Myocardial ischemia is the most common and primary cause of myocardium damage. Numerous conventional techniques and methods have been developed for ischemia and reperfusion studies. However, because of damage to the h...Myocardial ischemia is the most common and primary cause of myocardium damage. Numerous conventional techniques and methods have been developed for ischemia and reperfusion studies. However, because of damage to the heart sample, most of these techniques can not be used to continuously monitor the full dynamic course of the myocardial metabolic pathway. The nuclear magnetic resonnance (NMR) surface coil technique, which overcomes the limitations of conventional instrumentation, can be used to quantitatively study every stage of the perfused heart (especially after perfusion stoppage) continuously, dynamically, and without damage under normal or designed physiological conditions at the molecular level. In this paper, 31 P NMR was used to study the effects of ischemia and hypoxia on isolated perfused hearts. The results show that complete hypoxia caused more severe functional damage to the myocardial cells than complete ischemia.展开更多
文摘Myocardial ischemia is the most common and primary cause of myocardium damage. Numerous conventional techniques and methods have been developed for ischemia and reperfusion studies. However, because of damage to the heart sample, most of these techniques can not be used to continuously monitor the full dynamic course of the myocardial metabolic pathway. The nuclear magnetic resonnance (NMR) surface coil technique, which overcomes the limitations of conventional instrumentation, can be used to quantitatively study every stage of the perfused heart (especially after perfusion stoppage) continuously, dynamically, and without damage under normal or designed physiological conditions at the molecular level. In this paper, 31 P NMR was used to study the effects of ischemia and hypoxia on isolated perfused hearts. The results show that complete hypoxia caused more severe functional damage to the myocardial cells than complete ischemia.
基金This work was supported by the Major State Basic Research Development Program of People's Republic of China (No. G2000056905)the 985 Project of Peking University.
文摘目的探讨以阿片δ受体激动剂能否诱导心脏缺血预处理的延迟保护效应及其保护机制。方法健康成年雄性大鼠随机分4组,A和B组以阿片δ受体激动剂DADLE处理(2 mg/kg),C和D组注射生理盐水,24 h后4组都制成离体心脏,低温缺血3 h,复灌1 h。观测心功能、ATP等。其B和D组在缺血前以优降糖阻止心肌ATP敏感性钾通道的开放。结果A左室压力变化最大速率恢复率和心肌ATP含量都高于B,C和D组,差异有显著性(P<0.01 or P<0.05),而B,C和D组间无明显差异。A组心肌丙二醛含量与CK-MB漏出活性明显低于B,C和D组(P<0.01 or P<0.05)。结论阿片δ受体可以诱导健康成年大鼠产声预处理延迟保护效应,而ATP敏感性钾通道参与介导其效应机制。
