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研究生:劉家全
研究生(外文):Chia-Chyuan Liu
論文名稱:甲型內皮素受體拮抗劑和羥乙基澱粉對實驗熱中風之影響
論文名稱(外文):Effects of ETA receptor antagonist and hydroxyethyl starch on experimental heatstroke
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:145
中文關鍵詞:熱中風內皮素-1甲型內皮素受體拮抗劑羥乙基澱粉體積擴張腫瘤壞死因子-阿爾法
外文關鍵詞:heatstrokeendothelin-1ETAR antagonisthydroxyethyl starchvolume expansiontumor necrosis factor-alpha
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  • 被引用被引用:2
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  • 下載下載:9
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臨床發現,中風、腦缺血或是腦創傷患者體內血漿和腦脊髓液中,可觀察到內皮素-1濃度明顯比正常人來得高。另一方面,羥乙基澱粉在許多腦部缺血實驗模式中也被認為具有良好的效用。本論文主要的目的在於觀察內皮素受體拮抗劑的前處理或羥乙基澱粉的處理是否可減輕在實驗熱中風中所致動脈壓低落和腦部缺血的情形。現今研究,是將成年大白鼠麻醉後,置於42 ℃環境溫度下誘發熱中風的生成。隨熱中風誘發過程,當動物體動脈血壓從高點突然呈現不可恢復性低落的瞬間,此一時間點稱為熱中風生成點。而當動物體持續置於42 ℃環境溫度下約80分鐘後,會表現出有高體溫、動脈低血壓、低心輸出量(由於心搏量和總周邊阻力皆表現低落所致)、與高血中內皮素-1濃度和腫瘤壞死因子-阿爾法、和高腦缺血及腦損傷標記濃度的情形。事先於熱中風加熱起始點前60分鐘,給予處理甲型內皮素受體拮抗劑BQ-610 (0.5 mg/kg, i.v.),而非乙型內皮素受體拮抗劑BQ-788 (0.5 mg/kg, i.v.),明顯觀察到可改善動物體高體溫、動脈血壓低落、心輸出量降低與血中高濃度腫瘤壞死因子-阿爾法和高濃度腦缺血及損傷標記的情形。此外,於熱中風生成點立即給予羥乙基澱粉11 ml/kg處理後,經由增加體積擴張效用,可使熱中風所致動脈血壓低落、心搏量和總周邊阻力低落、血液酸化和動脈氧分壓低落、腦氧分壓低落和增加腦缺血及損傷標記濃度的情形亦獲得改善。因此,實驗結果指出,於實驗熱中風中,甲型內皮素受體拮抗劑的前處理具有預防效用,而羥乙基澱粉則具有治療的效用。
In clinical situation, the patients with stroke, cerebral ischemia and trauma showed higher levels of endothelin-1 (ET-1) than normal subjects in plasma and cerebrospinal fluid. On the other hand, hydroxyethyl starch (HES) had beneficial effects in several cerebral ischemic models. The aim of the present study was to assess whether endothelin receptor antagonists pretreatment or HES treatment is able to attenuate both the arterial hypertension and cerebral ischemia exhibited during experimental heatstroke. In the present study, heatstroke was induced by putting the anesthetized adult rats to an ambient temperature of 42 ℃. The moment in which the mean arterial pressure dropped irreversibly from the peak was taken as the onset of heatstroke. When exposed animals to 42 ℃ for 80 min, hyperthermia, arterial hypotension, decrement of cardiac output (CO) (due to decreased stroke volume and decreased total peripheral resistance), increment of plasma ET-1 and tumor necrosis factor-alpha, and increment of cerebral ischemia and injury makers were manifested. Prior antagonism of endothelin tape A receptor (ETAR) with BQ-610 (0.5 mg/kg, i.v.), but not endothelin tape B receptor with BQ-788 (0.5 mg/kg, i.v.) 60 min before the initiation of heat exposure, appreciably alleviated hyperthermia, arterial hypotension, decreased CO, increment of tumor necrosis factor, and increment of cerebral ischemia and injury makers exhibited during heatstroke. In addition, the heatstroke-induced arterial hypotension, decreased stroke volume and total peripheral resistance, decreased blood pH and PaO2, decreased brain PO2, and increased levels of cerebral ischemia and injury markers were all attenuated significantly by increasing the volume expansion with 11 ml/kg of HES administered immediately at the onset of heatstroke. The data indicated that ETAR antagonist had a preventive effect, whereas HES therapy had a therapeutic effect during heatstroke.
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