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研究生:周岳廷
研究生(外文):Yueh -Ting Chou
論文名稱:低溫治療實驗性熱中風之機轉的探討
論文名稱(外文):The mechanisms underlie the hypothermia therapy in 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:2003
畢業學年度:91
語文別:中文
論文頁數:194
中文關鍵詞:熱中風低溫
外文關鍵詞:heatstrokehypothermia
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熱中風好發在熱的環境中休息、在熱的環境中工作和在冷的環境中過度運動。通常熱中風的臨床症狀是高體溫、多器官的功能失調和中樞神經的損傷。在治療熱中風方面以降低體溫為最有效。但是降低體溫到底是透過何種機轉去達成治療的效用是本研究想要探討的。
本研究採用林茂村教授所發展的熱中風動物模式,將動物放置於42℃高溫的環境誘導熱中風,當動物熱中風後給於16℃低溫治療,來觀察1.生理的參數:肛溫、平均動脈壓、心跳速率和腦血流的變化 2.生化的參數:週邊動脈血液氣體分析包括PaO2、PaCO2、pH值、lactate and glucose 3.腦中的生化參數:包括glutamate(細胞缺血指標),dopamine,glycerol(細胞損傷指標),lactate/pyruvate(細胞缺血指標) and glucose。另外本實驗同時採用非侵入性的方式:功能性磁振造影(fMRI)和正子造影(PET)來觀察熱中風的動物及降低體溫後之腦功能的改變,例如相對腦容積的變化和腦中基底核多巴胺神經核功能的變化,透過以上各項研究來探討低溫療法到底是經由何種機轉來達到治療熱中風的目的。
在熱中風後沒有低溫治療組其平均動脈壓、局部腦血流、直腸溫度、心跳速率、動脈血中氧分壓、動脈血中二氧化碳分壓、酸鹼值和腦部相對腦血容積自我調節功能明顯比控制組別動物來得低。而在血中乳酸含量、神經損傷分數、神經膠質增生、海馬回細胞外麩胺酸、甘油、乳酸、乳酸/丙酮酸、紋狀體細胞外多巴胺濃度和紋狀體之基底核比上小腦之 FDOPA比例比控制組動物來得高。若在熱中風後給予低溫治療之組別,可以改善因熱中風所造成低血壓、腦部缺血、神經細胞的損傷、神經膠質細胞增生、乳酸血症、低氧合、酸血症以及海馬回過多麩胺酸、甘油、乳酸、乳酸/丙酮酸、紋狀體過多的多巴胺及基底核比上小腦 FDOPA 比例和腦部相對腦血容積自我調節功能失調的現象。
由以上的資料顯示低溫治療對熱中風動物之保護作用是多方面的,換句話說,就是抑制1. 乳酸血症 2. 組織酸中毒 3. 低氧合 4. 低動脈血壓 5. 腦部缺血 6. 腦部過多多巴胺,甘油,麩胺酸和乳酸/丙酮酸7. 神經膠質細胞增生 8. 神經細胞的損傷 9.腦部自我調節功能失調。說明了低溫療法主要是透過抑制循環性休克以及腦神經細胞缺血與損傷,因而延長熱中風動物之存活時間。
Heatstroke develops at rest in a hot environment、physical work in warm environments or strenuous exercise in other than cold environments. In general, the symptoms of heatstroke are (a) hyperthermia, (b) multiple organ failure, and (c) neural dysfunction. The good efficient treatment of heatstroke is cooling. The present study attempted to ascertain the possible mechanisms underlie the hypothermia therapy in experimental heatstroke.
The present study used a well-characterized experimental heatstroke model. Animals under urethane anesthesia were exposed to water blanket temperature (Tblanket) of 42℃ until mean arterial pressure (MAP) and regional cerebral blood flow (CBF) began to decrease from their peak levels, which was arbitrarily defined as the onset of heatstroke. Control animals were exposed to 26℃. Cooling was accomplished by decreasing Tblanket from 42℃ to 16℃. The following parameters were assessed:1. colonic temperature (Tco)、mean arterial pressure (MAP)、heart rate (HR)、and cerebral blood flow (CBF). 2. The arterial blood gas including: PaO2、PaCO2、pH、lactate and glucose;3. The extracellular levels of glutamate (a cellular ischemia marker), dopamine、glycerol (a cellular injury marker), lactate / pyruvate ratio (a cellular ischemia marker ) and glucose in brain;and 4. cerebral tissue O2 contents、intracranial pressure (ICP) and brain temperature. In addition, the present study used noninvasive methods including both MRI and PET to monitor brain functional alteration in experimental heatstroke. Relative cerebral volume (rCBV) and cerebral basal ganglia dopamine system was also assessed during heatstroke. The values of MAP、CBF、Tco、HR、PaO2、PaCO2、pH、and rCBV after the onset of heatstroke in heatstroke rats received no cooling were all significantly lower than those in control rats. On the other hand, the values of the arterial blood lactate、neuronal damage score、GFAP、extracellar ischemia and damage markers in the hippocampus、extracellular levels of dopamine in the striatum、basal ganglia / cerebellum FDOPA ratio in the striatum were all greater. Cooling immediately after the onset of heatstroke reduced the heatstroke-induced circulatory shock, tissue hypoxemia, lactacidemia, hyperthermia, neuronal damage, cerebral gliosis and cerebral ischemia, and surge of dopamine, basal ganglia / cerebellum FDOPA ratio, rCBV autoregulation failure in the striatum, and surge of cellular levels of ischemia, and injury markers in the hippocampus, and resulted in prolongation of the time to death (the interval between the start of heat stress and cardiac arrest).
The mode of protective action of cooling is apparently multi-focal reactions in heat stroke animals, namely, suppressing (1) lactacidemia;(2) tissue acidification;(3) low oxygenation;(4) arterial hypotension (5) cerebral ischemia (6) surge of dopamine, glycerol, glutamate, and lactate / pyruvate in brain;(7) proliferation of glial cells (8) production of cerebral neuronal damage;and (9) cerebral autoregulation failure. In particular, cooling suppresses circulatory shock, cerebral ischemia and neuronal injury and and results in prolongation of survival in heat stroke animals.
摘要 7
壹、緒論 13
一、熱中風 13
二、低溫治療熱中風 17
三、磁振造影與相對腦血容積 19
四、正子造影與腦中多巴胺神經元功能 20
伍、研究目的 24
貳、實驗材料與方法 25
一、實驗動物及麻醉 25
二、生理及週邊生化參數的測量 25
三、局部腦血流(Cerebral blood flow, CBF)的測定 26
四、局部腦溫度(Cerebral temperature, Tc)、腦血流(Cerebral
blood flows, CBF)及腦氧氣分壓(Cerebral oxygen pressure,
PO2)的測定 28
五、顱內壓(Intracranial pressure, ICP)的測定 28
六、腦部單胺類神經傳遞物質多巴胺(Dopamine, DA)之測定 29
七、腦部神經損傷及神經膠質細胞增生的測定 32
八、腦部麩胺酸(Glutamate)、甘油(Glycerol)、乳酸(Lactate)
及丙酮酸(Pyruvate)的測定 35
九、相對腦血容積(Relative cerebral blood volume, rCBV)
的測定 39
十、腦部單胺類多巴胺(Dopamine, DA)之測定:利用Positron
emission tomography (PET) 40
十一、熱中風(Heat stroke)之誘導及低溫治療 43
十二、病理組織學鑑定 44
十三、實驗步驟 47
十四、統計方法 52
參、結果 53
肆、圖表及說明 61
伍、討論 159
陸、結論與展望 166
柒、參考文獻 168
捌、附錄 194
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