Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 30 experiments in isolated canine hearts perfused with whole donor blood disorders in myocardial contractions were studied following the termination of paired stimulation. It was concluded that the cause of depression of cardiac contractions following paired stimulation is not myocardial hypoxia and energy reserve exhaustion during enhanced mechanical activity of the heart, but a dissociation of the electric and mechanical processes in the myocardium; switching off the second (stand-by) action potential together with the termination of the paired stimulation caused disorders in the regimen of coupling processes that have established themselves under this form of electric stimulation. This suggestion is supported by the fact that repeated paired stimulation during depression is capable of producing the same stimulating effect upon the cardiac contractions as the initial one. The depression was eliminated by the administration of potassium ions and catecholamines.
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PMID:[Analysis of depression of contractions of the isolated dog heart following paired stimulation]. 101 51

The effects of a single vs repeated bouts of exhaustive exercise on myocardial integrity were evaluated in the rodent. Rats were randomly divided into three groups: a sedentary control, single swim-to-exhaustion, and seven consecutive daily swims-to-exhaustion groups (n = 5 in each group). Overall morphology was evaluated histologically and sarcolemmal (SL), sarcotubular (ST), and mitochondrial (MITO) membranes were examined ultrastructurally using transmission electron microscopy. Neither single nor repeated bouts of exhaustive exercise produced myocardial hypoxia, as assessed by MITO morphology. However, increased interstitial space as well as significant swelling (P less than 0.01) was observed in ST from both 1- and 7-day exhausted animals. These findings were not observed at all in control myocardium. Higher magnification (x 45,000) in some instances revealed whole disruption of sarcotubular membranes in myocardium from swim-exhausted animals. The incidence of membrane disruption was higher (P less than 0.01) in 7-day vs 1-day swim-exhausted groups and not observed at all in control rats. Although in no instance did we observe disruption of SL membranes, their convoluted nature in myocardium from both exercised groups indicated exhaustion-induced fluid and/or ionic shifts within the left ventricle. These findings provide a structural basis for the reduction in myocardial sarcoplasmic reticulum and MITO Ca++ uptake previously observed following repeated bouts of exhaustive exercise.
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PMID:Effects of repeated exhaustive exercise on myocardial subcellular membrane structures. 318 55

Heart muscle fibres always undergo severe functional and structural alterations, finally resulting in necrotization, if free extracellular Ca2+ ions penetrate abundantly through the sarcolemma membrane into the myoplasm, so that the capacities of the Ca2+ binding or extrusion processes become overpowered. The crucial reaction consists of high-energy phosphate exhaustion which is brought about (a) by excessive activation of Ca2+-dependent intracellular ATPases, and (b) by Ca2+-induced impairment of the mitochondria. Intracellular Ca2+ overload proved to the common denominator in the pathogenesis of severe myocardial fibre injury and death produced under the following circumstances: Overdoses of beta-adrenergic catecholamines, dihydrotachysterol or vitamin D3, alimentary K+ or Mg2+ deficiency, hereditary cardiomyopathy of Syrian hamsters. Moreover, intracellular Ca2+ overload develops in the course of myocardial hypoxia or ischaemia thus causing additional precipitous damage of the mitochrondria. Following our first observations made in 1968, it has turned out that in all these cases, Ca2+ antagonists are capable of protecting myocardial cell integrity in that they prevent excessive transmembrane Ca2+ uptake. This is also true of the Ca2+ paradox: Ca2+ antagonists possibly inhibit the development of sarcolemmal leaks in the Ca2+-deprived myocardium. However, it is more likely that Ca2+ antagonists restrict the exaggerated influx of Ca2+ through these leaks, when the Ca+-deprived myocardial fibres return to a normal Ca2+-containing medium.
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PMID:Consequences of uncontrolled calcium entry and its prevention with calcium antagonists. 666 32

Patients suffering from stress-induced angina pectoris subjected to exertion show a decreased level of non-protein SH-groups in blood plasma and erythrocytes which depends on the level of myocardial hypoxia and may indicate metabolic exhaustion of the organism. Lowered concentrations of non-protein SH-groups are not a result of lipid peroxidation. Adrenalin is known to antagonize the depletion of non-protein SH-groups under exertion, while noradrenaline promotes the process of their oxidation. When the level of non-protein SH-groups decreases under exertion, the content of atherogenic lipids in blood does not increase, which implies that SH-groups are involved into the mechanism of appearance of atherogenic lipids in blood under exertion.
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PMID:[Non-protein sulfhydryl groups in the blood of patients with stenocardia induced by physical stress]. 775 64