The role of glycogen content in the heart for the development of isoprenaline-induced myocardial lesions (IML) was studied in Wistar rats and in two inbred rat strains: In IR rats (resistant to the development of IML) and in IS rats (sensitive to IML development). Glycogen content in the heart can be dramatically lowered or increased by various interventions. IML develop during the period of very low heart glycogen content (about 0.6 mg.g-1) induced by isoprenaline administration. In animals with increased resistance to IML, either due to genetic factors or induced by isoprenaline pretreatment a high glycogen content in the heart is found (up to 7.5 mg.g-1). The increase of resistance to IML development and increased glycogen content induced by isoprenaline pretreatment were accompanied by lower basal or ISO-, guanylylimidodiphosphate- (Gpp/NH/p) and forskolin-stimulated activities of adenylyl cyclase. On the other hand, these parameters did not differ between IR and IS rats in spite of the presence of significant differences in the resistance to the development of IML and in heart glycogen content in these two rats strains. These results suggest that genetically determined differences between two inbred rat strains in the resistance of the heart to the development of IML and in the heart glycogen content are caused by factors which are independent of the receptor-adenylyl cyclase complex and are therefore different from those involved in the increase of resistance and glycogen content due to isoprenaline pretreatment.

• MeSH
• Adenylyl Cyclases metabolism   MeSH
• Adrenergic beta-Agonists pharmacology   MeSH
• Glycogen metabolism   MeSH
• Guanylyl Imidodiphosphate pharmacology   MeSH
• Isoproterenol pharmacology   MeSH
• Colforsin pharmacology   MeSH
• Rats MeSH
• Myocardium metabolism   MeSH
• Rats, Wistar MeSH
• Propranolol pharmacology   MeSH
• Heart drug effects   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Adenylyl Cyclases MeSH
• Adrenergic beta-Agonists MeSH
• Glycogen MeSH
• Guanylyl Imidodiphosphate MeSH
• Isoproterenol MeSH
• Colforsin MeSH
• Propranolol MeSH

Two inbred rat strains, differing in their resistance to the induction of myocardial lesions by the administration of isoprenaline (ISO), have been developed. The extent of ISO-induced myocardial lesions (IML) was three to five times lower in the ISO-resistant (IR) strain as compared to that in the ISO-sensitive (IS) strain. The two strains differ also in a number of other genetically determined features, e.g., a higher myocardial glycogen content (MGC) and higher adipose tissue weight in IR rats. Between IML extent and MGC a significant negative correlation has been demonstrated in 2nd filial generation of IR and IS hybrids. By contrast, no correlation has been found between the resistance to the development of IML and the other genetically determined features studied. High resistance to the development of IML and a high MGC were also noted in another inbred strain, the hypertriacylglycerolemic (HTG) rats. Comparison of IML extent in HTG, IR and IS rats has revealed that the extent of IML, while depending on MGC, is independent of triacylglycerolemia. MGC can be raised in IR and IS rats by various interventions (e.g., repeated administration of ISD or fasting). Regardless of the intervention used, it entails a simultaneous increase in resistance to the development of IML. In vivo administration of glucose and insulin, however, exerts only a minimal effect on MGC and on the extent of IML. It may be concluded, therefore, that under our experimental conditions the enhanced resistance to the development of IML, whether genetically determined (IR, HTG rats) or induced by some interventions (fasting, repeated ISO administration), is closely related to an increased MGC.

• MeSH
• Adrenergic beta-Agonists toxicity   MeSH
• Glycogen metabolism   MeSH
• Rats, Inbred Strains MeSH
• Isoproterenol toxicity   MeSH
• Rats MeSH
• Myocardium metabolism   MeSH
• Heart drug effects   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Comparative Study MeSH
• Names of Substances
• Adrenergic beta-Agonists MeSH
• Glycogen MeSH
• Isoproterenol MeSH

Excessive release or administration of beta-mimetic catecholamines may induce cardiomegaly, necrotic lesions and accumulation of connective tissue in the heart of adult homoiotherms. It was examined here whether similar changes can also be observed at different stages of evolution of the cardiovascular system, i.e. in poikilotherms and in homoiotherms during embryonic life. Sensitivity of the poikilothermic hearts (carp, frog, turtle) to isoproterenol (IPRO) was significantly lower than in the homoiotherms. Necrotic lesions, if present, were localized in the inner spongious musculature which has no vascular supply but which exhibits higher activities of enzymes connected with aerobic oxidation. Moreover, the IPRO-induced decrease of the phospholipid content was also significantly more expressed in the spongious layer. IPRO treatment did not influence the total weight of the fish heart but the proportion of the outer compact layer was significantly higher. These changes were accompanied by an increase of collagen, higher water content and an increase of isomyosin with a lower ATPase activity. The response of the poikilothermic heart to IPRO-induced overload thus differs significantly from that in the homoiotherms. The administration of IPRO during embryonic life of homoiotherms (chick) induces serious cardiovascular disturbances, including cardiomegaly and cellular oedema. Necroses of myofibrils, characteristic of IPRO-induced lesions of adults, were, however, rather exceptional. IPRO did not elevate the concentration of 85Sr (as a calcium homologue) in the immature myocardium; it seems, therefore, that IPRO-induced changes of the embryonic heart are not necessarily due to an intracellular calcium overload. It may be concluded that the character of catecholamine-induced cardiomyopathy is not uniform and depends strictly on the stage of cardiac development.

• MeSH
• Adrenergic beta-Agonists toxicity   MeSH
• Biological Evolution MeSH
• Phospholipids metabolism   MeSH
• Isoproterenol toxicity   MeSH
• Cardiomyopathies chemically induced   metabolism   pathology   MeSH
• Rats MeSH
• Chick Embryo MeSH
• Myocardium metabolism   pathology   MeSH
• Necrosis MeSH
• Fishes MeSH
• Heart drug effects   embryology   growth & development   MeSH
• Anura MeSH
• Turtles MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Chick Embryo MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Comparative Study MeSH
• Names of Substances
• Adrenergic beta-Agonists MeSH
• Phospholipids MeSH
• Isoproterenol MeSH