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  4. ─心電生理特性,抗心律不整效力及不整脈誘發性之測定,包括CARVEDIOLO及THALIDOPARHINE與LIRIODENINE等新研發
 
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─心電生理特性,抗心律不整效力及不整脈誘發性之測定,包括CARVEDIOLO及THALIDOPARHINE與LIRIODENINE等新研發

Date Issued
1999
Date
1999
Author(s)
吳美環
DOI
882314B002124M48
URI
http://ntur.lib.ntu.edu.tw//handle/246246/29833
Abstract
1. Carvedilol,一種所謂"第三代β-拮 抗劑",對對於心衰竭之長期療效已經 多數臨床試驗證實。其機轉目前被認 為是抑制因心衰竭引起自主神經過度 代償之影響,且由於其α-拮抗效果, 可使在急性期投藥時,藉α-拮抗引起 之血管阻力下降,使病人之心衰竭不 致惡化,因此此種α與β拮抗比率應 可藉作長期抗心衰竭藥物設計之參 考。 2. 本實驗室工作群長期致力於由天然植 物萃取有效之化合物。經評估後,目 前有兩大類化合物,一為 thalidiporphine,一為 liriodenine,兩者皆具有適宜之心肌 收縮促進效果及抗心律不整效力。 3. 因此本群體計劃之目的在(1)將此兩大 類化合物予以改變部份結構,使具有 部份α與β拮抗作用(2)且能維持充份 之心臟收縮促進效果及抗心律不整效 力。 4. 本子計劃之主要工作在執行(1)第一 年:先界定carvedilol是否有直接抗 心律不整效力,或對心臟電生理特性 有直接影響,若有,其機轉為何?(2) 其次,第二年:將予界定 thalidoporplinie各類衍生物之抗心 律不整之效力及對心臟傳導系統之影 響(3)第三年:將予界定liriodenine 各類衍生物之抗心律不整之效力及對 心臟傳導系統之影響。 5. 方法:(1)心臟電生理特性之評估:以 Langendorff灌流之離體心臟作評估, 以自製特別之電極導線放入心房、心 室及希氏束處,記錄並刺激,以得到 各項組織之電生理特性資料(2)抗心律 不整之效力檢定:以Langendorff定壓 灌流之模式,經綁住再放鬆左冠狀動 脈支以誘發ischemia-reperfusion不 整脈,比較carvedilol 及其他衍生物 pretreatment或treatment與control 之差異。 6. 第一年計劃結果顯示:結果顯示 Carvedilol確能直接改變心電生理特 性,可縮短房室結之傳導及心室組織 之抑阻期。對於再灌流不整脈之誘發 概率亦能略減少(100%降到81%)。此外 並能停止再灌流不整脈,但最多只有 50%效力(1.5μM與5.4μM皆然)。
Background. Two compounds, thalidoporphine and liriodenine, had been identified with an antiarrhythmia potential and † 八十六年度及以前的一般 國科會專題計畫(不含產學 合作研究計畫)亦可選擇適 用,惟較特殊的計畫如國科 會規劃案等,請先洽得國科 會各學術處同意。 a low negative inotropy from our team. Further modification of the prototype will refer to a "third generation" ß blocking agent, carvedilol, that at therapeutic doses blocks all three adrenergic receptors, with a rank order of potency of ß1> a1 > ß2. Because of its a- blocking effect, carvedilol is a moderate vasodilator on acute administration and therefore has a good initial tolerability in patients with heart failure. Besides, carvedilol has been shown as a strong antioxidant. The clinical efficacy had been well shown several clinical trials. Methods. The direct modification by various interventions on cardiac conduction system was performed by intracardiac recording and stimulation in isolated, Langendorff perfused hearts. The and proarrhythmic potential was assessed by the incidence of ischemia /reperfusion arrhythmias after various interventions. Results. Carvedilol may directly shorten progressively the conduction through the AV node as well as the ventricular refractory period (1.5 and 4.5 mM). However, theses changes were irreversible as compared to the time-control data. As to the conduction through the atrial, His-Purkinje system and their refractoriness were not significantly modified by carvedilol. Carvedilol can modestly convert the ventricular tachyarrhythmias induced by ischemiareperfusion. At 1.5 mM and 4.5 mM, carvedilol could covert half of the reperfusion arrhythmias. Pretreatment by carvedilol (1.5 or 4.5 mM) could decrease the incidence of reperfusion arrhythmias from 100% (5/5) to 81% (9/11). Conclusions. Direct electropgysiological effects of carvedilol and the potential of ameliorating ischemia-reperfusion arrhythmias had been documented. However, the antiarrhythmic potential related to the direct carvediolol electrophysiological effects may be weak. Clinical therapeutic potential of carvedilol may be more closely related to the ß blocking as well as a-blocking
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臺北市:國立臺灣大學醫學院小兒科
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