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

Previously it was found that during the loss of postural support induced by combined administration of haloperidol and morphine, rats became markedly hypothermic. The present work was a more detailed study of this hypothermia. Morphine alone (20 mg/kg) produced a slight hyperthermia (1 degrees C) in female rats and no effect in males. Haloperidol alone (5 mg/kg) elicited a hypothermia of about 3 degrees C in females and no effect in males. The combination of both elicited a greater decrease of temperature (about 5 degrees C) in female rats and, unexpectedly, a decrease of 3 degrees C in males. According to these data, increased endorphinic activity with a concomitant decrease in dopamine in some unidentified regions of the central nervous system causes hypothermia.
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PMID:Sex differences in the effects of haloperidol, morphine, and their combination on colonic temperature in rats. 356 61

In spontaneously hypertensive rats (SHR) a diminished responsiveness for nociceptive stimuli is present, which might be associated with alterations in endogenous opioid peptide and receptor systems. In SHR, normotensive Wistar-Kyoto controls (WKY) and in Wistar rats the effects of acute morphine administration on pain sensitivity and body temperature have been investigated. Morphine potency decreases significantly in the rank order Wistar, SHR, WKY. Concerning body temperature, a low dose (2.5 mg/kg i.p) results in an initial and transient decrease in body temperature in SHR, which is not elicited in Wistar rats and WKY. After higher doses (10 and 20 mg/kg. i.p) in Wistar rats profound hypothermia occurs whilst SHR and WKY show a modest increase in body temperature. These differential effects in the three strains could not be explained by altered morphine concentrations in subcortical brain tissue.
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PMID:Differential sensitivity to morphine in spontaneously hypertensive and normotensive Wistar-Kyoto and Wistar rats. 362 33

delta 8-Tetrahydrocannabinol (THC)- and 8 beta, 9 beta-epoxyhexahydrocannabinol (EHHC)-tolerant mice were tolerant to the hypothermia produced by morphine while 8 alpha, 9 alpha-EHHC-tolerant mice were not. Morphine-tolerant mice acquired partial tolerance to the hypothermic effect of 8 alpha,9 alpha-EHHC, but not to the effect of delta 8-THC and 8 beta,9 beta-EHHC. Cataleptogenic effects of all cannabinoids were enhanced in morphine-tolerant mice as compared to non-tolerant animals. It seems that morphine-tolerant mice exhibited hypersensitivity to the cataleptogenic effect of the cannabinoids without potentiation of the hypothermia. These results suggest that the morphine-tolerant mouse may acquire 'latent' cross-tolerance to the hypothermic effect of the cannabinoids.
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PMID:Change in hypothermia and catalepsy induced by cannabinoids or morphine in mice tolerant to these substances. 366 37

Morphine administration (20 mg/kg s.c.) slowed renal elimination of phenol red in mice, raising plasma levels of this dye and reducing its levels in urine. After 9 days of twice daily morphine injections up to 100 mg/kg, an acute 20 mg/kg morphine challenge did not produce analgesia or hypothermia as in naive mice. This multiple dose morphine regimen also induced tolerance to the effects of the narcotic on plasma and urine levels of phenol red. Morphine, 20 mg/kg, reduced plasma p-aminohippurate clearance by 72% in naive mice but only by 56% in tolerant mice. However, reduction of iothalamate clearance after an acute morphine challenge did not show a statistically significant difference between naive and tolerant mice. These findings suggest that tolerance is more readily induced to the effects of narcotic on renal blood flow and/or tubular function than to reduction of glomerular filtration. Tolerance to the acute effects of morphine on phenol red disposition is probably due to lessened response of blood flow or tubular function in chronically dosed mice.
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PMID:Tolerance to morphine effects on renal disposition of xenobiotics in mice. 377 98

Morphine administration acutely reduced plasma clearance of sulfobromophthalein (BSP) in mice and increased hepatic retention of this dye. Increasing morphine doses from 5 to 40 mg/kg s.c. progressively raised plasma and liver BSP levels. Morphine-treated mice, warmed to reverse hypothermia, still had higher plasma and liver BSP levels. The narcotic also raised plasma levels of two dyes which are not conjugated, indocyanine green and dibromosulfophthalein. Naloxone reversed morphine-induced elevation of plasma BSP levels. In bile duct-ligated mice, plasma BSP levels were very high but hepatic BSP levels remained low, both after saline or morphine. Thus, the effects of morphine on BSP disposition differed from those of biliary occlusion. BSP content in bile was reduced by morphine, as dye levels were raised in plasma and hepatic parenchyma. In bile duct-cannulated mice morphine increased BSP levels in plasma and liver whereas reducing the amount of dye eliminated in bile.
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PMID:Opioid effects on hepatic disposition of dyes in mice. 397 20

