Role of potassium concentration in cardioplegic solutions in mediating endothelial damage

Abstract

We studied the effect of potassium concentration in cardioplegic solutions on endothelial function by examining its influence on 5-hydroxytryptamine- (5-HT) and nitroglycerin-induced vasodilation in the isolated rat heart. Forty-eight rat hearts were perfused on a modified Langendorff preparation. After a baseline record of increase in coronary flow induced by 10 −7 M 5-HT and 10 μg/mL nitroglycerin, the hearts were perfused for 30 or 60 minutes with either St. Thomas' solution or Bretschneider solution containing 20 mmol/L of potassium or for 30 minutes with either solution containing 30 mmol/L of potassium (n = 8 in each). Initially, 5-HT and nitroglycerin caused a 39.0% ± 3.3% and 39.7% ± 2.8% increase in coronary flow, respectively. After 30 or 60 minutes' perfusion with St. Thomas' solution containing 20 mmol/L of potassium, there was little change in the response to 5-HT or nitroglycerin (5-HT, 43.1% ± 4.1%; nitroglycerin, 38% ± 3.2%). Similarly, perfusion with Bretschneider solution (20 mmol/L K +) for 30 or 60 minutes did not alter the degree of vasodilation (5-HT, 39.2% ± 2.9%; nitroglycerin, 38.0% ± 3.3%). However, perfusion with St. Thomas' solution containing 30 mmol/L of potassium for 30 minutes abolished the endothelial-dependent 5-HT-induced vasodilation (5-HT, −1.6% ± 1.4%; nitroglycerin, 36.9% ± 2.2%). Perfusion with Bretschneider solution (30 mmol/L K +) gave similar results (5-HT, −2.1% ± 1.2%; nitroglycerin, 36.4% ± 1.7%). We conclude that the concentration of potassium in cardioplegic solutions plays a critical role in causing functional endothelial damage.