title: Histochemical and enzymehistochemical alterations during experimental cardiomyopathy.
abstract: Investigation of ethiology, pathogenesis, morphogenesis, pathokinesis, treatment and prevention of cardiomyopathy is one of the most important problems of cardiology. Last years many scientific forums have been devoted to cardiomyopathy problems and still many issues remain disputable and needs further investigation and definition. In particular, investigation of metabolic processes in cardiac muscle seems of great importance. Obtained data will promote elaboration of adequate means toward the correction of cardiac decompensation during cardiomyopathy. The main goal of present study was the investigation of oxidation-reduction and electron transport associated protein activity in myocardium during experimental cardiomyopathy. Experiments were carried out on 30 male rats (180 - 200 g weight). Based on histological, histochemical, enzymehistological investigations conclusion has been made that during experimental autoimmune cardiomyopathy activity of oxidation-reduction and electron transport enzymes is sharply decreased along with the decrease of ascorbic acid and tiny granule glycogen amount (with altered topographic distribution) determining energy deficiency and weakening of cardiac muscle contractile function. It is possible to consider that the present study will open the way for future research and prompt us to select optimal therapeutic agents.
authors.affiliation: Tbilisi State Medical University; Tbilisi Scientific Practical Center of Clinical Pathology.
authors.forename: I
authors.initials: I
authors.lastname: Kirvalidze
authors.forename: R
authors.initials: R
authors.lastname: Khetsuriani
authors.forename: T
authors.initials: T
authors.lastname: Jorbenadze
authors.forename: A
authors.initials: A
authors.lastname: Shukakidze
authors.forename: T
authors.initials: T
authors.lastname: Kipiani
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000032:analysis; D009202:Cardiomyopathies / Q000201:enzymology* / Q000473:pathology*; D004579:Electron Transport; D006003:Glycogen / Q000032:analysis; D008297:Male; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology*; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains; D013385:Succinate Dehydrogenase / Q000032:analysis
chemical_list: D006003:Glycogen; D013385:Succinate Dehydrogenase; D001205:Ascorbic Acid