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

Young (90 days) and old (15 months) male, Sprague-Dawley rats were subjected to an acute and massive myocardial infarct by giving them two injections of a large dose of isoproterenol. The animals were autopsied at sequential time intervals to ascertain the similarities or dissimilarities in the pathophysiologic events which attend acute myocardial infarction and repair in young vs old rats. Although the signs and severity of hypotensive shock appeared to be equal, mortality was higher in the old rats, especially during the acute necrosis phase. The older rats also manifested more severe and persistent congestive heart failure, i.e., hydrothorax. Serum enzymes (CPK, SGOT, SGPT, and LDH), lipids (triglycerides, free fatty acids, and cholesterol), glucose, and BUN levels manifested a dynamic rise and fall concomitant with the induced myocardial necrosis and repair phases with distinct differences in these metabolic changes between young and old rats. Despite initially higher circulating levels of corticosterone in the old vs young rats, the older animals manifested little or no increase in circulating corticosterone levels during the acute stress of myocardial infarction. This apparent lack of adrenocortical responsiveness was accentuated by the concomitant finding of greatly hypertrophied, hemorrhagic, and lipid-depleted adrenal glands in the old rats vs a dynamic increase in circulating corticosterone levels and alterations in the weight of adrenal and thymus glands of the young rats. During the myocardial repair phase, the young rats manifested extensive endocardial fibrosis whereas the old rats displayed little or no endocardial fibrosis but copous and persistent myocardial edema and ground substance in keeping with their higher concentration of cardiac hexosamine. The pathophysiologic course of events which attends myocardial necrosis and repair is quite different in young vs old rats and may be related to the degree of responsiveness of the pituitary-adrenal axis which changes with age.
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PMID:Myocardial infarction in young vs old male rats: pathophysiologic changes. 65 13

A comparative histological investigation of the thymus, spleen and inguinal lymph nodes has been performed in the rats flown for 18.5 days on board the biosatellite "Cosmos-936" under the conditions of weightlessness and artificial gravitation (acceleration 1 g) imitating terrestrial magnetism. It has been stated that in the animals that were under the conditions of weightless ness during the flight and were sacrificed 4.5--13 h after they have landed the Earth, accidental involution of lymphoid organs is noted with morphological signs in them of an acute stress in the form of massive degeneration of the thymus lymphocytes and neutrophilic infiltration of the spleen. In rats that during the flight were subjected to the effect of artificial gravitation there was noted neither involution of the lymphoid organs nor morphological signs of acute stress in them. One of the main cause of acute stress in the rats subjected to weightlessness during the space flight is supposed to be transition to the terrestrial gravitation.
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PMID:[Comparative study of the lymphoid organs of rats aboard a space flight under weightless and artificial gravity conditions]. 73 99

The thymus, spleen and inguinal lymphatic nodes of rats flown for 19.5 and 22.5 days on board of the Earth artificial satellites Cosmos-605 and Cosmos-782 were examined histologically. It was shown that prolonged space flights brought about accidental involution of lymph organs due to a decrease of the lymphocytes amount. It is suggested that hypoplasia of lymph organs resulted from stress effects of space flight factors. The mass disintegration of lymphocytes and accumulation of nuclear detritus in the thymus as well as neutrophil infiltration of the spleen can be attributed to the acute stress of the reentry and weightlessness--1 g transition stages. It is emphasized that inhibition of erythroid hemopoiesis in the spleen cannot be ascribed to stress effects of space flight factors. Possible contribution of the changes found in lymph organs to the immunological state of the animal body is discussed.
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PMID:[Changes in the lymphoid organs of rats during space flight]. 90 Dec 2

Experiments were undertaken to test the general validity of the assumption that potentiation of tumour transplantability by sublethal whole body irradiation (WBI) implies some degree of immunological resistance in the intact host. A transplantable carcinoma of spontaneous origin in CBA mice which exhibits a large WBI effect was assayed quantitatively in mice which had been immunologically crippled in terms of allograft acceptance by depletion of thymus derived lymphocytes. The mean number of tumour cells required for 50% successful takes (TD50) in these mice was found to be not significantly different from that in normal controls but highly significantly greater than in WBI mice. On the other hand, in mice which underwent laparotomy immediately before assay, the TD50 was reduced significantly though not to the same extent as in WBI mice. It was concluded that WBI effect was not due to impaired host immunity but possibly to physiological changes resulting from acute stress. The hypothesis that hyperfibrinogenaemia which occurs after both WBI and laparotomy might increase tumour transplantability was rejected because of the lack of correlation between TD50 and fibrinogen levels at different times after each procedure. From this and other work it is apparent that TD50 data, in themselves, give no reliable indication of host immunity.
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PMID:Enhancement of syngeneic murine tumour transplantability by whole body irradiation--a non-immunological phenomenon. 115 15

