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作 者:贾可亮[1] 陈芝喜[1] 林炳鎏[1] 邱卓嶷 欧明[2]
机构地区:[1]广州中医学院核医学研究室 [2]广州中医学院附院内科
出 处:《广州中医学院学报》1992年第2期79-82,共4页
摘 要:业已证明,毛冬青甲素(IA)对抑制血小板凝聚,松驰血管平滑肌和增强心肌收缩力都有显著的效应。进一步的研究证明IA在平滑肌具有钙拮抗作用,在心肌则具有钙激动作用。此文证明毛冬青甲素明显提高心肌的cAMP和cGMP水平。在血管平滑肌,IA只提高cAMP水平而不影响cGMP的含量。结果提示,心肌内cAMP的增加可能是IA促进心肌钙内外交换速率增加进而表现正性肌力作用的机理之一。而心肌内cGMP的增加则提示IA对心肌的作用可能是多方面的。另外,IA所具有的血管松驰效应可能也与其增加平滑肌cAMP水平有关。至于IA只提高心肌的cGMP水平而不影响平滑肌cGMP水平的机理尚待研究。The significant effects of llexonin A on the inhibition of the platetle aggregation, the vascular relaxation and the positive inotropic action have been demonstrated. Further studies showed that llexonin A possessed an antagonistic action of calcium in the smooth muscle and an agoristic action of calcium in the myocardium. It is reported that llexonin A markedly increased both cAMP and cGMP levels in the isolated rabbit myocardium. In the isolated smooth muscle, llexonin A enhanced cAMP level significantly, but did not affect cGMP content. Our study suggests that the increase of the rate of exchange of intracellular calcium in the heart which results in the direct positive inotropic action may be associated with the phosphorylation of the calcim channel (or a closelyassociated regulatory protein) which can be caused by cAMP-dependent protein kinase. The increase of cGMP level in the heart suggests that the effect of llexonin on cardiac function is likely complicated. This repost also indicates that one or all mechanisms of the vascular relaxtion of llexonin A may involve cAMP. In addition, llexonin A increased cGMP level only in the heart,but not in the smooth muscle. The mechanism of such an action needs further investigation.
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