Myocardial dysfunction in diabetic rats: influence of beta-adrenoceptor blockade (propranolol).

The effects of a beta-blocker, propranolol, on the enzyme and isoenzyme activities in the heart muscle in vitro and concomitant histopathology of the component cells of the islets of Langerhans were studied in the Wistar rats after treatment with streptozotocin and isoproterenol. The biochemical data indicated that the isoproterenol induced myocardial infarction (MI) precipitates an acute diabetic response in the rat heart. The superimposition of MI in diabetes mellitus caused significant inhibition of phosphofructokinase and hexokinase in the heart muscle. The lactate dehydrogenase depicted shifting of H-type to M-type in diabetes with or without MI. The drugs, when administered in combination, brought distinctive histopathological changes in beta-cells of the pancreatic islets including degranulation, hyalinosis and a near-total destruction; however A and D cells remained more or less unaffected. The effect of propranolol in diabetes mellitus was uncertain but in MI with or without prior diabetes, the drug inversely altered the activities of all the cardiac enzymes, besides stimulating a mild recuperation of the cells of the endocrine parenchyma.

Carbohydrates, lipids and lipoproteins and islet changes in diabetes with superimposed myocardial infarction.

Short-term metabolic and concomitant morphologic effects of streptozotocin diabetes on isoproterenol-induced myocardial infarction was studied in Wistar rats, Of particular significance was the observation that myocardial infarction in concert with diabetes brought about a distinctive exacerbation of the severity and complexity of the histopathological lesions. Of all the biochemical parameters, serum glucose and free fatty acids registered maximum elevation and serum lactate and cardiac glycogen levels a maximum reduction. Among the lipoproteins, an inverse relationship was found between high density lipoproteins and low density and very low density lipoproteins; while high density lipoproteins, ratio of high density lipoprotein to low density lipoprotein and the percentage of high density lipoprotein were decreased, there was a significant increase in low density lipoprotein concentration and percentage values of low density and very low density lipoproteins. In diabetes, the Β cell of the endocrine pancreas depicted selective necrosis. Loss of insulin granules and wide-spread necrobiosis of cellular elements of the pancreatic islets were observed, respectively, in myocardial infarction and in diabetes plus myocardial infarction combinations. Pathological evidence of chemical-induced mild toxicity was present in the exocrine parenchyma. Mitotic features and the presence of centroacinar cells in the damaged Langerhans’ islets supposedly formed the basis of regeneration of the tissue in diabetes, with or without vascular complications.

Effects of some drugs on islet function in catfish.

Blood glucose variations and concomitant bioptical cytopathological changes in the pancreatic islets following treatment with certain drugs were studied in the catfish. Glucose loading produced a dose-related hyperglycemia, maximum within 3 hr, while alloxan caused a biphasic rise in glucose level without induction of permanent diabetes. Streptozotocin elicited a monophasic hyperglycemic state at a lower dose and biphasic response at higher doses. Glybenclamide produced hypoglycemia in normal and sham-operated fish; the depancreatized animals were unresponsive to this treatment. In all the cases, normoglycemic values were restituted within 4 days of the treatment. The beta-cells of the islets underwent varying histopathological changes with signs of regenerative activity. A depletion in heavy metal (zinc) in these cells was also evident after treatment with streptozotocin.