Temperature changes of > or = 1 degree C alter functional neurologic outcome and histopathology in a canine model of complete cerebral ischemia.
Temperature changes of > or = 1 degree C alter functional neurologic outcome and histopathology in a canine model of complete cerebral ischemia.
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发表时间：
1995
期刊：
影响因子：
8.8
通讯作者：
C. Wass;W. Lanier;R. E. Hofer;B. Scheithauer;A. G. Andrews
中科院分区：
文献类型：
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作者：
C. Wass;W. Lanier;R. E. Hofer;B. Scheithauer;A. G. Andrews
基础温度的变化>或= 1 ℃（例如，发热引起的体温过高或麻醉相关的体温过低）在神经受损的患者中是常见的。目前的研究验证了这样一个假设，即温度变化小至1 ℃或2 ℃会显著改变缺血后功能性神经病学结果和脑组织病理学。在短暂性完全脑缺血的犬模型中检验了该假设。在机构批准后，将21只犬随机分配至三个温度特定组之一：（1）维持在37.0 +/- 0.3 ℃（目标温度+/-范围）的参考组;（2）38.0 +/- 0.3 ℃组;或（3）39.0 +/- 0.3 ℃组（每组n = 7）。使用已建立的动脉低血压加颅内高压模型产生持续时间为12.5分钟的完全脑缺血。右心房和颅骨（颞肌下方）温度保持在目标值，缺血前20分钟开始，缺血后1小时停止。此后，所有犬的体温均恢复至37.0 +/- 0.3 ℃。从重症监护环境出院后，将所有犬置于温度受控的恢复区。由设盲观察者在缺血后24、48和72小时使用100分评分量表进行神经系统评估。在72小时检查后（犬麻醉）或缺血相关死亡时，切除脑并保存。随后由不知道治疗组的神经病理学家对大脑进行组织学评分。所有21只犬均纳入神经功能分析;然而，仅存活>或= 24 h的犬纳入组织病理学分析。结果在整个研究过程中，犬的全身生理变量匹配良好，但体温除外。在缺血后72小时检查期间，保持在37 ℃的犬正常或接近正常。相比之下，保持在39摄氏度的狗要么昏迷，要么死于缺血相关的原因。保持在38摄氏度的狗是介于37摄氏度和39摄氏度之间的狗。与对照组相比，38 ℃和39 ℃犬的神经功能评分（分别为P < 0.01和P < 0.001）和组织病理学评分（均为P < 0.01）均显著较差。神经功能评分与组织病理学评分之间也存在显著相关性（rs = 0.96; P < 0.001）。结论：微小的、临床相关的温度变化（1 ℃或2 ℃）导致缺血后神经功能和脑组织病理学的显著改变。假设我们的研究结果可转移到人类，结果表明，在缺血性神经损伤的患者中，应密切监测体温。此外，临床医生应积极治疗所有高热发作，直到患者不再有缺血性神经损伤的风险。
BACKGROUND Changes in basal temperature of > or = 1 degree C (e.g., fever-induced hyperthermia or anesthesia-related hypothermia) are a common occurrence in neurologically impaired patients. The current study tested the hypothesis that temperature changes as small as 1 degree C or 2 degrees C would significantly alter post-ischemic functional neurologic outcome and cerebral histopathology. The hypothesis was tested in a canine model of transient, complete cerebral ischemia. METHODS After institutional approval, 21 dogs were randomly assigned to one of three temperature-specific groups: (1) a reference group maintained at 37.0 +/- 0.3 degree C (target temperature +/- range); (2) a 38.0 +/- 0.3 degree C group; or (3) a 39.0 +/- 0.3 degree C group (n = 7 per group). Complete cerebral ischemia 12.5 min in duration was produced using an established model of arterial hypotension plus intracranial hypertension. Right atrial and cranial (beneath the temporalis muscles) temperatures were maintained at the target value, beginning 20 min before ischemia and ceasing 1 h postischemia. Thereafter, temperatures were returned to 37.0 +/- 0.3 degree C in all dogs. After discharge from the intensive care environment, all dogs were placed in a temperature-controlled recovery area. Neurologic assessment was performed by a blinded observer at 24, 48, and 72 h postischemia using a 100-point scoring scale. After the 72 h examination (with the dogs anesthetized) or at the time of ischemia-related death, the brains were excised and preserved. The brains subsequently were histologically scored by a neuropathologist who was unaware of the treatment groups. All 21 dogs were included in the analysis of neurologic function; however, only dogs that survived for > or = 24 h postischemia were included in the histopathology analysis. RESULTS Dogs were well matched for systemic physiologic variables throughout the study, with the exception of temperature. During the 72 h postischemic examination, dogs maintained at 37 degrees C were either normal or near normal. In contrast, dogs maintained at 39 degrees C were either comatose or died from ischemia-related causes. Dogs maintained at 38 degrees C were intermediate between 37 degrees C and 39 degrees C dogs. When compared with the reference group, both 38 degrees C and 39 degrees C dogs had significantly worse neurologic function scores (P < 0.01 and < 0.001, respectively) and histopathology scores (P < 0.01 for both). There also was a significant correlation between neurologic function and histopathology rank scores (rs = 0.96; P < 0.001). CONCLUSIONS Small, clinically relevant changes in temperature (1 degree C or 2 degrees C) resulted in significant alterations in both postischemic neurologic function and cerebral histopathology. Assuming that our results are transferable to humans, the results suggest that, in patients at imminent risk for ischemic neurologic injury, body temperature should be closely monitored. Further, the clinician should aggressively treat all episodes of hyperthermia until the patient is no longer at risk for ischemic neurologic injury.