TITLE

MYOCARDIAL NECROSIS INDUCED BY ISO- PROTERENOL IN RATS

AUTHOR(S)
Wexler, Bernard C.; Judd, Joseph T.; Kittinger, George W.
PUB. DATE
December 1968
SOURCE
Angiology;Dec1968, Vol. 19 Issue 11, p665
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Changes in various metabolic parameters in nonarteriosclerotic and arteriosclerotic male and female rats, were compared following the induction of myocardial infarction with the potent catecholamine, isoproterenol. Rats of the Sprague-Dawley strain were used in all of these experiments. The animals having no pre-existing arteriosclerosis were male and female virgin rats comparable in age to the one-time breeder rats. The male breeder rats have microscopic arterial lesions in the aorta and had been used as studs long enough to sire four to live litters; the female breeders were divided into two groups: (1) one-time breeders with microscopic arterial lesions similar in intensity to breeder males and (2) four- to five-time breeder females having advanced, grossly visible arteriosclerosis. Isoproterenol was injected subcutaneously at 24-hr, intervals on the first and second day of the experiment. Control animals were sacrificed at the outset of the experiment, i.e., "0 days." Each day thereafter, for 7 days, a minimum of 40 animals per group consisting of male and female virgin and breeder rats were sacrificed. The metabolic response pattern could be linked to an acute myocardial necrosis phase and a more time-extended repair phase. Hyperglycemia, hyperlipidemia of certain lipid fractions, changes in total protein and in the relative ratio of protein and lipoprotein fractions, i.e., albumin to a- to �-, were observed during the acute cardiac necrosis phase with reversal of these patterns during the repair phase. Fatty infiltration of the liver, during the active myocardial necrosis phase, is believed to be due lo a temporary decreased availability of lipoproteincarrying agents leading to temporary accumulation of fat in the liver. There was a ronsiderablo difference in the overall metabolic response to the drug-induced myocardial infarction between animals with and without arteriosclerosis.
ACCESSION #
16370971

 

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