Myocyte and endothelial injury with ischemia reperfusion in isolated rat hearts

Abstract

We determined the time course of ischemic injury, the effects of reperfusion, and the protective effects of prostacyclin, oxygen radical scavengers, and diltiazem on myocardial myocyte and endothelial cell functions in isolated rat hearts. Left ventricular power and coronary microvascular permeability were used as indexes of myocyte and endothelial cell function, respectively. Neither 5- nor 10-min ischemia reperfusion significantly changed power or permeability. However, with reperfusion following 20 and 30 min of ischemia, power was reduced 50 and 60% and permeability increased 70 and 90%. In 30-min ischemic hearts the ischemia-induced increase in permeability was apparent after 4 min reperfusion and further exacerbated at 20 min. Hypoxic reperfusion did not prevent increased permeability. Prostacyclin or a combination of superoxide dismutase, catalase, and mannitol also did not prevent increased permeability, and the radical scavengers did not ameliorate depressed power. In contrast, perfusion with diltiazem during ischemia reperfusion blunted the reduction in power and prevented the increase in permeability. We conclude that ischemia reperfusion causes similar time course of injury to myocytes and endothelial cells; reperfusion contributes to endothelial injury, and diltiazem affords protection to both cell types.

FLIP Protects against Hypoxia/Reoxygenation-Induced Endothelial Cell Apoptosis by Inhibiting Bax Activation

“…Additionally, I/R may cause injury through the recruitment of proinflammatory leukocytes. Endothelial cells represent the first cell type injured by reactive oxygen species generated during I/R (30). In vitro, the mechanisms of endothelial cell death caused by H/R remain poorly understood and may involve both necrotic and apoptotic forms of cell death.…”

Hepatocyte Growth Factor Protects against Hypoxia/Reoxygenation-induced Apoptosis in Endothelial Cells

“…H/R, which generates cytotoxic reactive oxygen species and promotes the recruitment of inflammatory leukocytes, causes lung injury and cell death involving both necrotic and apoptotic events. Endothelial cells appear to be the first cell type injured by reactive oxygen species generated during I/R (19). The mechanisms of apoptotic cell death induced by H/R, however, are not well understood, especially in endothelial cells.…”

The Effects of Tetrandrine on the Contractile Function and Microvascular Permeability in the Stunned Myocardium of Rats.

“…Pretreating heart with nisoldipine could prevent the macromolecular leakage after ischemia [26]. Sunnergren et al [27] reported that reperfusion following 20 and 30 min of ischemia resulted in a reduction of contractile power by 50 and 60%, and increase of permeability by 70 and 90%. If the heart underwent 30 min of ischemia, the increase in permeability was evident after 4 min reperfusion and further exacerbated at 20 min.…”