By Bohuslav Ost'ádal, Frantisek Kolár
Cardiac Ischemia: From damage 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 outcomes of ischemia. the second one half offers with the mechanisms of cardiomyocyte dying in ischemia, structural elements 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 quick description of reperfusion damage, its medical 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 chances for expanding cardiac resistance to ischemia and hypoxia, i.e. long-lasting edition to power hypoxia and short-lasting preconditioning. The final a part of the booklet bargains with comparative and ontogenetic facets of cardiac sensitivity to oxygen deprivation; this bankruptcy additionally summarizes the ontogenetic modifications and obstacles in endogenous and exogenous safety of the ischemic/hypoxic heart.
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Extra resources for Cardiac Ischemia: From Injury to Protection
The supplementation of the myocardium with these compounds results in an increased tissue camitine content, a stimulation of pyruvate oxidation, lessening of the severity of ischemic injury, and improvement in the recovery of heart function during reperfusion (8tanley et al. 1997). Conversely, inhibition of long-chain acyl-CoA transport into mitochondria by etomoxir (carnitine palmitoyltransferase 1 inhibitor) seems to exert a beneficial effect, not only by directly inhibiting fatty acid oxidation but also indirectly by increasing the rate of glycolysis (Opie, 1996a).
Induction of ischemic quiescence can be considered a protective mechanism as it allows a drastic reduction of mitochondrial oxidation and, in turn, of the oxygen need ofthe myocytes. 18 Table 2 Causes of impaired contractility in acute severe ischaernia Accumulation of metabolites Intracellular acidosis with displacement of Ca2+ from intracellular binding sites on contractile proteins Accumulation of inorganic phosphate with an interaction with Ca2+ Accumulation of neutral lactate Changes in high-energy phosphate levels or availability Decreased tumover of ATP Decreased level of cytosolic phosphocreatine with irnpaired phosphocreatine shuttle Decreased level of A TP in a "contractile" subcompartment Decreased free energy change of ATP hydrolysis (related to rise of inorganic phosphate) Mechanical effects of decreased coronary flow Reversed "garden hose" or "erectile" effect From Opie, 1998, with perrnission.
No data are available. From Bolli and Marban, 1999, with permission. 22 Table 4 Mechanisms proposed for myocardial stunning Most plausible Oxyradical hypothesis (generation of oxygen-derived free radicals) Calcium hypothesis Calcium overload Decreased responsiveness of myofilaments to calcium Less plausible Excitation-contraction uncoupling due to sarcoplasmic reticulum dysfunction Not plausible Insufficient energy production by mitochondria Impaired energy production by mitochondria Impairment of sympathetic neural responsiveness Impairment of myocardial perfusion Damage of the extracellular collagen matrix Impaired excitation From Bolli and Marban, 1999, with permission.
Cardiac Ischemia: From Injury to Protection by Bohuslav Ost'ádal, Frantisek Kolár