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研究生:牛江山
研究生(外文):Chiang-Shan Niu
論文名稱:糖尿病鼠對熱不適應之神經藥理學基礎及其治療
論文名稱(外文):The neuropharmacological basis of heat intolerance and its treatment in diabetic rats
指導教授:林茂村林茂村引用關係
指導教授(外文):Mao-Tsun Lin
學位類別:博士
校院名稱:國立陽明大學
系所名稱:生理學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2004
畢業學年度:92
語文別:中文
論文頁數:90
中文關鍵詞:糖尿病熱中風
外文關鍵詞:diabetes mellitus(DM)heat stroke
相關次數:
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  • 下載下載:23
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證據顯示熱中風時,大腦因過度產生麩胺酸鹽及氫氧自由基,引發低血壓和腦缺血現象。在熱中風的病人中,大部分是高血糖的糖尿病病患。糖尿病產生熱中風高發病率之神經藥理學基礎尚待釐清。
當STZ誘發之糖尿病鼠曝露在43 ℃的高溫環境下50分鐘後,產生與正常鼠類似的熱中風症狀;體溫上升、平均動脈壓下降、心跳加速、腦血流下降,這些現象因給予NMDA受體的拮抗劑MK-801而減緩。在高溫環境下,會促進紋狀體麩胺酸鹽的釋放量。而且,STZ誘發之糖尿病鼠紋狀體的麩胺酸鹽更大量表現,且存活時間縮短。因此,STZ誘發的糖尿病鼠在高溫環境,乃因紋狀體麩胺酸鹽高分泌量,以致易誘發熱中風的生成。胰島素及phlorizin的治療似乎有助於預防STZ誘發之糖尿病鼠熱中風的發生機率。
正常鼠或是STZ誘發之糖尿病鼠經由熱處理後(42 ℃, 15分鐘),均能誘發大腦產生熱休克蛋白72。然而,熱休克蛋白72無法保護STZ誘發之糖尿病鼠熱中風產生的低血壓和腦缺血的傷害。α-tocopherol(自由基清除劑)亦不能預防STZ誘發之糖尿病鼠熱中風時的症狀。另外,在正常鼠或是STZ誘發之糖尿病鼠經由外頸靜脈直接逆行性灌流冰生理食塩水,因改善感壓反射敏感度,增強動物對熱的抵抗力。
總之,我們成功地證明MK-801、胰島素、phlorizin 或者非經心肺途徑的由外頸靜脈直接逆行性灌流冰生理食塩水,能保護STZ誘發之糖尿病鼠熱中風時的傷害。但α-tocopherol的治療或熱休克蛋白72誘發則無保護之功效。STZ誘發的糖尿病鼠在高溫刺激,因紋狀體產生高量麩胺酸鹽,造成容易誘發熱中風。胰島素、phlorizin、 MK-801的治療或者大腦降溫皆有助於預防糖尿病鼠熱中風的生成。
There is evidence that overproduction of both glutamate and hydroxyl radicals in brain are associated with arterial hypotension and cerebral ischemia exhibited during heatstroke. Among the patients with heatstroke, most of them had diabetes with high plasma glucose. The neuropharmacological basis for the high incidence of diabetes in heatstroke needs to be clarified.
In heatstroke related symptoms in streptozotocin-induced diabetic rats (STZ-diabetic rats) exposed to a high temperature (43 ℃) for 50 min, like that in normal rats, the high colon temperature and the decreases of mean arterial pressure, heart rate and cerebral blood flow were abolished by MK-801, the NMDA receptor antagonist. Also, striatal glutamate was markedly released in both animals by this exposure while the release was higher and the survival time was shorter in STZ-diabetic rats were markedly reduced. Therefore, heatstroke was easily induced via the elevated striatal glutamate in STZ-diabetic rats by high temperature exposure. Insulin and phlorizin treatment seem helpful in the prevention of heatstroke in STZ-diabetic rats.
Heat shock (42 ℃for 15 min) pretreatment was found to be able to induced heat shock protein 72(HSP 72)expression in brains of either normal or STZ-diabetic rats. However, HSP 72 preconditioning failed to protect the STZ-diabetic rats from the heatstroke-induced arterial hypotension and cerebral ischemia.
Furthermore, pretreatment with α-tocopherol (a free radical scavenger)did not prevent the heatstroke-induced arterial hypotension and cerebral ischemia in STZ-diabetic rats.
Finally, direct retrograde hypothermic perfusion via the jugular vein protects against the heatstroke-induced arterial hypotension and cerebral ischemia by potentiality the baroreceptor sensitivity in both normal and STZ-diabetic rats.
In conclusion, we successfully demonstrated that MK-801, insulin, phlorizin or direct retrograde ice saline infusion in the jugular vein without cardiopulmonary bypass, but not α-tocopherol or HSP 72 preconditioning, protect against arterial hypotension and cerebral ischemia during heatstroke in STZ-diabetic rats. Heatstroke was more easily induced via the elevated brain glutamate in STZ-diabetic rats by heat stress. Treatment with insulin, phlorizin, MK-801, or brain cooling seems helpful in the prevention of heatstroke in STZ-diabetic rats.
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