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Ann Thorac Surg 1991;51:89-93
© 1991 The Society of Thoracic Surgeons
a National Heart and Lung Institute, London, United Kingdom
b Harefield Hospital, Harefield, United Kingdom
Accepted for publication September 10, 1990.
* Address reprint requests to Mr Mankad, Harefield Hospital, Harefield, Uxbridge, Middlesex UB9 6JH, United Kingdom.
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.
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