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熱中風的發生，常困暴露於高熱環境中所造成；臨床診斷出現高體溫及合併中樞神經系統異常現象，其包括昏迷，譫妄和意識不清等複雜之症狀。最近的研究發現，當急性熱中風後，所致大腦紋狀體缺血及神經細胞損傷與黑質紋狀體多巴胺神經系統明顯活化有關。有證據指出，當腦部缺血時，引發多巴胺神經系高度活化而導致紋狀體神經細胞損傷。而高容積稀釋法，先前學者已常使用於實驗性腦部缺血的治療。因此，我們假設高容積稀釋法可藉抑制多巴胺神經系活化來保護紋狀體神經細胞而免於缺血性損傷。為了證實此一假設，我們比較有及無使用高容積稀釋法 (熱中風前，靜脈給予10%人類白蛋白溶液或0.9%食鹽水)，大鼠的平均血壓、直腸溫度、紋狀體血流率、多巴胺釋放、和酪胺酸水解酵素活性表現，以及紋狀體神經細胞損傷情況。
熱中風之誘發係先將實驗動物以氨基甲酸乙酯(Urethane, 1.4g/kg, i.P.)麻醉，暴置於高溫環境下(42℃)；當動物之平均動脈座壓、紋狀體血流自其最高點做急遽降落時視為熱中風之誘發開始。當熱中風誘發時，動物表現高體溫，平均動脈壓、紋狀體腦血流值則下降，而紋狀體多巴胺釋放、酪胺酸水解酵素活性表現以及紋狀體神經細胞損傷均較無誘發熱中風之動物提高。然而，事先給予高容積稀釋法處理之誘發熱中風動物均可將熱中風所誘發的上述反應明顯減輕。除此，高容積稀釋也可延長動物之存活時間(熱中風之誘發至死亡之間)。由這些結果推論：熱中風之症狀發作與大腦黑質紋狀體多巴胺神經系統明顯活化有關；若以高容積稀釋法抑制其活性，可有效保護紋狀體神經細胞免受熱中風時缺血性之損傷。
The clinical diagnosis of heatstroke is strongly suggested when hyperthermia is associated with neurological abnormalities ( including coma, delirium and confusion ) after exposure to high amibient temperature. In recent studies, marked activation of the nigrostriatal dopaminergic system in association with striatal ischemia and cell injury was found in rats after heatstroke. This dopaminergic hyperactivity was proposed to contribute to the selective vulnerability of striatal neurons to ischemia. Hypervolemic hemodilution has been frequently used in the treatment of cerebral ischemia. We hypothesized that hypervolemic hemodilution protects the striatal neurons from ischemic injury by inhibiting the dopaminergic activity. To deal with this question, we compared the temporal profile of mean arterial pressure (MAP), colon temperature, striatal blood flow (SBF), striatal dopamine (DA) release and tyrosine hydroxylase (TH) expression, striatal neuronal damage, and survival time in rats with and without hypervolemic hemodilution produced by administration of 10 % human albumin before onset of heatstroke.
Heatstroke was induced by exposing the animals under urethane anesthesia to a high ambient temperature (42℃); the movement at which MAP and SBF began to decrease from their peak levels was taken as the onset of heatstroke. During onset of heatstroke, the animals displayed hyperthermia, increased level of striatal DA, increased expression of TH, striatal neuronal damage, decreased MAP, and decreased SBF compared to normothermic controls. The marked activation of dopaminergic system in striatum, arterial hypotension, striatal ischemia and neuronal damage after heatstroke onset were significantly attenuated by pretreatment with hypervolemic hemodilution. In addition, the survival time (interval between onset of heatstroke and death) of the rats with heatstroke was extended by pretreatment with hypervolemic hemodilution. These results suggest that marked activation of nigrostriatal dopamine system is important for the development of heatstroke syndromes and it's inhibition after hypervolemic hemodilution can effectively protect striatal neurons from ischemia and cell injury in rat heatstroke.
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