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J Thorac Cardiovasc Surg 1994;107:829-837
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Early effects of hypothyroidism on the contractile function of the rat heart and its tolerance to hypothermic ischemia

London, United Kingdom

Supported in part by grants from STRUTH.

Received for publication June 17, 1993. Accepted for publication Aug. 27, 1993. Address for reprints; Manuel Galiñanes, MD, PhD, Cardiovascular Research, The Rayne Institute, St. Thomas' Hospital, London SEI 7EH, United Kingdom.

Abstract

We have investigated the early effects of hypothyroidism on cardiac function and tolerance to hypothermic ischemia. Hypothyroidism was induced by thyroidectomy. Five days after operation, sham-operated and thyroidectomized rats were anesthetized and cardiac function was assessed. At this time, the plasma levels of triiodothyronine and thyroxine had fallen by eightfold and threefold, respectively, in thyroidectomized rats compared with the values in sham-operated rats. In vivo pump function was assessed by measuring mean arterial pressure, cardiac index, and stroke volume index: all were reduced by thyroidectomy (respectively 95 ± 5 mm Hg, 22 ± 2 ml/min/100 gm body weight, and 67 ± 7µl/beat/100 gm body weight versus 112 ± 4 mm Hg, 35 ± 1 ml/min/100 gm body weight and 85 ± 4µl/beat/100 gm body weight in the sham-operated group; p < 0.05 in each instance). Systemic vascular resistance index was higher in thyroidectomized than in sham-operated rats (4.4 ± 0.4 versus 3.1 ± 0.2 mm Hg/ml/min/100 gm body weight; p < 0.05). In vivo indices of contractile function were also reduced by thyroidectomy: maximum rate of left ventricular pressure development fell by almost 50% (5190 ± 790 versus 9600 ± 900 mm Hg/sec; p < 0.05) and left ventricular developed pressure and heart rate also fell (respectively 92 ± 8 mm Hg and 340 beats/min versus 129 ± 6 mm Hg and 398 ± 6 beats/min; p < 0.05 in each instance). After excision, hearts were blood-perfused and ex vivo function assessed with intraventricular balloons. Systolic and diastolic functions were significantly impaired in the thyroidectomized group and the myocardial Na+-K+-adenosinetriphosphatase activity was reduced from a control value of 8.3 ± 0.3 to 5.8 ± 0.4 mean integrated extinction x 100. The hearts were then subjected to 2 minutes of cardioplegic infusion, 6 hours of hypothermic (4° C) ischemia, and 40 minutes of reperfusion. In control hearts, left ventricular developed pressure (at an end-diastolic pressure of 8 mm Hg) recovered to 76% of its preischemic value (131 ± 8 versus 173 ± 8 mm Hg; p < 0.05); in hearts from thyroidectomized rats, left ventricular developed pressure recovered to 81% of its preischemic value (110 ± 8 versus 136 ± 12 mm Hg; p = not significant), an absolute value that was not significantly different from that in the sham-operated group. Diastolic function recovered to the same extent in both groups. Myocardial high-energy phosphate content was unaffected by thyroidectomy and was depleted to a similar extent in both sham-operated and thyroidectomized groups by hypothermic ischemia. In conclusion, thyroidectomy leads to a deterioration of systolic and diastolic functions but this does not adversely affect the tolerance of the heart to extended periods of hypothermic ischemic storage. (J THORACCARDIOVASCSURG1994;107:829-37)

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