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Abundant information is now available about changes in subcellular organelles that are responsible for the impaired intracellular calcium homeostasis in diabetic cardiomyopathy. Some of these changes concern heart sarcolemma and include decrease in the following variables: calcium binding, influx of calcium through the L-type calcium channels, (Na,K)-ATPase(More)
Rats with streptozotocin-diabetes develop mechanisms of endogenous protection (MEP) that participate actively in functional remodeling of cardiac sarcolemma. Remodeling of sarcolemma is a sign of damage but it also protects the cells of the diabetic heart (DH) against additional energy disbalance due to excessive Ca(2+) entry. Since yet, cardiac(More)
Contrary to clinical trials, experimental studies revealed that diabetes mellitus (DM) may initiate, besides increased myocardial vulnerability to ischemia-reperfusion injury (I/R) and pro/antioxidant dysbalance, development of adaptation leading to an enhanced tolerance to I/R. The aims were to characterize 1) susceptibility to ischemia-induced ventricular(More)
A new concept of cardioprotection based on the exploitation of endogenous mechanisms is known as ischemic preconditioning (IPC). It has been hypothesized that substances released during brief ischemic stress (e.g. catecholamines) stimulate the receptors and trigger multiple cell signaling cascades. Opening of ATP-sensitive K+ channels [K(ATP)] has been(More)
Different from clinical studies of diabetes mellitus (DM), experimental data reveal both, higher and lower vulnerability of the heart to ischemic injury. We have previously demonstrated an enhanced resistance to ischemia-induced arrhythmias in isolated rat hearts in the acute phase of DM. Our objectives were thus to extend our knowledge to the effects of DM(More)
Statins, the inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, are most frequently used drugs in the prevention of coronary artery disease due to their cholesterol-lowering activity. However, it is not exactly known whether these effects of statins or those independent of cholesterol decrease account for the protection against(More)
Chronic intermittent high altitude (IHA) hypoxia results in long-term adaptation protecting the heart against acute ischemia/reperfusion injury; however, molecular mechanisms of this phenomenon are not completely elucidated so far. The present study was aimed at investigation of a modulating effect of IHA hypoxia on the expression and/or activation of(More)
There is some evidence that diabetic hearts are more resistant to ischaemia/reperfusion injury due to alterations in Ca2+ handling. Our objective was to explore this hypothesis in the model of Ca2+ overloaded heart (calcium paradox, CaP). Diabetes was induced by streptozotocin (45 mg/kg, i.v.). Despite regular insulin treatment blood glucose was increased.(More)
Mitochondrial contact sites (MiCS) are structures in the mitochondrial membrane containing the structure-bound mitochondrial isoenzyme of creatine phosphokinase that participates in the transfer of energy into the cytoplasm. This explains the increased formation of MiCS found in hearts with high metabolic activity. Earlier we demonstrated that enhanced MiCS(More)
The purpose of this study was to focus on the role of the sarcolemma and intercalated disc in the induction and prevention of calcium paradox. Perfusion of the heart with Ca deficient solution produces only minor cytoplasmic ultrastructural changes. More obvious changes are seen in the sarcolemma. The cell surface shows a separation between the layers of(More)