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Zapytanie: ZIEGELH”FFER
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Tytuł oryginału: Fluidising effect of resorcylidene aminoguanidine on sarcolemmal membranes in streptozotocin-diabetic rats: blunted adaptation of diabetic myocardium to Ca**2+ overload.
Autorzy: Waczulikova I., Ziegelh”ffer A., Orszaghova Z., Carsky J.
Źródło: J. Physiol. Pharmacol. 2002: 53 (4) p. 2 s.727-739, il., tab., bibliogr. 36 poz.
Sygnatura GBL: 302,092

Hasła klasyfikacyjne GBL:
  • endokrynologia
  • farmacja
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: The "remodeling" of cardiac sarcolemma in diabetes is belived to underline the reduced sensitivity of diabetic hearts due to their overload with extracellular calcium. Along with a non-enzymatic glycosylation and the free radical-derived glycxidation of sarcolemmal proteins there is ongoing reduction in cardiomyocyte membrane fluidity, the modular of cardiac sarcolemmal functioning. Aminoguanidine derivative, that inhibit glycation and glycoxidation, might suppress myocardium "remodelling" occurring in diabetic heart. To verify this hypothesis, we studied physical parameters of cardiac sarcolemma from the streptozotocin-induced diabetic rats (45 mg.kg**-1 i.m.) treated with resorcylidene aminoguanidine (RAG, 4 or 8 mg.kg**-1 i.m.). The treatment with RAG not only completely abolished protein glycation and a generation of free oxygen species (p 0.001) in treated diabetic animals, but also considerably attenuated the decrease in sarcolemmal membrane fluidity (p 0.001). In diabetic animals the "normalization" of the sarcolemmal membrane fluidity was accompanied by the vastly increased susceptibility of diabetic hearts to be overload with external calcium. We concluded that the decreased fluidity of the sarcolemmal membrane, apparently linked to the excessive glycation of sarcolemmal membrane proteins, might be intimately connected the adaptation mechanism(s) that are likely to develop in diabetic heart to protect it against to overload with external calcium.

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