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. 1984 Jul;88(1):49-56.

Reperfusion of inflow-limited myocardium following hypothermic potassium-induced cardioplegia

  • PMID: 6738102

Reperfusion of inflow-limited myocardium following hypothermic potassium-induced cardioplegia

W R Chitwood Jr et al. J Thorac Cardiovasc Surg. 1984 Jul.

Abstract

Previous studies have shown that transmural reperfusion patterns may be markedly abnormal following periods of ischemia. The present study was done to elucidate the effects of hypothermic potassium cardioplegia on pressure-flow characteristics during reperfusion of myocardial regions with chronically compromised arterial inflow. Prior to cardiopulmonary bypass studies. Ameroid constrictors were placed on the circumflex coronary artery of 10 adult dogs to create a myocardial region subserved by inflow-restricting collaterals. Subsequently, during cardiopulmonary bypass at 80 mm Hg, 10 minutes of ischemic arrest was induced with hypothermic potassium cardioplegia (15 degrees C, pH 7.4, potassium chloride 25 mEq/L). Transmural myocardial flow was measured in normal and collateral-dependent regions during control conditions and at 1, 5, and 10 minutes of reperfusion. Also, retrograde circumflex pressures were monitored as an additional index of perfusion of the collateral regions. A normal endocardial/epicardial flow ratio was maintained in the normal regions at 1, 5, and 10 minutes of reperfusion. In contrast, a marked decrease in endocardial/epicardial flow ratio occurred transiently in the collateral regions at 1 minute of reperfusion (0.28 +/- 0.05). Simultaneously, retrograde circumflex pressures fell from 55 +/- 3.5 mm Hg to 42 +/- 3.0 mm Hg (p less than 0.001). By 5 minutes of reperfusion, retrograde circumflex pressure, mean flow, and transmural endocardial/epicardial ratios returned to normal in collateral regions. These data suggest that, even with optimal myocardial protection, changes in transmural flow occur very early during reperfusion and are exaggerated in inflow-restricted myocardial regions. Mechanisms responsible for these changes may include refilling of epicardial vessels emptied during the cross-clamp period or an early epicardial hyperemic response. Despite these alterations, normal transmural flow patterns are reestablished rapidly. Thus, when detailed attention is paid to adequate myocardial protection, abnormal reperfusion characteristics are obviated, and this is particularly important in myocardium supplied by inflow-compromised coronary vessels.

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