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J Thorac Cardiovasc Surg 1996;111:74-84
© 1996 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

IMPROVEMENT IN FUNCTIONAL RECOVERY OF THE ISOLATED GUINEA PIG HEART AFTER HYPERKALEMIC REPERFUSION WITH ADENOSINE

Milwaukee, Wis.

Supported by Deutsche Forschungsgemeinschaft, grant Ha 1651/5-1 (H. H.) and VA Merit Grant 8204-04P (D. F. S.).

Received for publication Dec. 5, 1994. Accepted for publication April 19, 1995. Address for reprints: Helmut Habazettl, MD, Institute for Surgical Research, University of Munich, Marchioninistrasse 15, 81366 Munich, Germany.

Abstract

The aim of this study was to examine the effect of initial hyperkalemic reperfusion (HKR), with and without added adenosine, on coronary flow, myocardial function, and endothelium-dependent and endothelium-independent coronary vascular function. Cardioplegic arrest was induced in 40 isolated guinea pig hearts by infusing oxygenated cardioplegic (high in potassium ion) Krebs solution for 5 minutes. Hearts were then stored at room temperature for 3.5 hours. On reperfusion, hearts were divided into four groups of 10 hearts each: control, reperfusion with regular Krebs solution (4.6 mmol/L potassium chloride); base hyperkalemic reperfusion, initial reperfusion with 37º C oxygenated, cardioplegic Krebs solution for 5 minutes; hyperkalemic reperfusion with addition of 1 mmol/L adenosine during HKR; and hyperkalemic reperfusion with addition of 5 mmol/L adenosine. Coronary reserve (adenosine bolus 2 mmol/L) and responses to acetylcholine (1µmol/L) and nitroprusside (100µmol/L) were examined before and after ischemia and reperfusion. Flow did not return to preischemic values in any group after reperfusion. Adenosine treatment during initial reperfusion increased coronary flow (percentage of baseline ± standard error of the mean) from 57% ± 4% in control and 45% ± 3% in hearts with hyperkalemic reperfusion to 79% ± 3% and 83% ± 5% in hearts with hyperkalemic reperfusion also treated with, respectively, 1 mmol/L adenosine and 5 mmol/L adenosine (p < 0.05). At 30 and 60 minutes of reperfusion, however, flow remained elevated only in the group treated with 5 mmol/L adenosine. Coronary reserve and responses to acetylcholine and nitroprusside were equivalently depressed in all groups after reperfusion. Recovery of left ventricular systolic and diastolic function was improved in all groups after hyperkalemic reperfusion (54% ± 4% of preischemic value) compared with control (39% ± 3%), and recovery was further enhanced in the group treated with 5 mmol/L adenosine (60% ± 4%). In this ex vivo model, hyperkalemic reperfusion improved myocardial function after cardioplegic arrest and the addition of 5 mmol/L adenosine improved coronary flow. Adenosine may counteract the potassium chloride–induced vasoconstriction that occurs during hyperkalemic reperfusion and may thus improve coronary flow and myocardial function. Postischemic depression of endothelium-dependent or endothelium-independent vascular functions, however, was not alleviated by hyperkalemic reperfusion with or without adenosine. (J THORACCARDIOVASCSURG1996;111:74-84)

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