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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

Little is known about adrenocortical function after coronary bypass surgery in which moderate to deep hypothermia and cardiopulmonary bypass are used particularly with intraoperative steroid administration. Therefore, we performed a pilot study in which immediately preoperative and 18-hour postoperative serum cortisol levels were determined in eight patients who received 1.0 to 1.5 gm of methylprednisolone intravenously during surgery; postoperative serum cortisol (3 +/- 1 microgram%) levels were lower than preoperative levels (15 +/- 3 microgram%, p less than 0.05). To determine the possible cause of these striking findings, the effects of moderate to profound hypothermia and cardiopulmonary bypass upon adrenocortical functioning were investigated without the influence of intraoperative steroid administration. Serum cortisol and aldosterone levels and their response to adrenocorticotropic hormone (ACTH) (Cortrosyn) were determined before coronary bypass surgery and at various postoperative intervals in seven patients. Postoperative cortisol and aldosterone levels increased markedly over their preoperative values, reaching a maximum at 6 to 12 hours (cortisol 16 +/- 8 vs 63 +/- 23 micrograms%, p less than 0.05, aldosterone 15 +/- 5 vs 51 +/- 22 ng%, p less than 0.05). Adrenal response to ACTH was normal preoperatively, during rewarming from hypothermia, and 18 hours, and 7 days postoperatively. In summary, normal adrenal responsiveness occurs after coronary bypass surgery, in spite of hypothermic cardiopulmonary bypass and the effects of anesthesia, and a single dose of methylprednisolone during surgery is associated with markedly lower serum cortisol levels and prevents the usual adrenal stress response to bypass surgery for at least 18 hours postoperatively.
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PMID:Adrenal function following coronary bypass surgery. 299 Jan 87

We have shown previously that repeated restraint stress results in differential adaptation at both macrophysiological and cellular levels. Chronic stress accentuates vasopressinergic control of adrenocorticotropic hormone secretion in the pituitary. The present work determined whether endogenous vasopressin plays a role in response to repeated restraint. The first experiment explored changes in the response of repeatedly stressed animals to intracerebral vasopressin infusions. The second determined the effect of pretreating rats with a vasopressin V1a receptor antagonist on the way that they adapted to repeated restraint. Experiment 1: rats were subjected either to daily 60-min restraint for 10 days or transferred to the testing room where restraint sessions took place (controls). On the 11th day, they were infused with either artificial cerebrospinal fluid or 250 pmol vasopressin. The behavioural response to vasopressin was unaltered by previous stress. Plasma corticosterone was lowered in vasopressin-treated rats only after previous stress. Sixty minutes after vasopressin infusion, the central amygdala, locus coeruleus, the nucleus of the solitary tract and the dorsal vagal nucleus expressed increased levels of c-fos, and there were significant two-way interactions between stress and infusion for dorsal paraventricular nucleus, locus coeruleus and dorsal vagal nucleus. One-way analysis suggested that previous stress also reduced the c-fos response to vasopressin in the nucleus of the solitary tract. These results show that previous stress causes differential alterations in behavioural, endocrine and cellular responses to vasopressin. Experiment 2: rats were implanted with a transmitter which monitored heart rate and core temperature and a lateral cerebroventricular cannula. For 10 days, either artificial cerebrospinal fluid or 2500 pmol V1a antagonist, [d(CH2)1(5)-O-Me-Tyr2-Arg8]-vasopressin were infused i.c.v. 10 min prior to a 60-min restraint session. On the 11th day, no infusions were carried out, but rats received the usual period of restraint. The vasopressin antagonist was followed by motor responses (freezing, grooming and burrowing), more evident during the third and fifth days of stress. Core temperature responses were altered by the antagonist: stress-induced hypothermia was greatly reduced. Reduced baseline core temperatures, observed in controls as successive stress proceeded, were absent in antagonist-treated rats. By contrast, there were no significant effects of vasopressin antagonism on stress-induced tachycardia, nor in the way that this adapted to repeated restraint. On the 11th day (no i.c.v. infusions), hypothermic responses were no different in rats previously receiving either antagonist or control vehicle, but secondary hyperthermia was greater in the first group. Corticosterone levels were not altered by previous i.c.v. infusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in sensitivity to intracerebral vasopressin and the effects of a V1a receptor antagonist on cellular, autonomic and endocrine responses to repeated stress. 771 81

