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

The neuroendocrine stress response is a dynamic process involving multiple hormonal alterations with distinct features in the acute and chronic phase of critical illness. In the initial response to an acute stress event, the anterior pituitary actively releases its hormones into the circulation while in the periphery, anabolic target organ hormones are inactivated. This response is thought to be beneficial and adaptive. When critical illness becomes prolonged, pulsatile secretion of anterior pituitary hormones becomes uniformly reduced due to reduced (hypothalamic) stimulation, and this underlies reduced activity of the respective target tissues and impaired anabolism. This difference in the acute and chronic stress response may not be trivial. It was the (inappropriate) assumption that acute stress responses, such as GH resistance, persist throughout the course of critical illness, which had formed the (inappropriate) justification to administer high doses of GH to long-stay intensive care patients to induce anabolism [102]. The concomitant endocrine changes in chronic critical illness may have predisposed to severe side effects of high doses of GH. In view of the significant benefits of strict glycemic control using exogenous insulin recently demonstrated in ICU patients [101], GH-induced insulin resistance and hyperglycemia may have played a role. It remains to be studied whether endocrine intervention with releasing factors such as TRH and GHRP in prolonged critical illness will accelerate recovery of patients who have entered the vicious circle of prolonged intensive care dependency.
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PMID:Neuroendocrine pathobiology of chronic critical illness. 1214 Sep 11

This study investigated the effect of an acute stress on food intake and on the expression of neuropeptide Y (NPY), corticotropin-releasing hormone (CRH), and ghrelin and its receptors, growth hormone secretagogue receptors (GHSRs) in the tilapia (Oreochromis mossambicus). Food intake was significantly (P < 0.01) reduced in fish after a 30-min crowding and handling stress. In a second group of animals exposed to the same 30-min stressor, tissue samples were collected immediately after the stressor to determine changes in the neuroendocrine regulators of food intake. Although CRH and NPY are considered the major mediators of appetite during stress, both mRNA levels were unaltered in the telencephalon/pre-optic area and in the hypothalamic/optic tectum. Interestingly, there was an elevation in the ghrelin transcript (P < 0.05) in the telencephalon/pre-optic area and elevation of its functional receptor (GHSR1a-LR) (P < 0.001) in the hypothalamic/optic tectum. Elevation of GHSR-LR heteronuclear RNA (P < 0.01) in the telencephalon/pre-optic area and suppression in the hypothalamic/optic tectum (P < 0.001) suggest rapid control of the ghrelin regulatory system in response to acute stress. These results suggest that ghrelin signaling is altered during acute stress. It is not clear if these changes result in altered feeding behavior because no changes in CRH or NPY mRNA expression were observed or if ghrelin is playing a role in regulating overall metabolic changes after acute stress.
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PMID:Acute stress inhibits food intake and alters ghrelin signaling in the brain of tilapia (Oreochromis mossambicus). 2329 Oct 12