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Background: Abnormal vascular responsiveness to vasoconstrictors may play an important role in peripheral vascular resistance in hyperthyroidism. The aim of the present study was to evaluate whether the vascular response to potassium chloride and phenylephrine is abnormal in a rat model of thyroxine-induced cardiac hypertrophy., Methods: Left ventricular hypertrophy was induced in Wistar rats by subcutaneous administration of L-thyroxine for two weeks ("THYR"), n=17. Animals treated with normal saline served as controls, ("NORM"), n=20. The thoracic aorta was dissected and cut into rings that were suspended in an isolated organ bath with Krebs-Henseleit buffer. Maximal tension, Tmax, in g was measured in response to KCl and PE at the highest concentration in rings with endothelium (+E) and without endothelium (-E) in both groups. Relaxation response (Relax percent) to acetylcholine administration was expressed as percent of the maximal tension induced by phenylephrine., Results: Left ventricular weight was 0.9 (SEM, 0.04) g for THYR group vs 0.7 (0.02) g for the NORM group, p<0.05. With KCl, Tmax was not different between the THYR and NORM groups with and without endothelium. With PE, there was a difference in Tmax between THYR+E and NORM+E, 1.2 (0.05) g vs 1.5 (0.09) g, p<0.05. Tmax was also different between THYR-E and NORM-E, 1.5 (0.08) g vs 1.7 (0.07) g, p<0.05. Relax percent was not significantly different between THYR+E and NORM+E (45.9 percent vs 42.8 percent, p>0.05)., Conclusions: We conclude that: a) Vascular tension of the thoracic aorta in response to PE is lower in thyroxine-treated rats as compared to controls, probably due to enhanced PE-induced vasorelaxation at high concentration. b) Relaxation response of the thoracic aorta to acetylcholine is not different between THYR and NORM groups.

This study was undertaken to define the contributions of left ventricular hypertrophy (LVH) and increased adrenergic activity to the acceleration of ischemic contracture (IC) that occurs in chronic hyperthyroid rat heart. Acute and chronic hyperthyroidism (THYR) were induced by thyroxine administration for 2 and 14 days, respectively, and normal animals (NORM) served as controls. Isolated hearts were perfused in a Langendorff mode. NORM alpha acute, n = 6; THYR alpha acute, n = 8; and THYR alpha, n = 13; and NORM alpha, n = 13 were subjected to 20-min zero-flow global ischemia (I) and 45-min reperfusion (R). Additional THYR and NORM hearts treated with propranolol (prop) were subjected to 30-min I; THYR beta prop, n = 6 and NORM beta prop, n = 8, and THYR beta, n = 6, NORM beta, n = 8 served as controls. Acceleration of IC was measured by the time to peak contracture (Tmax). Left ventricular hypertrophy (LVH) was assessed by the ratio of left ventricular weight in milligrams (LVW) to animal body weight (BW) in grams. Cardiac hypertrophy developed in chronic but not acute hyperthyroidism. Propranolol reduced the extent of LVH. Contracture occurred earlier in chronic than in acute hyperthyroid and normal hearts. Propranolol did not alter contracture. In conclusion, IC is accelerated by thyroxine administration, and this is probably not due to LVH or increased beta-adrenergic activity. Propranolol diminishes LVH in hyperthyroidism.

Background: The present study was undertaken to define the effects of thyroxine administration on ischaemic preconditioning (PC) and the ischaemic contracture., Methods: Hyperthyroidism was induced by administration of L-thyroxine in rats (THYR) while normal animals served as controls (NORMa). Isolated rat hearts were perfused in a Langendorff preparation. NORMa control (n = 16) and THYR control (n = 9) hearts underwent 20 min of ischaemia and 45 min reperfusion while NORMa PC (n = 16) and THYR PC (n = 14) were subjected to PC before ischaemia. Additional normal hearts were subjected to 30 min of ischaemia with and without PC, NORMb control, n = 8 and NORMb PC, n = 6. Postischaemic recoveries of left ventricular (LV) developed pressure were expressed as % of the initial value (LVDP%). Severity of contracture was measured by the time (Tmax) and magnitude (Cmax) of peak contracture., Results: LVDP% was significantly higher after PC, both in NORMa and THYR rats. In NORMa control hearts, ischaemic contracture had not yet reached a plateau at 20 min of ischaemia. Contracture appeared earlier in THYR control and PC than in NORMa control and PC groups. Tmax was 22.1 (0.9) vs 16.8 (1.4) min for NORMb control and PC, p < 0.05 and 12.5 (1.0) vs 9.3 (1.1) min for THYR control and PC hearts, p < 0.05. Tmax was earlier in both THYR groups compared to NORMb groups, p < 0.05. Cmax was significantly higher in both THYR groups compared to both NORMb groups., Conclusion: Ischaemic contracture is both accelerated and accentuated in thyroxine treated hearts while preconditioning capacity is preserved. Preconditioning and thyroxine administration shorten Tmax in an additive way, whereas Cmax in hyperthyroid hearts did not further increase by preconditioning.