Soon after birth, mammals are often confronted with the challenges of hypoxia, hypothermia and hypoglycemia. The incidence of the latter in the human population is roughly 2-20% of all live births. We characterized the glucose profile over the first 24 h of postnatal life in a large population of suckling, nonfasted rats. Approximately 63% were hypoglycemic (plasma glucose < 60 mg/dl) during the first 4 h after birth; from 6 to 24 h after birth this number was reduced to 10%. Low glucose levels in the first hours after birth were significantly associated with high plasma glucocorticoid and adrenocorticotropic hormone levels. Glucocorticoid injections 2 h after birth that elevated plasma corticosterone to high physiological levels for 1-2 additional hours significantly increase plasma glucose levels compared to vehicle-injected controls. These results suggest that, like the human newborn, rat pups are susceptible to developing neonatal hypoglycemia with about the same frequency as in babies. Also, the hypothalamic-pituitary-adrenocortical (HPA) axis appears to be active from birth and may be responsive to hypoglycemia stress during this early period (contrary to later neonatal ages when the HPA axis is quiescent in rats). Finally, glucocorticoids appear to prevent the development of hypoglycemia shortly after birth.
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PMID:Twenty-four hour profiles of glucose, corticosterone and adrenocorticotropic hormone during the first postnatal day in rats. 826 May 62

The effects of the selective 5-HT1A receptor agonist flesinoxan on neuroendocrine function, temperature, and behavior were assessed in male healthy volunteers using a double-blind, placebo-controlled crossover design. Flesinoxan (7 and 14 micrograms/kg), administered intravenously in 11 healthy volunteers, elicited a dose-related decrease in body temperature and increases in growth hormone, adrenocorticotropic hormone (ACTH), cortisol, and prolactin plasma levels. In a second independent study, 12 healthy volunteers were pretreated sequentially, at one-week intervals, with either the 5-HT1A antagonist pindolol (30 mg, PO), the nonselective 5-HT1/2 antagonist methysergide (4 mg, PO), or placebo, prior to being administered flesinoxan (1 mg, IV). The growth hormone response to flesinoxan was blocked by pindolol but not by methysergide, whereas the prolactin response was blocked by methysergide but not by pindolol. The ACTH and cortisol responses to flesinoxan were potentiated by methysergide. The flesinoxan-induced hypothermia was attenuated by both methysergide and pindolol, although the latter effects did not reach statistical significance. The present results suggest that the growth hormone response and the hypothermic response to the intravenous infusion of flesinoxan may serve as a valid index of 5-HT1A receptor function in humans.
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PMID:Serotonin1A receptor activation by flesinoxan in humans. Body temperature and neuroendocrine responses. 859 27

Hypothermic and hormonal responses to a challenge with a selective 5-HT1A receptor agonist ipsapirone are considered to provide an index of 5-HT1A receptor function in humans. To examine the effects of divalproex sodium (DVP) on 5-HT1A receptor function in humans, we measured the hypothermic, adrenocorticotropic hormone (ACTH) cortisol, and behavioral responses to ipsapirone in 10 healthy male volunteers. After obtaining a blood sample for baseline hormone levels and measuring body temperature, a single dose of 0.3 mg/kg of ipsapirone was given orally to all the subjects and further bloods and temperature reading were obtained at regular intervals for three hours. The ipsapirone challenge tests were repeated after the subjects had been treated with DVP (1000 mg/day) for one week. The results showed that the hypothermia induced by ipsapirone was significantly attenuated by the DVP treatment, whereas the ACTH/cortisol release and the behavioral responses following ipsapirone challenges were not altered. Our findings suggest that DVP may enhance 5-HT neurotransmission in humans via a subsensitization of 5-HT1A autoreceptors but does not appear to affect postsynaptic 5-HT1A receptors.
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PMID:Effects of divalproex sodium on 5-HT1A receptor function in healthy human males: hypothermic, hormonal, and behavioral responses to ipsapirone. 939 26

In the rat dorsal hippocampus and dorsal raphe nucleus, the microiontophoretic application of ergotamine and 5-HT suppressed the firing activity of CA3 pyramidal neurons and 5-HT neurons, an effect antagonized by selective 5-HT1A receptor antagonists. Co-application of ergotamine prevented the inhibitory action of 5-HT on the firing activity of CA3 pyramidal neurons but not of 5-HT neurons, indicating that ergotamine acted as a partial 5-HT1A receptor agonist in the dorsal hippocampus and as a full agonist at 5-HT1A autoreceptors. Ergotamine decreased, in a concentration-dependent manner, the electrically evoked release of [3H]5-HT in preloaded rat and guinea pig hypothalamus slices; this effect was prevented by the nonselective 5-HT receptor antagonist methiothepin but not by the selective 5-HT1B/1D receptor antagonist GR 127935 or the alpha 2-adrenoceptor antagonist idazoxan. Although body temperature in humans remained unchanged following inhaled ergotamine, in the rat, subcutaneously injected ergotamine produced a hypothermia that was prevented by a pretreatment with the 5-HT1A/1B receptor/beta-adrenoceptor antagonist pindolol. Finally in humans, ergotamine did not alter prolactin or adrenocorticotropic hormone levels, but increased growth hormone level, which was prevented by pindolol. Cortisol level was increased in humans by ergotamine, but this enhancement was unaltered by pindolol. In conclusion, the present results suggest that ergotamine acted in the rat brain as a 5-HT1A receptor agonist and as an agonist of terminal 5-HT autoreceptor of a yet undefined subtype. In humans, ergotamine also displayed some 5-HT1A receptor activity but, probably because of lack of receptor selectivity, it did not present the same profile as other 5-HT1A receptor agonists.
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PMID:Effect of ergotamine on serotonin-mediated responses in the rodent and human brain. 977 59

