Τίτλος:
Propranolol diminishes cardiac hypertrophy but does not abolish acceleration of the ischemic contracture in hyperthyroid hearts
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
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 α acute, n = 6; THYR α acute, n = 8; and THYR α n = 13; and NORM α, 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 β prop, n = 6 and NORM β prop, n = 8, and THYR β, n = 6, NORM β, 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 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 β-adrenergic activity. Propranolol diminishes LVH in hyperthyroidism.
Συγγραφείς:
Pantos, C.I.
Mourouzis, I.S.
Tzeis, S.M.
Malliopoulou, V.
Cokkinos, D.D.
Asimacopoulos, P.
Carageorgiou, H.C.
Varonos, D.D.
Cokkinos, D.V.
Περιοδικό:
Journal of Cardiovascular Pharmacology
Εκδότης:
Lippincott Williams and Wilkins
Λέξεις-κλειδιά:
propranolol; thyroxine, adrenergic activity; animal experiment; animal model; article; beta adrenergic stimulation; controlled study; drug effect; heart function; heart hypertrophy; heart left ventricle hypertrophy; heart muscle ischemia; hormone action; hyperthyroidism; hypoxia; isolated heart; nonhuman; priority journal; rat
DOI:
10.1097/00005344-200009000-00015
