Coronary vascular responsiveness to 5-hydroxytryptamine before and after infusion of hyperkalemic crystalloid cardioplegic solution in the rat heart. Possible evidence of endothelial damage.

Using the isolated, Langendorff-perfused rat heart (n = 8 per group), we have studied the effects of 5-hydroxytryptamine and papaverine on coronary flow before and after a 30-minute infusion of hypothermic (20 degrees C), nonoxygenated cardioplegic solution containing potassium in a concentration of either 25 or 40 mmol/L. Before infusion of the 25 mmol/L potassium cardioplegic solution, both 5-hydroxytryptamine (1 x 10(-7) mol/L) and papaverine (5 x 10(-6) mol/L) caused similar increases in flow (+21.2% +/- 1.6% and +22.8% +/- 1.6%, respectively). After cardioplegia, the vasodilatory response to 5-hydroxytryptamine was completely lost and a slight vasoconstriction was observed (-0.2% +/- 1.2%). However, there was no significant change in the response to papaverine, which maintained a +23.7% +/- 1.4% vasodilation. With the cardioplegic solution containing a 40 mmol/L concentration of potassium, the initial responses to 5-hydroxytryptamine and papaverine were again similar (+21.5% +/- 2.5% and +24.1% +/- 3.0%, respectively). After cardioplegia, 5-hydroxytryptamine caused a significant vasoconstriction (-4.3% +/- 1.1%), whereas the response to papaverine was again maintained (+19.1% +/- 2.3%). The results of this study support the concept that hyperkalemic crystalloid cardioplegic solutions cause vascular damage possibly involving the endothelium or its function, which may adversely affect vascular responsiveness.