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J Thorac Cardiovasc Surg 1994;107:1050-1058
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Hypothermic potassium cardioplegia impairs myocyte recovery of contractility and inotropy

Charleston, S.C.

Supported by a grant-in-aid from the American Heart Association and National Institutes of Health grant R29-HL45024.

Received for publication May 11, 1993. Accepted for publication Sept. 7, 1993. Address for reprints: John R. Handy, MD, Division of Cardiothoracic Surgery, Medical University of South Carolina, 171 Ashley Ave., Charleston, SC 29425.

Abstract

Acute postoperative left ventricular dysfunction after hypothermic, crystalloid potassium cardioplegia occasionally occurs. This project examined myocyte contractility and inotropic responsiveness after hypothermic arrest with and without potassium cardioplegia. Isolated swine left ventricular myocytes were placed in a thermostatically controlled chamber (37° C) that contained a standard cell medium, pulse stimulated at 1 Hz, and steady-state contractions were measured by computer-assisted video microscopy with and without isoproterenol (25 nmol/L). After baseline measurements were taken the myocytes were randomly assigned to the following treatments: (1) control group with infusion of 37° C crystalloid solution and maintained at 37° C for 3 hours (n = 23), (2) hypothermia group with infusion of 4° C crystalloid without potassium and stored at 4° C for 3 hours (n = 22), (3) hypothermic cardioplegia group with infusion of a crystalloid cardioplegia (oxygenated, buffered 4° C Ringer's solution with 24 mEq/L K⁺) and then stored at 4° C for 3 hours (n = 35). After treatment the myocytes were then rewarmed to 37° C by infusion of medium, and contractile measurements were repeated. In the control group, the percent and velocity of shortening were identical to those in baseline measurements: 6.4% ± 0.4% and 53 ± 5µm/sec, respectively, and these values remained unchanged in the hypothermia group: 6.5% ± 0.4% and 51 ± 3µm/sec, respectively. However, in the hypothermic cardioplegia group, the percent and velocity of shortening were significantly lower with rewarming: 4.8% ± 0.4% and 35 ± 3µm/sec, respectively, p < 0.05). Isoproterenol caused increased percent and velocity of shortening in both the control and hypothermia groups: 10.0% ± 0.6% and 9.5% ± 0.9% and 81.6 ± 8µm/sec and 71.4 ± 8µm/sec, respectively. This response was significantly blunted in the cardioplegia group (8.9% ± 0.8% and 56.9 ± 7µm/sec, p < 0.05). With an isolated myocyte system that is independent of extracellular and perfusion effects, hyperkalemic cardioplegic solution resulted in depressed myocyte contractile performance after rewarming. Potassium cardioplegia also caused a blunted inotropic responsiveness on rewarming. A potential contributory factor for the depressed left ventricular function after the use of potassium cardioplegia is a direct depression in myocyte contractility. (J THORAC CARDIOVASC SURG1994;107:1050-8)

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