Calcium and the protective effect of ethanol in epinephrine-induced cardiac necrosis in the rat
Mallov, S.
Research Communications in Chemical Pathology and Pharmacology 26(1): 47-63
1979
ISSN/ISBN: 0034-5164 PMID: 515509 Document Number: 147723
The i.v. or i.p. as well as oral administration of ethanol to rats markedly reduced the severity of cardiac necrosis produced by the injection of a single large dose of epinephrine. Since ethanol also lowers plasma Ca levels in rats, it was postulated that it might exert its protective effect by reducing plasma Ca concentrations and hence decreasing the epinephrine-induced rise of Ca inflow into the heart. The effects of other blood Ca-lowering agents on epinephrine-induced cardiac necrosis were explored. The administration of phosphate buffer or calcitonin in doses that lowered plasma Ca to approximately the same degree elicited by ethanol, did not protect the rats against epinephrine-produced cardiac necrosis. Administration of ethanol solutions containing CaCl2 protected these animals although plasma Ca was not decreased. Ethanol does not appear to be protective as a consequence of its blood-Ca lowering activity. Urethane, a sedative-anesthetic agent which has also been reported to lower plasma Ca concentrations in rats, did inhibit the production of cardiac necrosis by epinephrine. Urethane is metabolized to ethanol in vivo. Large doses of calcitonin that lowered plasma Ca to a greater degree than ethanol also reduced the severity of epinephrine-induced cardiac necrosis. The protective action in this case might have been due to an interference with thrombus formation in the heart since blood clotting times were elevated in the rats given the large doses of calcitonin, and since heparin also reduced the severity of the cardiac necrosis produced by epinephrine.