Left ventricular performance in conscious thyrotoxic calves
Goldman, S.; Olajos, M.; Friedman, H.; Roeske, W.R.; Morkin, E.
American Journal of Physiology 242(1): H113-H121
1982
ISSN/ISBN: 0002-9513 PMID: 7058904 Document Number: 194796
The effects of thyroid hormone on the size and performance of the left ventricle (LV) were examined in 9 conscious calves with chronically implanted sonomicrometer crystals to record wall thickness, minor diameter, and the motion of a segment in the long axis of the ventricle. A solid-state pressure transducer was placed in the LV cavity, and pacing electrodes were sewn into the left atrium. After stable control measurements were obtained, the tachycardia and mild hypertension of thyrotoxicosis were simulated by pacing at 145 beats/min and infusion of phenylephrine to raise LV systolic pressure to about 146 mm Hg. Thyrotoxicosis then was induced by daily i.m. injection of L-thyroxine [T4] (200 .mu.g/kg) for 14 days. LV midwall sarcomere lengths also were measured EM in hearts rapidly fixed in diastole from 3 untreated and 3 thyrotoxic animals. T4 treatment produced significant increases in heart rate, cardiac output, LV dP/dt, end-diastolic diameter, end-systolic diameter, and peak wall stress. LV end-diastolic pressure, percent shortening, and the velocity of circumferential fiber shortening and LV diastolic wall thickness were not changed significantly. LV wt-to-body wt ratios for unoperated and thyrotoxic calves also were unchanged. Mean normalized sarcomere length in euthyroid LV (2.07 .+-. 0.05 .mu.m) was essentially the same as in thyrotoxic LV (2.06 .+-. 0.06). By comparison with the dramatic effects of T4, atrial pacing and phenylephrine infusion, alone or in combination, produced insignificant effects on LV performance. Thus T4 enhances the contractile performance of each contractile unit in a larger LV circumference by a positive inotropic action that is independent of the effects of tachycardia or the Frank-Starling mechanism. This enables the ventricle to work effectively from a larger end-diastolic volume in meeting the increased blood flow requirements of thyrotoxicosis.