Subject(s)
Lipids/analysis , Myocardium/chemistry , Physical Exertion , Subcellular Fractions/chemistry , Animals , Cholesterol/analysis , Fatty Acids, Nonesterified/analysis , Male , Microsomes/chemistry , Mitochondria, Heart/chemistry , Rats , Rats, Inbred Strains , Sarcoplasmic Reticulum/chemistry , Triglycerides/analysisABSTRACT
In the myocardial mitochondria (MCh) of persons who had died from ischemic heart disease (IHD) the content of phosphatidylcholine (PCh) and cardiolipin reduces while the amount of the products of their hydrolysis--free fatty acids (FFA) and lysophospholipids--increases. This is evidence of the breakdown of the membrane MCh phospholipids (PL). The content of PL, protein, FChS, FFA, and lysophosphatidylethanolamine in the sarcoplasmic reticulum increases. The increase in the amount of PL, protein, and free cholesterol (FChS) may be explained by an increase of their synthesis due to myocardial hypertrophy which was encountered in all of the cases studied. The accumulation of FFA and lysophosphatidylethanolamine is probably not linked with PL hydrolysis (their amount in this subcellular fraction increases) but is a consequence of other changes in myocardial lipid metabolism. Thus, in IHD hydrolysis of PL prevails in the myocardial MCh and their synthesis in the sarcoplasma reticulum. These changes in the metabolism of the subcellular fractions may lead to damage of the membranes of the cardiomyocyte MCh, which may be the cause of disorders of electrolyte metabolism and contractile properties of the myocardium in IHD.
Subject(s)
Coronary Disease/metabolism , Myocardium/metabolism , Coronary Disease/etiology , Death, Sudden/etiology , Heart Ventricles/metabolism , Humans , Lipid Metabolism , Male , Phospholipids/metabolism , Proteins/metabolism , Subcellular Fractions/metabolism , Wounds and Injuries/metabolismABSTRACT
It was established that in the persons who had died from acute ethanol intoxication the processes of calcium compartmentalization in myocardiocytes are disordered and characterized by a decrease of calcium content in mitochondria and sarcoplasmic reticulum and an increase of its concentration in the supernatant fluid. Alcohol-induced changes of calcium compartmentalization in myocardiocytes may cause cardiac disorders and be, in particular, one of the possible links in the thanatogenesis of sudden death.
Subject(s)
Alcoholic Intoxication/metabolism , Calcium/metabolism , Heart/drug effects , Myocardium/metabolism , Proteins/metabolism , Histocytochemistry , Humans , Male , Subcellular Fractions/drug effects , Subcellular Fractions/metabolism , Wounds and Injuries/metabolismABSTRACT
The content of Ca2+ was reduced in myocardiocyte mitochondria and sarcoplasmatic reticulum, and increased in the supra-sedimentary fluid following the sedimentation of sarcoplasmatic reticulum in cases of sudden coronary death, an evidence of disturbed Ca2+ deposition in subcellular myocardial fractions and elevated Ca2+ concentration in myocardiocyte sarcoplasm. The demonstrated disturbances of Ca2+ deposition may be responsible for cardiac contractility disorders, and incomplete diastolic relaxation of the myocardium, and thus provide an essential element of thanatogenesis of the sudden coronary death.