By Bohuslav Ost'ádal, Frantisek Kolár
Cardiac Ischemia: From harm to Protection has been divided into six components. the 1st half describes the diversities among hypoxia and ischemia, animal versions, the consequences of ischemia on myocardial functionality and metabolism, and the electrophysiological results of ischemia. the second one half bargains with the mechanisms of cardiomyocyte dying in ischemia, structural points of irreversible ischemic damage, necrosis and apoptosis of cardiac cells, the function of calcium, and the concept that of calcium antagonism. The 3rd bankruptcy is a short description of reperfusion harm, its scientific relevance, and attainable prevention. The fourth half summarizes adjustments in myocardial vasculature in the course of ischemia and reperfusion. The 5th half is the survey of 2 major probabilities for expanding cardiac resistance to ischemia and hypoxia, i.e. long-lasting edition to persistent hypoxia and short-lasting preconditioning. The final a part of the booklet offers with comparative and ontogenetic elements of cardiac sensitivity to oxygen deprivation; this bankruptcy additionally summarizes the ontogenetic changes and boundaries in endogenous and exogenous security of the ischemic/hypoxic heart.
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Additional info for Cardiac Ischemia: From Injury to Protection
E. e. , 1996). Ca2+ appear to playa key role in these mechanisms (Fig. 12). Abnormal impulse generation is favored by dirninished negativity of resting membrane potentials and by triggered activity precipitated by early or delayed afterdepolarizations. The inward current that Imtlates early afterdepolarizations, occurring during phase 2 or 3 of repolarization can most likely be attributed to L-type Ca2+ channels, so one could expect that it could be prevented by calcium antagonists. Indeed, verapamil and dihydropyridines both proved effective in abolishing early afterdepolarizations and triggering.
The K+ channels activated during ischemia may serve as conduits for cellular K+ loss and cause shortening of the action potential. The KATP channels, which open when ATP decreases during hypoxia, metabolic inhibition or ischemia, may be responsible for some of the K+ efflux accompanying 33 these conditions. Phannacological blockade of the KATP channel with sulfonylureas during ischemia reduces, but does not prevent, cellular K+ loss. , Vo ltage~ated cha nnsl. --~~~~ .. Oe .. ,olW 1 Ion exchangersltransporters Figure 9 Sarcolemmal and intracellular membrane channels, pumps, and exchangers that may contribute to the ionic and electrophysiological changes that occur during ischemia.
All of these changes reduce action potential duration and consequently also the Ca2+ influx into the myocyte (Norna 1983). Such a decreased intracellular Ca2+ concentration could then reduce contractile function and A TP consumption (Heusch and Schulz, 1996). Apart from changes in the absolute concentration of myocardial ATP decreases in the phosphorylation potential of the free energy change of ATP hydrolysis could be responsible for the decrease in contractile function (Clarke et 19 al. , 1987).