This study examined the effect of immobilization stress on the expression of muscarinic and beta-adrenergic receptors on thymocytes and lymphocytes obtained from 5-month-old L-E male rats. After 2 h immobilization (acute stress) there was a significant increase in specific binding of [3H]-DHA to beta-adrenergic receptors on thymocytes and on lymphocytes from the blood but not from the spleen, whereas [3H]-QNB binding to muscarinic receptors in those cells was not altered in comparison with the undisturbed control. Chronic immobilization stress (5 days, for 2 h) decreased the [3H]-QNB binding to lymphocytes collected from the spleen and blood but not from thymus; it caused neither a significant change in the 3H-DHA binding to thymocytes nor lymphocytes obtained from the blood and spleen.
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PMID:Stress-induced changes in muscarinic and beta-adrenergic binding sites on rat thymocytes and lymphocytes. 131 29

The responses of the hypothalamic-pituitary-adrenal axis during chronic stress are characterized by normal or slightly elevated plasma ACTH, increased hypothalamic corticotropin-releasing hormone (CRH) and vasopressin secretion, decreased pituitary CRH receptors and hypersensitivity of the ACTH and glucocorticoid responses to a novel stress. To determine the role of CRH and vasopressin in the pituitary hyperresponsiveness to a superimposed stress, pituitary CRH receptors and plasma ACTH responses were measured in rats receiving minipump infusions of CRH or a combination of CRH and vasopressin (VP), 50 ng/min of each for 50 h. Rats were killed by decapitation with or without exposure to ether vapor for 5 min or immobilization for 15 or 30 min, and blood was collected for ACTH and corticosterone determinations. The pituitary CRH receptor concentration measured by binding 125I-Tyr-oCRH, was reduced by 45 and 80% in CRH- and CRH-plus-VP-infused rats, respectively, with no changes in receptor affinity. Acute stress by ether exposure or immobilization had no effect on pituitary CRH receptors. Adrenal weight was significantly increased, and thymus weight decreased in CRH-infused animals, indicating activation of the pituitary adrenal axis. However, in contrast to the responses following chronic stress, the increases in plasma ACTH in response to an injection of 10 micrograms/kg CRH or acute stress were significantly lower in CRH- and CRH-plus-VP-infused rats. Furthermore the content and release of ACTH from quartered pituitaries were also decreased in chronically treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Desensitization of the hypothalamic-pituitary-adrenal axis following prolonged administration of corticotropin-releasing hormone or vasopressin. 133 16

We have used streptozotocin (STZ)-induced diabetes in rats to determine whether this represents a sustained stimulus to the adrenocortical system and whether STZ-diabetic rats are able to mount an acute stress response. Furthermore, we compared pituitary responsiveness to CRF and/or arginine vasopressin, and adrenal responsiveness to ACTH in STZ- vs. vehicle-treated rats. We also compared the efficacy of dexamethasone inhibitory feedback in STZ-diabetic and control rats. Our results show that STZ-treated rats chronically hypersecrete corticosterone (B) as evidenced by their decreased thymus weights, their increased urinary B excretion, and their elevated mean plasma B levels during the light hours of the day. Despite the evidence for sustained hypersecretion of B, STZ-treated rats showed greater and more prolonged ACTH and B responses to the acute stress of histamine injection. However, when tested separately, neither pituitary nor adrenal responsiveness to their secretagogues were increased in STZ-diabetic compared to control rats. Dexamethasone inhibition of stress-induced B secretion was tested using two different paradigms: pentobarbital-anesthetized rats were given iv injections of acid saline, and awake rats were given ip injections of histamine. In both experiments the STZ-treated rats were relatively resistant to glucocorticoid inhibition of stress responses. This finding, taken together with the exaggerated ACTH and B responses to stress, strongly suggests that the facilitatory effects of chronic STZ-diabetes are a consequence of changes in sensitivity of central neural components of the adrenocortical system to stimulatory and/or inhibitory inputs, in conjunction with changes in glucocorticoid feedback sensitivity.
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PMID:Chronic streptozotocin diabetes in rats facilitates the acute stress response without altering pituitary or adrenal responsiveness to secretagogues. 164 14

