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研究生:陳盈利
論文名稱:熱休克對空氣栓塞所造成急性肺損傷的保護作用
論文名稱(外文):Effects of heat shock on air embolism-induced acute lung injury
指導教授:黃坤崙黃坤崙引用關係
學位類別:碩士
校院名稱:國防醫學院
系所名稱:海底醫學研究所
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:2002
畢業學年度:90
語文別:中文
論文頁數:78
中文關鍵詞:空氣栓塞
外文關鍵詞:Air embolism
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潛水順應性是指潛水員每天進行深度時間相當的潛水工作,得減壓病的機會與日遞減;雖然有學者提出『補體去除學說』可能扮演重要的角色,但是潛水順應性的機轉到目前還不明瞭。另一方面,先決化(preconditioning)是一種生物保護機制,是指生物組織在經過多次非致命性的刺激後,對接踵而來較深的刺激將產生耐受性,避免嚴重的傷害。事先給予熱處置可以誘導熱休克蛋白的合成,可保護多種嚴重刺激所帶來的組織傷害。因此我們試著以『誘生保護因子理論』來解釋潛水順應性的機制。肺部空氣栓塞為潛水減壓症臨床表徵之一,可作為減壓症研究的動物模式。本研究目的在探討熱休克處置對肺部空氣栓塞所造成急性肺損傷的影響。
在麻醉狀況下,給予大白鼠靜脈空氣注射每分鐘25µl持續20或40分鐘,會導致低血氧的情形。靜脈空氣注射停止40分鐘後,將右肺門夾閉,右肺取下分析肺濕乾重量比及熱休克蛋白;左肺則進行支氣管肺泡灌洗收集肺灌洗液。靜脈空氣注射會增加肺濕乾重量比及肺灌洗液中蛋白質的含量及乳酸脫氫酵素的活性。利用西方墨點法分析熱休克蛋白,可發現熱處置後4 及16小時熱休克蛋白在肺組織的表現量最多。熱休克處置可加速靜脈空氣注射時所導致低血氧的恢復,且可減少肺濕乾重量比及肺灌洗液中的蛋白質濃度。熱休克處置後,動物肺組織中熱休克蛋白的含量與其靜脈空氣注射後肺濕乾重量比增加的程度成反比。我們的結果證實,熱處置的確會增加熱休克蛋白的產生,事先給予熱處置對肺部空氣栓塞,所造成的急性肺損傷有部分保護,其機轉可能是透過熱休克蛋白的合成。

Diving acclimatization has been described as an adaptive mechanism to decompression sickness (DCS) after repetitive pressure exposures. Although it has been reported that complement depletion may play a role, the mechanism of acclimatization to DCS remains unknown. On the other hands, preconditioning is a powerful form of endogenous protection against the subsequently severe insults via induction of cytoprotective factors. Thermal precondition has been proved to be able induce the production of heat shock protein (HSP) and to protect against organ damage., We therefore proposed an “induction theory” trying to explain the mechanism of diving acclimatization. The purposes of this study were to demonstrate an acute lung injury induced by pulmonary air embolism which is one of the manifestation of DCS and to investigate the effects of prior heat shock on air bubble-induced lung injury in rats.
Venous air infusion at rate of 25 µl/min for 20 or 40 min induced a profound hypoxemia in anesthetized rats. Forty min after stopping air infusion the right lung was cramped at hilum and was excised for wet/dry measurement and HSP determination and bronchoalveolar lavage (BAL) were done to the left lung. Air infusion increased protein concentration and LDH activity in BAL fluid as well as lung water content. Expression of heat shock protein 70(HSP70) in the lung, determined by Western blotting, was significantly higher than that of the control group 4 to 16 hours after heat shock. Prior heat shock accelerated the recovery of hypoxemia after air infusion and reduced the wet/dry weight ratio and BAL fluid protein concentration. The increase in W/D ratio after air infusion was inversely correlated to the level of HSP70 expression in the lung. Our results demonstrated that prior heat shock induces expression of HSP70 in the lung, which may be responsible for the protective effects against air embolism-induced lung injury.

目錄
頁次
目錄 ………………………………………………………………………………… I
圖次 ……………………………………………………………………………………. II
中文摘要..……………………………………………………………………………. III
英文摘要 …………………………………………………………………………….. V
第一章 前言 ………………………………………………………………………. 1
第二章 材料與方法 …………………………………………………………. 17
第三章 實驗結果 ……………………………………………………………… 31
第四章 討論……………………………………………………………………….. 38
第五章 結論 ……………………………………………………………………….. 47
第六章 參考文獻…………………… ………………………………………….. 67

第六章、參考文獻
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