期刊刊名：南台學報 　 卷期：37卷1期

篇名出版日期：2012年5月1日

作者：Hung-Jung Lin,林宏榮

語言：English

關鍵字：熱中風,間歇性低氧適應,循環性休克,大腦缺血,心輸出量, Heatstroke, Intermittent Hypoxia Adaptation, Circulatory Shock, Cerebral Ischemia, Cardiac Output

被點閱次數：2次

閱讀時間：153sec

摘要：
Heatstroke is a serious clinical problem in many parts of world. The symptoms of heatstroke include hyperthermia, central nervous system disorders and multiple organ failures in more than 50 % of the victims. In the animal model heatstroke, rats display arterial hypotension, intracranial hypertension, cerebral ischemia, cerebral dopamine, serotonin, cytokines and glutamate overload and cerebral neuronal damage. However, the above-mentioned heatstroke syndromes are attenuated by induction of heat shock protein 72 (HSP72) in rat brain. Other evidences have also demonstrated that HSP 72 can be detected in heart from rats with endurance exercise or hypoxia training. This raises the possibility that pretreatment of rats with physical exercise protects against the heatstroke-induced arterial hypotension, cerebral ischemia and cerebral neuronal damage via inducing HSP 72 and improves cardiovascular function of rats during heatstroke. Male SD rats are randomly assigned to either a heatstroke control group or to an intermittent hypoxia adaptation group. Trained animals were put in a hypoxia chamber 5 days/week, 4 hours/day with intensity 0.45 ATA for 2 weeks. Heatstroke is induced by exposing the animals to a high temperature (43℃); the moment at which mean arterial pressure (MAP) and cerebral blood flow (CBF) decreased from their peak values is taken as the time of heatstroke onset. To address the question properly, we will compare the temporal profiles of MAP, CBF, heart rate and cerebral neuronal damage score after heatstroke in rats with or without physical exercise training and detect the changes of cardiovascular parameters (cardiac output and heart stroke volume) through the heatstroke period. Implanting an intracranial microdialysis probe will help assess the NO, free radicals release and markers of cerebral ischemia and cellular injury (including glycerol, glutamate and lactate/pyruvate ratio) in brain. The HSP 72 in brain cortex tissue was analyzed by SDS-PAGE and Western blotting with monoclonal anti-HSP 72 antibody. The data indicate that intermittent hypoxia adaptation increased HSP72 expression and attenuated heatstroke induced neuronal damage.

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