Ethanol-induced cardiac hypertrophy: correlation between development and the excretion of adrenal catecholamines.
The progression of cardiac hypertrophy and the effects on adrenal medullary catecholamine content and release were determined in rats given ethanol, in conjunction with a supplementary diet, by gavage, every eight hours for periods up to 96 hours. Ethanol caused a marked depletion of adrenal medullary adrenaline content which fell to about 25 percent of control after the full time course. During this time, there were two- to fourfold increases in urinary noradrenaline content and five- to tenfold increases in urinary adrenaline. Cardiac hypertrophy, with increases in protein content and tissue weight of both ventricles, was evident at 24 hours of intoxication. By 96 hours of treatment these markers had increased more than 20% over control values. Proportional heart weight increases per day correlated significantly with daily urinary catecholamine excretion, providing support for the hypothesis that ethanol induced cardiac hypertrophy in the rat results from catecholaminergic stimulation, primarily of adrenal medullary origin.
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D006332:Cardiomegaly / Q000139:chemically induced*; D002395:Catecholamines / Q000652:urine*; D004032:Diet; D000431:Ethanol / Q000633:toxicity*; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D002395:Catecholamines; D000431:Ethanol; D009638:Norepinephrine