Alterations in Calcium-Binding Properties of Sarcoplasmic Reticulum Membrane Proteins Following Cardiac Injury

Abstract

Aims:The objective of present work is to investigate metabolic alterations associated with heart failure, particularly one of its manifestations, a sustained hypocalcemia that causes hemodynamic changes contributed to subsequent myocardial injury. Comparative study was carried out using experimental models of pancreatic necrosis (PN) and crush syndrome (CS) accompanied by cardiac damage down to myocardial infarction. Study design: Wistar adult male rats randomly divided into groups (n=12/group). The controls are healthy intact animals. The pancreatic necrosis (PN) and crush syndrome (CS) groups were then randomly subdivided: PN group-into 3, 24 and 72 h groups concerning hemorrhage, early and late pancreatic necrosis respectively; CS group -into 2, 4, 24, and 48 h decompression stages. The rats were sacrificed to analyze spectra and calcium-binding properties of the membrane proteins isolated from the cardiomyocyte sarcoplasmic reticulum (SR). Development of pathological changes in the heart and pancreas were also monitored. Place and Duration of Study: Department of Pathological Biochemistry and Radioisotope Methods, H. Buniatyan Institute of Biochemistry of Natl. Acad. Sci (NAS), Republic of Armenia (RA). Experiments conducted between May 2011 and October 2013. Methodology: To study pathogenesis of hypocalcemia underlying myocardial damage a translocation of radioactive 45 CaCI 2 into cardiomyocytes and its intracellular distribution was examined. Binding of 45 Ca 2+ to the SR membrane proteins was measured after proteins separation by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and radioactivity from the gel plates was counted by a gas-flow meter Berthold-II.

The effect of hypothalamic peptides, neurohormone C and proline-rich peptide-1on the Ca2+-handling system in heartin pathophysiological conditions

“…We then studied the processes 3 h after the onset of AP associated with vascular necrosis (edematous hemorrhagic AP), 24 and 72 h after the onset of AP associated with hemorrhagic pancreatic necrosis, and 7, 14 and 21 days after the onset of AP associated with chronic pancreatitis, characterized by symptoms of sclerosis and lipomatosisof organs, respectively, corresponding to reparative, chronic, and chronic recurrent stages of pancreatitis [30,31]. AP is accompanied by increased secretion of catecholamines in blood and elevated level of norepinephrine in heart, contributing to myocardial damage, similar to isoproterenol-induced HF and MI, resulting in 25-35% of mortality from AP [32].…”