The role of myocardial glycogen content for the development of isoprenaline-induced myocardial lesions in different inbred strains of rats
Jazyk angličtina Země Německo Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
8773192
DOI
10.1007/bf00788539
Knihovny.cz E-zdroje
- MeSH
- agonisté adrenergních beta-receptorů toxicita MeSH
- glykogen metabolismus MeSH
- inbrední kmeny potkanů MeSH
- isoprenalin toxicita MeSH
- krysa rodu Rattus MeSH
- myokard metabolismus MeSH
- srdce účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- agonisté adrenergních beta-receptorů MeSH
- glykogen MeSH
- isoprenalin 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.
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Arch Pathol Lab Med. 1993 Dec;117(12):1208-14 PubMed
Am J Cardiol. 1981 Aug;48(2):361-5 PubMed
Circulation. 1990 Sep;82(3 Suppl):II2-12 PubMed
J Biol Chem. 1956 Jun;220(2):583-93 PubMed
Jpn Circ J. 1963 Mar;27:282-93 PubMed
Nutr Dieta Eur Rev Nutr Diet. 1968;10(2):81-90 PubMed
Physiol Bohemoslov. 1983;32(4):307-17 PubMed
Am J Cardiol. 1983 Jul 20;52(2):72A-81A PubMed
Circulation. 1971 Jan;43(1):67-82 PubMed
AMA Arch Pathol. 1959 Apr;67(4):443-55 PubMed
Arch Pathol. 1970 Jan;89(1):79-83 PubMed
Eur Heart J. 1993 Nov;14 Suppl G:2-5 PubMed
J Mol Cell Cardiol. 1982 Nov;14(11):619-26 PubMed
J Pharmacol Exp Ther. 1993 Jan;264(1):135-44 PubMed
Eur Heart J. 1993 Nov;14 Suppl G:31-3 PubMed
Basic Res Cardiol. 1986 Jan-Feb;81(1):74-82 PubMed
Circ Res. 1970 Nov;27(5):835-49 PubMed
Ann N Y Acad Sci. 1993 Jun 14;683:57-68 PubMed
Radiol Clin North Am. 1994 May;32(3):477-500 PubMed
Ann N Y Acad Sci. 1994 Nov 25;741:252-62 PubMed
Physiol Bohemoslov. 1985;34(4):289-96 PubMed
Basic Res Cardiol. 1993 Jan-Feb;88(1):52-9 PubMed
Physiol Bohemoslov. 1980;29(4):323-31 PubMed
Physiol Bohemoslov. 1983;32(3):203-9 PubMed
Heart glycogen content and isoprenaline-induced myocardial lesions
