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

Recently progress has been made on O2 toxicity and pathology related to numerous environmental contaminants in insects. The pro-oxidants studied included: dioxin, paraquat, and an assorted array of quinones, 8-methoxypsorlen, arsenic, and mercury. The responses to these oxidants are diverse, but they arise from the reactive oxygen species. These pro-oxidants in insects cause lipid peroxidation, protein and enzyme oxidation, and GSH depletion. Potentially, they may also cause DNA oxidation, and form DNA adducts. Oxidative challenge is alleviated by antioxidant compounds, but more importantly by the induction of antioxidant enzymes, which are crucial for the termination of O2 radical cascade and lipid peroxidation chain reaction. Insects exhibit a wasting syndrome under sub-acute stress. In acute toxicity vital physiological processes impaired are hemolymph melanization and diuresis. Thus, insects resemble vertebrates in both the response to oxidative stress and its pathological consequences. These results raise the prospect that insects may serve as non-mammalian model species for monitoring the oxidative-stress component of environmental toxicity.
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PMID:Oxidative stress from environmental pollutants. 760 41

An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This 'wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus-pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here. The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially amplified or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and beneficial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-amplified by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.
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PMID:Novel insights into the neuroendocrinology of critical illness. 1087 25

The initial neuroendocrine response to critical illness illness consists primarily of activated anterior pituitary function, the peripheral anabolic pathways being inactivated. This response presumably provides metabolic substrates, establishes the host's defences and is thus considered to be adaptive and beneficial. It was previously assumed that the acute stress response persisted throughout the course of critical illness, but this assumption has now been disproved. Indeed, a uniformly reduced pulsatile secretion of growth hormone, thyroid-stimulating hormone, prolactin and luteinizing hormone has been observed in protracted critical illness, impairing the function of target organs. A reduced availability of thyrotropin-releasing hormone, gonadotropin-releasing hormone, the endogenous ligand of the growth hormone-releasing peptide receptor (possibly ghrelin) and, in very long-stay critically ill men, also growth hormone-releasing hormone seems to be involved. The pulsatile secretion of growth hormone, thyroid-stimulating hormone, prolactin and luteinizing hormone can be re-established by relevant combinations of releasing factors, which also substantially increase the circulating levels of insulin-like growth factor-1, growth hormone dependent binding proteins, thyroxine, tri-iodothyronine and testosterone. Active feedback inhibition loops prevent the target organs being overstimulated. The metabolism is altered in a beneficial way when growth hormone-secretagogues, thyrotropin-releasing hormone and gonadotropin-releasing hormone are administered together, whereas the effect of single-hormone treatment is minor and accompanied by side-effects. This new concept of a selectively reduced stimulation of pituitary function in the chronic phase of critical illness unveils new therapeutic perspectives to reverse the paradoxical wasting syndrome' and intensive care dependency.
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PMID:The neuroendocrine response to stress is a dynamic process. 1180 May 14