Alterations in norepinephrine pattern in the damaged myocardium in the rat.
In the albino rat, the evolvement of myocardial necrosis induced by a single injection of ISO was accompanied by a fall in total NE. Pretreatment with propranolol and pargyline protected against ISO-induced necrosis and myocardial hypertrophy, but did not influence the ISO-induced depletion of NE stores. The depletion of NE stores is not due to impairment in synthesis or increased intraneuronal metabolism of NE since, in ISO-treated rats, neither cardiac tyrosine hydroxylase activity nor MAO activity was altered. The decrease in endogenous NE is not due to a defect in the storage of NE. The ability of myocardium to take up and store NE returned to normal within 48 hours, whereas endogenous levels returned to normal within 5 days, even in the presence of demonstrable necrosis. Thus, there is lack of correlation between chemical and morphological changes, since catecholamine depletion occurred in the absence of morphologically demonstrable tissue injury, and the function of the adrenergic neuron returns to normal in the presence of demonstrable necrosis.
D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced; D009202:Cardiomyopathies / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D008995:Monoamine Oxidase / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D009336:Necrosis; D009638:Norepinephrine / Q000378:metabolism*; D010293:Pargyline / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D010293:Pargyline; D011433:Propranolol; D014446:Tyrosine 3-Monooxygenase; D008995:Monoamine Oxidase; D007545:Isoproterenol; D009638:Norepinephrine