Why the study?
Does isoproterenol-induced myocardial infarction alter liver lipids in adult male Long-Evans rats?
Does isoproterenol-induced myocardial infarction alter liver lipids in adult male Long-Evans rats?
Isoproterenol-induced myocardial infarction in rats is associated with acute, transient hyperlipidemia and fatty liver, characterized primarily by increased hepatic triglycerides and cholesterol.
Acute MI models show transient hepatic hyperlipidemia; leaves open relevance to human infarction or outcomes.
Adult, male Long-Evans rats were challenged with two subcutaneous doses of the potent catecholamine, isoproterenol. Within hours after the first injection myocardial ischemia and necrosis became apparent. On the second day, after the second injection, myocardial necrosis reached a zenith followed by myocardial repair during days 4–7 after the initial injection. During the development of myocardial ischemia and necrosis there is dramatic loss of body weight; dissolution of periadrenal, mesenteric, and other adipose tissue depots; hyperlipidemia; and grossly-visible fatty metamorphosis of the liver. During the myocardial repair phase the hyperlipidemia and the condition of fatty liver disappear rapidly. Chemical analysis of the hepatic lipid fractions demonstrate that there is a very considerable and rapid increase in hepatic triglycerides, a less marked and less rapid but significant increase in hepatic cholesterol, and only a modest fluctuation in hepatic phospholipid.
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Judd et al. (1969) studied this question.
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