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題 名 | Effect of Magnolol on Coronary Vascular Resistance in Rabbits: Measurement with Pulsed Doppler Velocimetry=以杜卜勒超音波血流測量術探討厚朴酚對白兔冠狀動脈血流阻力之影響 |
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作 者 | 黃正雄; 洪傳岳; 蔡勝國; 賴曉亭; | 書刊名 | 臺灣醫學會雜誌 |
卷 期 | 99:7 2000.07[民89.07] |
頁 次 | 頁554-558 |
分類號 | 415.3161 |
關鍵詞 | 杜卜勒超音波血流測量術; 厚朴酚; 白兔; 冠狀動脈; 血流阻力; Magnolol; Nitroglycerin; Coronary vascular resistance; Rabbits; Pulsed Doppler velocimetry; |
語 文 | 英文(English) |
英文摘要 | Background and purpose: Magnolol is an active component purified from Magnolia officinalis that has been reported to protect the myocardium against infarction and reperfusion injury. The purpose of this study was to investigate the effect of magnolol on the coronary circulation and to determine whether a change in coronary vascular resistance could be the mechanism underlying its myocardial protective effect. Methods: Male New Zealand white rabbits were anesthetized. A 3-mm suction-type pulsed Doppler velocimetry probe was applied to the proximal part of the left anterior descending coronary artery after median sternotomy. The 39 rabbits received intravenous injection of either vehicle (n = 5), magnolol (10 –6 g/kg, n = 6; 10 –5 g/kg, n = 5; 10 –4 g/kg, n = 5), or nitroglycerin (10 –5 g/kg, n = 6; 10 –4 g/kg, n = 6; 10 –3 g/kg, n = 6). The effects of magnolol and nitroglycerin on coronary vascular resistance were compared. Results: Magnolol did not change blood pressure or coronary blood flow velocity. However, at a dose of 10 –4 g/kg, it decreased coronary vascular resistance significantly more than vehicle (88 �b�n1% vs 95 �b�n1% of baseline coronary vascular resistance, p < 0.001). Nitroglycerin increased coronary blood flow velocity and decreased coronary vascular resistance in a dose-dependent manner (p < 0.01). Conclusions: Magnolol reduced coronary vascular resistance in anesthetized, open- chest rabbits only at a high concentration. Its effect was modest compared with that of nitroglycerin. Since magnolol protects the myocardium at relatively low doses, coronary vasodilatation is unlikely to be the underlying mechanism responsible for its myocardial protective effects. |
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