ROLE OF ADENOSINE IN THE TREATMENT OF MYOCARDIAL STUNNING

被引:18
作者
FORMAN, MB
VELASCO, CE
机构
[1] Department of Medicine, Division of Cardiology, Vanderbilt University School of Medicine, Nashville, TN
[2] Division of Cardiology, Vanderbilt University Medical Center, Nashville, 37232-2170, TN
关键词
ADENOSINE; ADENOSINE TRIPHOSPHATE; REGIONAL BLOOD FLOW; FREE RADICALS; CALCIUM HOMEOSTASIS; STUNNING;
D O I
10.1007/BF00053551
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Adenosine is an endogenous nucleoside produced from the breakdown of adenosine triphosphate (ATP) that possesses a number of complex cellular and metabolic effects that could ameliorate postischemic contractile dysfunction (myocardial stunning). Potential mechanisms include the repletion of high-energy phosphate stores, reduced myocardial oxygen consumption, a decrease in oxygen-derived free radicals, restoration of calcium homeostasis, and an increase in regional myocardial blood flow. Experimental studies have shown that adenosine can reduce myocardial stunning with or without a concomitant increase in the total myocardial ATP stores. Adenosine may be a useful pharmacologic strategy in the prevention and treatment of ventricular dysfunction following episodes of regional or global ischemia, although further studies are needed to clarify the precise cellular mechanisms involved.
引用
收藏
页码:901 / 908
页数:8
相关论文
共 65 条
[31]  
Przyklenk K., Whittaker P., Kloner R.A., Direct evidence that oxygen free radicals cause contractile dysfunction in vivo (Abstr), Circulation, 78, (1988)
[32]  
Bolli R., Jeroudi M.O., Patel B.S., Et al., Marked reduction of free radical generation and contractile dysfunction by antioxidant therapy begun at the time of reperfusion. Evidence that myocadial “stunning” is a manifestation of reperfusion injury, Circ Res, 65, pp. 607-622, (1989)
[33]  
Zweier J.L., Flaherty J.T., Weisfeldt M.L., Direct measurement of free radical generation following reperfusion of ischemic myocardium, Proc Natl Acad Sci USA, 84, pp. 1404-1407, (1987)
[34]  
Tribble D.L., Aw T.Y., Jones D.P., The pathophysiological significance of lipid peroxidation in oxidative cell injury, Hepatology, 7, pp. 377-386, (1987)
[35]  
Engler R., Granulocytes and oxidative injury in myocardial ischemia and reperfusion, Fed Proc, 46, pp. 2395-2396, (1987)
[36]  
Cronstein B.N., Kramer S.B., Weissmann G., Hirschhorn R., Adenosine: A physiologic modulator of superoxide anion generation by human neutrophils, J Exp Med, 158, pp. 1160-1177, (1983)
[37]  
Tanabe M., Terashita Z., Nishikawa K., Hirata M., Inhibition of coronary circulatory failure and thromboxane A<sub>2</sub> release during coronary occlusion and reperfusion, J Cardiovasc Pharmacol, 6, pp. 442-448, (1984)
[38]  
Steenbergen C., Murphy E., Levy L., London R.E., Elevation in cytosolic free calcium concentration early in myocardial ischemia in perfused rat heart, Circ Res, 60, pp. 700-707, (1987)
[39]  
Marban E., Kitakze M., Kusuoka H., Porterfield J.K., Yuo D.T., Chacko V.P., Intracellular free calcium concentration measured with <sup>19</sup>F NMR spectroscopy in intact ferret hearts, Proc Natl Acad Sci USA, 86, pp. 6005-6009, (1987)
[40]  
Krause S.M., Jacobus W.E., Becker L.C., Alterations in cardiac sarcoplasmic reticulum calcium transport in the postischemic “stunned” myocardium, Circ Res, 65, pp. 526-530, (1989)