Obese (f/f) Koletsky rats lack the leptin receptor (LR), whereas their lean (F/?) counterparts bear a fully functional LR. By using f/f and F/? rats, we studied whether the LR is involved in lipopolysaccharide (LPS)-induced fever and hypothermia. The body temperature responses to LPS (10 or 100 microg/kg iv) were measured in Koletsky rats exposed to a thermoneutral (28 degrees C) or cool (22 degrees C) environment. Rats of both genotypes responded to LPS with fever at 28 degrees C and with dose-dependent hypothermia at 22 degrees C. The fever responses of the f/f and F/? rats were identical. The hypothermic response of the f/f rats was markedly prolonged compared with that of the F/? rats. The prolonged hypothermic response to LPS in the f/f rats was accompanied by enhanced NF-kappaB signaling in the hypothalamus and an exaggerated rise in the plasma concentration of tumor necrosis factor (TNF)-alpha. The f/f rats did not respond to LPS with an increase in the plasma concentration of corticosterone or adrenocorticotropic hormone, whereas their F/? counterparts did. The hypothermic response to TNF-alpha (80 microg/kg iv) was markedly prolonged in the f/f rats. These data show that the LR is essential for the recovery from LPS hypothermia. LR-dependent mechanisms of the recovery from LPS hypothermia include activation of the anti-inflammatory hypothalamo-pituitary-adrenal axis, inhibition of both the production and hypothermic action of TNF-alpha, and suppression of inflammatory (via NF-kappaB) signaling in the hypothalamus.
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PMID:A new function of the leptin receptor: mediation of the recovery from lipopolysaccharide-induced hypothermia. 1538 70

We report the case of a 30-year-old woman with severe, prolonged refractory status epilepticus requiring more than 6 months of iatrogenic coma. Opinions on prognosis and clinical management were solicited from a number of experienced neurointensivists and epileptologists at multiple time-points during the clinical course. The ensuing discussion, annotated with references, is presented here. Several experts commented on isolated cases of young patients with encephalitis requiring up to 2-3 months of iatrogenic coma, yet still having good outcomes. Treatments discussed include ketamine, gammaglobulin, plasmapheresis, steroids, adrenocorticotropic hormone, very high-dose phenobarbital, isoflurane, lidocaine, electroconvulsive therapy, ketogenic diet, hypothermia, magnesium, transcranial magnetic stimulation, vagus nerve stimulation, deep brain stimulation, and neurosurgery. The patient eventually suffered a cardiac arrest but was resuscitated as requested by the family. Seizures then stopped, and the patient has remained in a persistent vegetative state since.
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PMID:Literature review, case report, and expert discussion of prolonged refractory status epilepticus. 1649 94

The physiological function of 5-HT(7) receptors is not yet fully determined. This study was designed to characterize the involvement of 5-HT(7) receptor in rat body temperature regulation and in adrenocorticotropic hormone (ACTH) and corticosterone secretion. In the first part of our study, acute administration of SB-269970 (0.1-1 mg/kg, i.p.), a potent and selective 5-HT(7) receptors antagonist, dose-dependently prevented 5-HT(1A/7) receptor agonist 8-OH-DPAT (0.1 mg/kg, s.c.)-induced hypothermia and when the 5-HT(1A) receptor antagonist WAY-100,635 was co-injected with SB-269970, a reduction of the latter hypothermia was obtained in an additive manner. In contrast, 1 mg/kg (i.p.) of SB-269970 failed to prevent 8-OH-DPAT (0.5 mg/kg, s.c.)-induced increase of ACTH and corticosterone plasma levels. In conclusion, the present results unveil an additive effect of both 5-HT(1A) and 5-HT(7) receptors in core body temperature regulation.
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PMID:Effects of the 5-HT7 receptor antagonist SB-269970 on rat hormonal and temperature responses to the 5-HT1A/7 receptor agonist 8-OH-DPAT. 1675 2


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