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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied ultrastructurally the influence acute stress, produced by formaldehyde, has on some aspects of the cardiac muscle metabolism in albino rats. The results showed that the cardiac muscle was induced to develop additional work, represented ultrastructurally by an increase in the number of lipid droplets and increased concentration and volume of mitochondria.
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PMID:[Some ultrastructural aspects of the cardiac muscle of albino rat during the acute stress produced by formaldehyde (author's transl)]. 57 69

ATP-sensitive potassium (K(ATP)) channels are evolutionarily conserved plasma-membrane protein complexes, widely represented in tissue beds with high metabolic activity. There, they are formed through physical association of the inwardly rectifying potassium channel pore, most typically Kir6.2, and the regulatory sulfonylurea receptor subunit, an ATP-binding cassette protein. Energetic signals, received via tight integration with cellular metabolic pathways, are processed by the sulfonylurea receptor subunit that in turn gates the nucleotide sensitivity of the channel pore thereby controlling membrane potential dependent cellular functions. Recent findings, elicited from genetic disruption of channel proteins, have established in vivo the requirement of intact K(ATP) channels in the proper function of cardiac muscle under stress. In the heart, where K(ATP) channels were originally discovered, channel ablation compromises cardioprotection under ischemic insult. New data implicate the requirement of intact K(ATP) channels for the cardiac adaptive response to acute stress. K(ATP) channels have been further implicated in the adaptive cardiac response to chronic (patho)physiologic hemodynamic load, with K(ATP) channel deficiency affecting structural remodeling, rendering the heart vulnerable to calcium-dependent maladaptation and predisposing to heart failure. These findings are underscored by the identification in humans that defective K(ATP) channels induced by mutations in ABCC9, the gene encoding the cardiac sulfonylurea receptor subunit, confer susceptibility to dilated cardiomyopathy. Thus, in parallel with the developed understanding of the molecular identity and mode of action of K(ATP) channels since their discovery, there is now an expanded understanding of their critical significance in the cardiac stress response in health and disease.
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PMID:Cardiac KATP channels in health and disease. 1591 Aug 78

Zinc plays a vital role in various cellular functions. Zinc deprivation is associated with severe disorders related to growth, maturation, and stress responses. In the heart, zinc affects differentiation and regeneration of cardiac muscle, cardiac conductance, acute stress responses, and recovery of heart transplants. Recent discoveries of the molecular players in zinc homeostasis revealed that the amount of intracellular free zinc is tightly controlled on the level of uptake, intracellular sequestration, redistribution, storage, and elimination, consequently creating a narrow window of optimal zinc concentration in the cells. Most of intracellular zinc is bound to numerous structural and regulatory proteins, with metabolically active, labile zinc present in picoto nanomolar concentrations. The central position of zinc in the redox signaling network is built on its unique chemical nature. The redox inert zinc creates a redox active environment when it binds to a sulfur ligand. The reversible oxidation of the sulfur ligand is coupled to the reversible zinc release from the protein, thereby executing the task of so-called protein "redox zinc switch." Clearly, the impairment of zinc homeostasis will have far reaching physiological consequences.
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PMID:Zinc dynamics in the myocardial redox signaling network. 1698 23

Our aim was to investigate the effects of moderate load, regular swimming exercise on stress-induced anxiety, and associated oxidative organ injury. Male Sprague-Dawley rats (n = 48) were either kept sedentary or submitted to swimming exercise for 8 weeks. Rats were then divided as non-stressed, acute stress, and chronic stress groups. After acute or chronic stress (electric foot shocks) applications, rats were placed on a holeboard and the exploratory behavior was recorded to assess the anxiety. Rats were decapitated after the stress application. Acute and chronic stress induction led to increased serum cortisol levels as compared to non-stressed groups. Plasma aspartate aminotransferase levels that were elevated in sedentary rats with both stress exposures were lower in trained rats. Malondialdehyde levels and myeloperoxidase activity were increased in the cardiac muscle, liver, stomach, and brain of the stressed rats with a concomitant reduction in the glutathione levels, while stress-induced changes in malondialdehyde, myeloperoxidase, and glutathione levels were reversed in the trained animals. Exercise, which led to increased malondialdehyde and reduced glutathione levels in the skeletal muscle of the non-stressed rats, also protected against stress-induced oxidative damage. Regular exercise with its anxiolytic and antioxidant effects ameliorates stress-induced oxidative organ damage by a neutrophil-dependent mechanism.
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PMID:Stress-induced multiple organ damage in rats is ameliorated by the antioxidant and anxiolytic effects of regular exercise. 2080 5