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J Thorac Cardiovasc Surg 1995;110:315-327
© 1995 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

PRETREATMENT WITH 3,5,3' TRIIODO-L-THYRONINE (T₃): Effects on myocyte contractile function after hypothermic cardioplegic arrest and rewarming

Charleston, S.C.

From the Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, S.C.

Received for publication July 20, 1994. Accepted for publication Nov. 28, 1994. Address for reprints: Francis G. Spinale, MD, PhD, Division of Cardiothoracic Surgery, Medical University of South Carolina, 171 Ashley Ave., CSB 418, Charleston, SC 29425

Abstract

Circulating levels of 3,5,3'triiodo-L-thyronine are depressed after cardiopulmonary bypass and have been implicated to play a contributory role in the alterations in left ventricular function after hypothermic cardioplegic arrest and rewarming. The central hypothesis of the present study was that pretreatment of isolated myocytes with triiodothyronine will have a direct and beneficial effect on contractile performance after hypothermic cardioplegic arrest and rewarming. Contractile function in isolated pig left ventricular myocytes was examined by video microscopy after the following treatment protocols: (1) 37° C incubation in medium (normothermia) for 2 hours with triiodothyronine followed by a 2-hour normothermic incubation with no triiodothyronine, (2) 4 hours of normothermic incubation with no triiodothyronine, (3) normothermic incubation for 2 hours with triiodothyronine followed by 2 hours of hyperkalemic, hypothermic cardioplegic arrest ([K⁺]: 24 mmol/L; 4° C) and subsequent rewarming, and (4) normothermic incubation for 2 hours with no triiodothyronine followed by 2 hours of hyperkalemic, hypothermic cardioplegic arrest and rewarming. Two hours of normothermia with triiodothyronine increased myocyte contractile function by 30% compared with values in untreated control myocytes, and this increase persisted after a subsequent 2-hour incubation under normothermic conditions with no triiodothyronine. For example, myocyte velocity of shortening in triiodothyronine-pretreated myocytes was 84 ± 4.9µm/sec compared with 62 ± 2.8µm/sec in control myocytes (p < 0.05). Cardioplegic arrest and subsequent rewarming caused a significant reduction in myocyte velocity of shortening from normothermic values (37 ± 3.4µm/sec, p < 0.05). However, in myocytes pretreated with triiodothyronine, myocyte contractile function was significantly higher after hypothermic cardioplegic arrest and rewarming (54 ± 2.5µm/sec, p < 0.05). In a second series of experiments,ß-adrenergic responsiveness was examined after pretreatment with triiodothyronine. In the presence of theß-adrenergic agonist isoproterenol (25 nmol/L), myocyte contractile function was increased by 26% in the triiodothyronine-treated myocytes compared with that in untreated control myocytes. This enhancedß-adrenergic responsiveness with triiodothyronine pretreatment persisted with subsequent exposure to hypothermic cardioplegic arrest and rewarming. In summary, triiodothyronine pretreatment caused an increase in myocyte contractile function andß-adrenergic responsiveness under normothermic conditions and after hypothermic cardioplegic arrest and rewarming. Thus the present study provides direct evidence to suggest that preemptive treatment with triiodothyronine may improve left ventricular contractile performance after hypothermic cardioplegic arrest and rewarming. (J THORACCARDIOVASCSURG1995;110:315-27)

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