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題 名 | Myocardial Effects of beta-Agonist Stimulation in Rats with Chronic Left Ventricular Dysfunction Treated with an Angiotensin-Converting Enzyme Inhibitor=乙型交感神經對轉化酶抑制劑治療慢性左心室衰竭老鼠心肌功能的影響 |
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作 者 | 程文俊; 王兆弘; 陳雪芬; 洪明銳; | 書刊名 | 長庚醫學 |
卷 期 | 22:4 1999.12[民88.12] |
頁 次 | 頁546-555 |
分類號 | 415.319 |
關鍵詞 | 心臟衰竭; 轉化酶抑制劑; 腎素血管活力素系統; Sprague-dawley大白鼠; Cardiac failure; Angiotensin-converting enzyme inhibitor; Renin-angiotensin system; Sprague-dawley rat; |
語 文 | 英文(English) |
中文摘要 | 背景:本研究利用形態學及血管行動力學的變化來探討Sprague-Dawley大白鼠心 肌梗塞後,乙型交感神經剌激對左心室及腎活素-血管張力素的影饗。 方法:大白鼠在接受左冠狀動脈結紮或控制組手術後,分成有無服用轉化□抑制劑兩組,經 12週治療後,測量其體內及體外的心臟功能,包括左心室功能及心臟乳突肌的機能。全部52 隻大白鼠依心肌梗塞範圍分成控制組,小範圍梗寒(心肌梗塞範圍小於30%),大範圍梗塞(梗 塞範圍大於30%)等三組。 結果:無論有無接受轉化晦抑制劑冶療,左心室舒張壓在大範圍梗塞組有明顯上升,而且左 心室導管在轉化□押制劑治療下有下降現象。左心室乳突肌在長度、重量及橫切面在轉化□ 抑制劑治療下,在大範圍梗塞組都有明顯下降。除此之外,在大梗塞組,沒有梗塞的左心室 後乳突肌對乙型交感神經刺激劑的反應在收縮及舒張功能方面都有影響。而在長期轉化□抑 制劑的治療下,其收縮功能有改善的空間。 結論:慢性轉化□抑制劑會改善心肌梗塞後大白鼠乙型交感神經刺激心肌的等長功能,其機 轉可能與乙型接收器路徑有關。 |
英文摘要 | Background: This study measured morphological and hemodynamic changes and renin-angiotensin responsiveness of the left ventricle (LV) toβ-agonist stimulation in a Sprague-Dawley rat model of myocardial dysfunction produced by coronary artery lig-ation. Methods: The LV function and papillary muscle mechanics were measured after 12 weeks of captopril treatment (2 g/l in drinking water) following left coronary artery lig-ation or a sham operation. Fifty-two rats were divided into three groups: those with sham operations, those with small infarcts (infarct size [ISI <30% LV] and those with large infarcts (IS ≧30% LV). Results: The results showed that LV end-diastolic pressures were elevated in the large-infarct group regardless of treatment with the angiotensin-converting enzyme inhibitor (ACEI), and the LV weight was reduced in the ACEI-treated rats. In addition, the uninfarcted LV posterior papillary muscle of the large-infarct rats showed an impaired response to isoproterenol stimulation, including the developed tension, positive and negative rate of tension development, lime to peak tension, and time to half relaxation. Conclusion: Chronic captopril treatment improved isoproterenol-stimulated muscle isometric function in rats following myocardial infarction, possibly through the β -receptor pathway. |
本系統中英文摘要資訊取自各篇刊載內容。