后,将大鼠随机分为亚低温组(n = 12、33摄氏度)或常温组(n = 12、38摄氏度)。在第一和第二阶段期间,每组的直肠温度均保持不变。在基线以及I和II期结束时通过Sonoclot分析(SA)评估了全血凝血病。还监测了凝血酶-抗凝血酶III复合物和血浆-α-2-纤溶酶抑制剂复合物的纤溶参数。结果:在第72小时,12只低温组大鼠中的10只和12只正常体温组大鼠中的5只仍然存活(p <0.05)。与基线(33%+/- 5%; p <0.05)相比,液体复苏显着降低了血细胞比容(20%+/- 5%)。 SA在阶段I结束时组间无显着差异。但是,在阶段II结束时,SA血凝块速率/ min降低,凝块速率降低为34凝块信号/ min +/- 14凝块信号/ min。 p <0.05)和体温过低的“高峰时间”延长(15分钟+/- 5分钟与6分钟+/- 2分钟; p <0.05)。在整个实验过程中,各组之间的凝血酶-抗凝血酶III复合物和血浆α-2-纤溶酶抑制剂复合物值均无差异。结论:33摄氏度的治疗性亚低温未在HS期间引起凝血病,但在液体复苏期间未损害SA凝血参数,可能是由于稀释。体温过低也可延长HS后的生存期。凝血参数的损害并没有使大鼠HS模型的结局恶化。

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