Iwamoto Shinichiro, Takasu Akira, Sakamoto Toshihisa
Department of Traumatology and Critical Care Medicine, National Defense Medical College, Saitama, Japan.
J Trauma. 2010 Mar;68(3):669-75. doi: 10.1097/TA.0b013e3181a0fbb3.
: 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.
: 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and spontaneous breathing, 24 rats underwent HS (phase I) for 90 minutes, during which 2.5 mL/100 g blood was withdrawn over 15 minutes; fluid resuscitation (phase II) for 60 minutes, during which no blood was reinfused but 5.0 mL/100 g lactated Ringer's solution was infused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.
: 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" in hypothermia compared with normothermia (22 clot signal/min +/- 11 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.
: 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.
在大鼠失血性休克（HS）模型中，确定治疗性低温对HS及液体复苏过程中凝血参数的影响以及对生存率的影响。
在浅麻醉和自主呼吸状态下，24只大鼠经历90分钟的HS（I期），在此期间15分钟内抽取2.5 mL/100 g血液；60分钟的液体复苏（II期），在此期间不回输血液，但在30分钟内输注5.0 mL/100 g乳酸林格氏液；以及无麻醉的观察期（III期）直至72小时。在容量控制性出血后，大鼠被随机分为低温组（n = 12，33℃）或常温组（n = 12，38℃）。在I期和II期维持每组大鼠的直肠温度。在基线以及I期和II期结束时通过Sonoclot分析（SA）评估全血凝固性障碍。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。
72小时时，低温组12只大鼠中有10只存活，常温组12只大鼠中有5只存活（p < 0.05）。与所有大鼠的基线（33%±5%）相比，液体复苏显著降低了血细胞比容（20%±5%；p < 0.05）。SA显示在I期结束时两组之间无显著差异。然而，在II期结束时，SA显示低温组与常温组相比“凝血速率”降低（22个凝血信号/分钟±11个凝血信号/分钟对34个凝血信号/分钟±14个凝血信号/分钟；p < 0.05），且低温组“达到峰值的时间”延长（15分钟±5分钟对6分钟±2分钟；p < 0.05）。在整个实验过程中，两组之间凝血酶 - 抗凝血酶III复合物和血浆α-2-纤溶酶抑制剂复合物的值未见差异。
33℃的治疗性轻度低温在HS期间未引起凝血障碍，但在液体复苏期间确实损害了SA凝血参数，可能是由于稀释作用。低温也延长了HS后的生存期。在大鼠HS模型中，凝血参数的损害并未使结果恶化。
