Propranolol diminishes cardiac hypertrophy but does not abolish acceleration of the ischemic contracture in hyperthyroid hearts

This study was undertaken to define the contributions of left ventricular h ypertrophy (LVH) and increased adrenergic activity to the acceleration of i schemic contracture (IC) that occurs in chronic hyperthyroid rat heart. Acu te and chronic hyperthyroidism (THYR) were induced by thyroxine administrat ion for 2 and 14 days, respectively, and normal animals (NORM) served as co ntrols. Isolated hearts were perfused in a Langendorff mode. NORM ct acute, n = 6; THYR or acute, n = 8; and THYR alpha, n = 13; and NORM alpha, n = 1 3 were subjected to 20-min zero-flow global ischemia (I) and 45-min reperfu sion (R). Additional THYR and NORM hearts treated with propranolol (prop) w ere 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 (T-max). Left ventricular hypertrophy (LVH) was assessed by the ratio of left ventricular weight in m illigrams (LVW) to animal body weight (BW) in grams. Cardiac hypertrophy de veloped in chronic but not acute hyperthyroidism. Propranolol reduced the e xtent of LVH. Contracture occurred earlier in chronic than in acute hyperth yroid and normal hearts. Propranolol did not alter contracture. In conclusi on, IC is accelerated by thyroxine administration, and this is probably not due to LVH or increased beta-adrenergic activity. Propranolol diminishes L VH in hyperthyroidism.