Silbergleit R, Satz W, Lee D C, McNamara R M
Department of Emergency Medicine, George Washington University, Washington, DC, USA.
Ann Emerg Med. 1998 Mar;31(3):339-43. doi: 10.1016/s0196-0644(98)70344-0.
To correlate changes in core body temperature with changes in mean arterial pressure (MAP) and cardiac output (CO) and with the administration of room-temperature intravenous fluids in a clinically relevant large-animal model of uncontrolled hemorrhage.
Ten swine were subjected to uncontrolled hemorrhage through a flow-monitored shunt placed between the femoral artery and the peritoneal cavity. Animals were randomly assigned to a treatment or a control group. The control group (n=5) received no intravenous fluids. The treatment group (n=5) received 80 mL/kg (3:1 crystalloid/blood loss) ambient-temperature lactated Ringer's solution over a 10-minute resuscitation phase initiated 10 minutes after injury. CO and core body temperature, measured with the use of a pulmonary artery catheter, and MAP were the primary outcomes. We analyzed differences between groups with the use of repeated-measures ANOVA. Change of temperature was analyzed against the change in CO, and against fluid infusion for each interval, by means of regression analysis.
The unresuscitated control animals had no change in core temperature despite profound hemorrhagic shock and hypotension. The animals treated with fluids had a mean 2.6 degrees C decrease in core temperature during fluid resuscitation (95% confidence interval [CI], 1.8 to 3.5). A 1.5 degrees C decrease in core temperature (95% CI, .1 to 2.0) persisted at the end of 60 minutes (40 minutes after fluid resuscitation was discontinued). Core temperatures in control animals were 2.8 degrees C lower than those in treated animals after fluid resuscitation (95% CI, .8 to 4.8). Decreases in core temperature correlated with fluid infusion (beta=-35.2 mL/kg x degrees C, R2=.75) and increases in CO (beta=-1.46 L/min x degrees C, R2=.69).
Ambient-temperature crystalloid resuscitation in a clinically relevant large-animal model of hemorrhagic shock causes small decreases in core body temperature. Resuscitation rather than shock is the main cause of decreased body temperature in this model.
在一个具有临床相关性的未控制出血的大型动物模型中，将核心体温的变化与平均动脉压（MAP）和心输出量（CO）的变化以及室温静脉输液的使用情况进行关联分析。
通过在股动脉和腹腔之间放置的流量监测分流器，对10头猪进行未控制出血。将动物随机分为治疗组或对照组。对照组（n = 5）未接受静脉输液。治疗组（n = 5）在受伤10分钟后开始的10分钟复苏阶段接受80 mL/kg（3:1晶体液/失血量）的常温乳酸林格氏液。主要观察指标为使用肺动脉导管测量的CO、核心体温和MAP。我们使用重复测量方差分析来分析组间差异。通过回归分析，针对每个时间间隔，分析温度变化与CO变化以及液体输注的关系。
未复苏的对照动物尽管出现严重失血性休克和低血压，但核心体温没有变化。接受液体治疗的动物在液体复苏期间核心体温平均下降2.6℃（95%置信区间[CI]，1.8至3.5）。在60分钟结束时（停止液体复苏40分钟后），核心体温持续下降1.5℃（95% CI，0.1至2.0）。液体复苏后，对照动物的核心体温比治疗动物低2.8℃（95% CI，0.8至4.8）。核心体温的下降与液体输注（β = -35.2 mL/kg×℃，R² = 0.75）和CO的增加（β = -1.46 L/min×℃，R² = 0.69）相关。
在具有临床相关性的失血性休克大型动物模型中，常温晶体液复苏会导致核心体温小幅下降。在该模型中，复苏而非休克是体温下降的主要原因。
