Panjwani G D, Mustafa M K, Muhailan A, Aneja I S, Owunwanne A
Department of Physiology, Faculty of Medicine, Kuwait University, Safat.
Electroencephalogr Clin Neurophysiol. 1991 Sep-Oct;80(5):384-91. doi: 10.1016/0168-5597(91)90086-d.
In the rat heat stroke model, established by heating to a climatic chamber temperature of 42 degrees C, the brain temperature was found to be consistently lower than the rectal temperature, suggesting efficient brain cooling mechanisms in the rat. In response to heating, with increasing brain temperature, the latencies of the somatosensory evoked potentials (SEPs) showed an initial decrease followed by an increase (inflection point). Studies were done on rats heated up to, before, or after the inflection point and then cooled. Reversibility with cooling of functional and structural changes induced by heat was evaluated by analysis of SEPs, survival time, brain blood perfusion and histopathology. The evidence from these studies demonstrated that the brain temperature at which the inflection in wave P2 latency occurred was critical, beyond which hyperthermia produced irreversible changes in the SEP, shorter survival time, relative reduction in brain blood perfusion and evidence of brain histopathological damage. The suggestion that endorphins may mediate brain dysfunction in hyperthermia was investigated. In rats heated and then cooled after wave P2 latency inflection naloxone, the endorphin antagonist, was injected (10 mg/kg, intravenously) just prior to the inflection. It produced reversibility of SEP changes as well as longer survival time (P less than 0.001) compared to saline-treated rats.
在通过将气候箱温度加热至42摄氏度建立的大鼠中暑模型中，发现脑温始终低于直肠温度，这表明大鼠存在有效的脑冷却机制。随着脑温升高，体感诱发电位（SEP）的潜伏期在加热过程中先缩短后延长（转折点）。对在转折点之前、之时或之后加热然后冷却的大鼠进行了研究。通过分析SEP、存活时间、脑血流灌注和组织病理学来评估热诱导的功能和结构变化在冷却后的可逆性。这些研究的证据表明，P2波潜伏期出现转折点时的脑温至关重要，超过此温度，体温过高会导致SEP发生不可逆变化、存活时间缩短、脑血流灌注相对减少以及出现脑组织病理学损伤的证据。研究了内啡肽可能介导体温过高时脑功能障碍这一假说。在大鼠P2波潜伏期出现转折点后加热然后冷却，在转折点前静脉注射内啡肽拮抗剂纳洛酮（10mg/kg）。与生理盐水处理的大鼠相比，纳洛酮使SEP变化可逆，且存活时间更长（P<0.001）。
