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研究生:劉惠惠
研究生(外文):Liu, Hui-Hui
論文名稱:大鼠熱中風時心血管參數與血漿白介質乙型濃渡之變化
論文名稱(外文):Alteration of Cardiovascular Parameters and Plasma Interleukin-1 Levels in Rat Heatstroke
指導教授:林茂村林茂村引用關係
指導教授(外文):Lin Mao-Tsun
學位類別:碩士
校院名稱:國立成功大學
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:1996
畢業學年度:84
語文別:中文
論文頁數:56
中文關鍵詞:熱中風白介質乙型心血管參數
外文關鍵詞:HeatstrokeInterleukin-1Cardiovascular parameters
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為了探究熱中風所導致的低血壓情形時,血流動力變數
及白介質乙型受器所參與的機制,將實驗分為三組來進行:控制組、細菌
內毒素(白介質乙型誘導物)處理組與白介質乙形受器拮抗劑處理組。觀
察此三組實驗動物在熱中風時心血管參數及血漿之白介質乙型之變化。熱
中風的誘導是將全身麻醉之大鼠暴露於42℃的高溫環境中,當動物的平均
動脈壓由上升至最高點突然降低時,即是熱中風之生成時。與常溫之控制
組大鼠比較,熱中風大鼠具有較低之R波振幅、P-R波間期、Q-T波間期、
收縮壓波振幅、舒張壓波波寬、dicrotic wave 波寬、平均動脈壓、心收
縮指數、及心輸出指數等,但卻具有較高之心跳速率以及直腸溫度。進一
步地在熱中風生成前70分鐘時,由靜脈注射200μg/kg的白介質乙型受器
拮抗劑時,可有效地抑制熱中風時所導致之上述參數的降低,但對於熱中
風時所造成的心跳增加及高溫並無明顯影響。除此之外,靜脈注射400μ
g/kg的細菌內毒素除了增加血漿中白介質乙型的含量外,也導致了心收縮
指數、心輸出指數、以及血壓的下降。但細菌內毒素或是熱中風之生成皆
不影響周邊血管阻力。而造成熱中風的潛伏時間(及熱實驗起至熱中風產
生時)及存活時間(即熱中風生成至動物死亡這段時間)可經由注射細菌
內毒素而縮短;但經由注射白介質乙型受器拮抗劑卻可有效延長熱中風動
物的存活時間。在過去我們實驗室已證實由靜脈注射腎上腺素拮抗劑所表
現的心血管參數反應則與熱中風大鼠所表現的反應相似。本研究結果顯示
心跳增加(由於高溫所引起)以及心收縮量減少(由於心肌收縮力降低)
是造成熱中風時之低血壓之兩個主要原因。而熱中風時白介質乙型受器被
活化可能會降低心臟交感神經之活性,更進而導致心肌收縮力的降低,以
致血壓下降。白介質乙型受器拮抗劑對於熱中風之療效乃經由抑制白介質
乙型受器活性,而導致心肌收縮力及血壓降低之延緩所致。
英 文 摘 要In order to ascertain the hemodynamic contributing
factors and the Interleukin-1 (IL-1) receptor mechanisms
underlying the heatstroke-induced arterial hypotension,
experiments were carried out to assess alterations in either
cardiovascular parameters or plasma IL-1 levels in control rats,
in rats treated lipopolysaccharide (LPS, an IL-1 inducer) , or
in rats treated with an IL-1 receptor antagonist during
heatstroke. Heatstroke was induced by exposing the anesthetized
rats to an ambient temperature of 42℃; the moment at which mean
arterial pressure (MAP) began to drease from its peak was taken
as the onset of heatstroke. As compared to these of normothermia
controls, the heatstroke rats had lower values of R wave
amplitude (Ra), P-R interval (PR), Q-T interval (QT), systolic
wave amplitude (Sya), diastolic wave duration (Dd), dicrotic
wave duration (Dw), MAP, stroke index (SI) or cardiac index
(CI), but higher values of heart rate or colonic temperature.
The decreased values of Ra, Sya, Syd, Wd, Dd, Dw, MAP, SI or CI
occurred during heatstroke were attenuated by an I.V. dose of
200μg/kg of IL-1 receptor antagonist, 70 min before the onset
of heatstroke. However, blockade of IL-1 receptors did not
affect the heatstroke-induced tachycardia and hyperthermia.
Intravenous administration of LPS (400μg/kg) in addition to
increasing IL-1 level in the plasma also produced a decrease in
SI, CI or MAP. Neither the LPS nor the heatstroke affected the
total peripheral vascular resistance. Either the latency of
onset of heatstroke or the survival time (interval between the
onset of heatstroke and death) was shortened by LPS, but
prolonged by an IL-1 receptor antagonist. Our previous results
have demonstrated that intravenous injection of adrenergic
receptor antagonists share with heatstroke the similar
cardiovascular parameter responses in rats. The present results
indicate that tachycardia (due to hyperthermia) and decreased
stroke volume (due to decreased myocardial contraction) are two
contributing factors responsible for development of arterial
hypotension in heatstroke. Activation of IL-1 receptor
mechanisms during rat heatstroke may decrease cardiac
sympathetic (adrenergic) mechanisms and result in reduction of
myocardial contraction.

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