Key result
Induction of diabetes in rats with post-infarction cardiac remodeling led to suppression of the increase in lipid peroxidation activity and maintenance of myocardial rhythmoinotropic reactions.
Why the study?
Does the concomitant induction of diabetes mellitus alter lipid peroxidation and myocardial rhythmoinotropic reactions in rats with post-infarction cardiac remodeling?
Does the concomitant induction of diabetes mellitus alter lipid peroxidation and myocardial rhythmoinotropic reactions in rats with post-infarction cardiac remodeling?
In a rat model, the induction of diabetes during post-infarction cardiac remodeling paradoxically suppressed lipid peroxidation and maintained myocardial contractile responses.
Rat myocardial data in combined ischemic HF and diabetes require validation; leaves open human relevance.
The features of the functional state of the rat myocardium and the activity of the lipid peroxidation processes were studied under the conditions of concomitant development of heart failure of ischemic etiology and diabetes mellitus. The rhythmoinotropic myocardial reaction and the content of active products of thiobarbituric acid and diene conjugates in the blood plasma of rats with postinfarction and diabetic heart remodeling were assessed separately and under their combined development. Under experimental conditions with the development of post-infarction cardiac remodeling, it was shown that the induction of diabetes leads to suppression of the increase in the activity of lipid peroxidation and maintenance of myocardial rhythmoinotropic reactions.
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Kondratieva et al. (2019) studied Postinfarction cardiosclerosis and diabetes mellitus. Concomitant development of postinfarction cardiosclerosis and diabetes mellitus vs. Separate development of postinfarction cardiosclerosis or diabetes mellitus was evaluated on Rhythmoinotropic myocardial reaction and content of active products of thiobarbituric acid and diene conjugates in blood plasma. Induction of diabetes in rats with post-infarction cardiac remodeling led to suppression of the increase in lipid peroxidation activity and maintenance of myocardial rhythmoinotropic reactions.
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