Ogura K, Takayasu M, Dacey R G
Department of Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri.
J Neurosurg. 1991 Sep;75(3):433-9. doi: 10.3171/jns.1991.75.3.0433.
The effects of hypothermia and hyperthermia on the cerebral microcirculation were studied using isolated perfused intracerebral (parenchymal) arterioles obtained from rats. In a temperature-dependent manner, hypothermia (20.0 degrees to 35.0 degrees C) dilated the spontaneous tone developed by the arterioles and also diminished their contractile response to potassium and prostaglandin F2 alpha. In contrast, hyperthermia (40.0 degrees to 45.0 degrees C) induced a biphasic response consisting of initial vasoconstriction and secondary vasodilation. Exposure of the vessels to 45.0 degrees C for 30 minutes irreversibly abolished the spontaneous tone and responsiveness of the arterioles when the temperature of the preparation was returned to 37.5 degrees C. In calcium-free solutions, however, the arteriolar diameter was not affected within a temperature range of 20.0 degrees to 45 degrees C. Furthermore, arterioles that had been in a calcium-free solution during exposure to 45 degrees C temperature recovered their viability at 37.5 degrees C. These results suggest that changes in ambient temperature alter calcium-induced contraction in arteriolar smooth muscle, and that the irreversible effects of hyperthermia on the arterioles are dependent upon extracellular calcium. These studies indicate that alterations in brain temperature may affect the pathogenesis of cerebral ischemia by mechanisms that are in part independent of parenchymal metabolism.
利用从大鼠获取的离体灌注脑实质小动脉，研究了低温和高温对脑微循环的影响。低温（20.0℃至35.0℃）以温度依赖的方式扩张小动脉产生的自发张力，并减弱其对钾和前列腺素F2α的收缩反应。相比之下，高温（40.0℃至45.0℃）诱导出一种双相反应，包括初始血管收缩和继发性血管舒张。当制剂温度恢复到37.5℃时，将血管暴露于45.0℃30分钟会不可逆地消除小动脉的自发张力和反应性。然而，在无钙溶液中，在20.0℃至45℃的温度范围内小动脉直径不受影响。此外，在暴露于45℃温度期间处于无钙溶液中的小动脉在37.5℃时恢复了活力。这些结果表明，环境温度的变化改变了小动脉平滑肌中钙诱导的收缩，并且高温对小动脉的不可逆影响取决于细胞外钙。这些研究表明，脑温的改变可能通过部分独立于实质代谢的机制影响脑缺血的发病机制。