This is an attempt to find a teleological rationale for the involution of the thymus with aging. The thymus is the first organ in the body to age, which seems incongruent considering its cardinal role in the immune system. An analogical incongruency can be seen in the fact that acute stress is generally accompanied by a reversible involution of the thymus. We hypothesized earlier, that this reversible involution might protect the organism from the danger of autoimmune diseases. It stands to reason that, in nature, conditions leading to stress frequently entail massive tissue destruction. This may cause the appearance of "altered self" components, leading to the formation of autoantibodies. Hence, the temporary shut-off of thymic activity would be beneficial. A similar argument holds in the case of aging and will be elaborated as follows: 1) Formation of antibodies per se entails the danger of autoimmune mechanisms, hence the process is controlled at various levels; 2) The aging process is characterized by the increasing appearance of non-self components as a result of DNA errors and post-translational changes due to free radicals and other high energy oxygen derivatives; 3) Early involution serves, in our opinion, to reduce the risk of autoimmune diseases which increases with aging, and should therefore be regarded as an adaptation of the organism to aging; 4) If this notion proves to be correct the desirability of restoring full thymic activity in old people becomes questionable.
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PMID:Hypothesis: involution of the thymus with aging--programmed and beneficial. 192 91

In previous studies we showed that in mice the pineal gland modulates the immune response via the circadian synthesis and release of melatonin. Exogenous melatonin proved also to exert immunoenhancing effects and to counteract completely the immunologic effect of acute stress. Melatonin was active only in vivo, in mice primed with T-dependent antigens and its effects on the primary antibody response and thymus weight were abolished by the specific opioid antagonist naltrexone. Here we demonstrate that physiologic concentrations of melatonin stimulate, in vitro, activated L3T4+ (CD4+) cells to release opioid agonist(s) that can reproduce in vivo the immunoenhancing and anti-stress effects on thymus cellularity and antibody production of melatonin and compete with specific binding of [3H]naloxone to mouse brain membranes. Similar results were obtained when mitogen-activated human immunocompetent cells were incubated with melatonin. In the human model the results were, however, less consistent than those obtained with murine cells, in that only four out of ten blood donors provided cells that were responsive to melatonin. This finding elucidates the mechanism of a novel immuno-neuroendocrine connection with relevant implications for our understanding of the neuroendocrine factors that may influence the immune response in vivo in normal and stressful situations. In addition, it opens new perspectives in a wide range of research fields.
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PMID:The pineal neurohormone melatonin stimulates activated CD4+, Thy-1+ cells to release opioid agonist(s) with immunoenhancing and anti-stress properties. 197 43

We have recently demonstrated that the pineal neurohormone melatonin can enhance immune reactivity in normal mice and counteract the effects of acute stress or corticosterone treatment on antibody production, thymus weight and anti-viral resistance. These remarkable immunopharmacologic effects of melatonin were abolished by naltrexone, suggesting an involvement of the endogenous opioid system. Here we compared the immunopharmacologic action of beta-endorphin, dynorphin 1-13, leu-enkephalin and metenkephalin with that of melatonin in restraint-stressed or prednisolone-treated mice and in normal nonstressed animals. We found that beta-endorphin and dynorphin 1-13 can mimic the immunoenhancing and antistress effect of melatonin. However, at variance with the pineal neurohormone, these opioids were effective in umprimed mcie, too. We found also that restraint stress or prednisolone treatment decreases the immunopharmacologic potency of beta-endorphin and augments that of dynorphin 1-13. In fact, at the doses used, beta-endorphin enhanced the antibody response in normal but not in stressed or prednisolone-treated mice, while dynorphin 1-13 was effective only in counteracting the effect of stress or prednisolone treatment. Most interestingly, all these effects proved to be dependent on the time of administration, i.e. showed a circadian rhythm in analogy with the effects of melatonin. Again, naltrexone abolished all the opioid effects, indicating that their action was exerted via opioid receptors. These findings have important scientific and practical implications.
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PMID:Beta-endorphin and dynorphin mimic the circadian immunoenhancing and anti-stress effects of melatonin. 257 Jul 59


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