Morphine (M) was administered in different doses intraperitoneally (i.p.) or 50 micrograms intraventriculary (i.c.v.) to restrained and unrestrained guinea-pigs. The systemic administration of M induces a fall in body temperature which is more evident in restrained than in unrestrained guinea-pig. The intraventriculary administration of M produces a fall in body temperature in unrestrained animals, however no significant hypothermic effect was observed in restrained guinea-pig. Dexamethasone antagonized the hypothermic effect observed after the highest dose of M given i.p. The hypothermia observed after the highest dose of M was antagonized by naloxone in all conditions. These findings reemphasize the importance of restraint in determinating the action of M on body temperature and suggest that this effect probably results from stress-related hormone release from the anterior pituitary.
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PMID:Effects of morphine and their antagonism by dexamethasone on body temperature in restrained and unrestrained guinea-pigs. 401 54

Unanesthetized rats, made physically dependent over 5 days by chronic intra-arterial infusion of increasing concentrations of morphine (35-100 mg/kg/day) underwent withdrawal by naloxone (6 micrograms) injection into either the lateral ventricle (i.c.v.), fourth ventricle (V4), intrathecal subarachnoid space (i.t.), or intra-arterially (i.a.) and were evaluated for cardiovascular and behavioral signs of precipitated abstinence. Naloxone i.c.v. produced a significantly greater increase in the magnitude and duration of withdrawal hypertension than did V4 injection. Naloxone i.t. produced a distinctively different, persistent, pressor response as compared to i.c.v., V4 or i.a. routes of administration, although no quantitative differences in behavioral signs of withdrawal were observed. Morphine-dependent, spinal transected (C1) animals generated an augmented pressor response to i.c.v. or i.t. naloxone. This pressor response was accompanied by a significant reduction in core temperature (0.50-0.79 degrees C). Both the naloxone-induced pressor and hypothermic responses were abolished by ganglionic (hexamethonium, 100 mg/kg, i.a.) or peripheral alpha-adrenergic (phentolamine 4 mg/kg, i.a.) blockade. The hypertensive and hypothermic effects of naloxone also were prevented in transected dependent rats by prior spinal pithing. We conclude that in morphine-dependent rats: supraspinal sites rostral to the V4 mediate a more intense naloxone-induced pressor response than caudal regions; cardiovascular and behavioral signs of withdrawal can be precipitated via the spinal cord of intact animals; and the production of withdrawal hypertension and hypothermia in spinal transected morphine-dependent rats indicates that these abstinence signs can be mediated through neuronal pathways within the spinal cord.
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PMID:Supraspinal and spinal mediation of naloxone-induced morphine withdrawal in rats. 403 93

The effects of morphine on body temperature were studied in rats in two different states - stressed and non-stressed. Morphine injected subcutaneously (s.c.) produced a dual action on body temperature in non-stressed rats. Hyperthermia occurred at lower doses (2.5-10 mg/kg) while hypothermia was produced with a higher dose (20 mg/kg). Both of these effects of morphine were reversed by naloxone (0.1-5.0 mg/kg). Stressing the rats (immobilization with wire mesh) produced slight hypothermia which was markedly potentiated by morphine (5-20 mg/kg) in a dose-dependent manner. Enhancement of hypothermia by morphine in the stressed animals was antagonized by pretreatment with naloxone (0.1-5.0 mg/kg). When rats were treated with morphine (10 mg/kg) 1 h before stress, and were then exposed to immobilization stress, the hyperthermia exhibited in the non-stressed state changed to hypothermia in the stressed state. When the rats which were treated with morphine and then stressed for 1 h were released from stress, the hypothermia observed in the stressed state progressively changed to hyperthermia. Furthermore, these morphine effects, i.e. hyper- and hypothermia in the non-stressed and stressed states, respectively, were reversed but not eliminated by naloxone. These results suggest that the effects of morphine on core temperature in rats are altered depending upon the state of the animals. That is, morphine appears to have a dual action, hyperthermia in the non-stressed state and hypothermia in the stressed state. It also appears that these actions are mediated via opiate receptors.
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PMID:Differential effects of morphine on core temperature in stressed and non-stressed rats. 404 Apr 69

Morphine injected intraseptally in the amounts of 35 and 70 nmol prolonged pentobarbital-induced narcosis in the rat. Pentobarbital-induced hypothermia was also potentiated by intraseptal injection of 70 nmol of morphine. These effects were antagonized when morphine was injected together with naltrexone (29 nmol). Naltrexone injected by itself into the septum did not significantly affect pentobarbital-narcosis and hypothermia. It is concluded that activation of mu opioid receptors in the septal region could affect the actions of pentobarbital.
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PMID:Intraseptal morphine potentiates pentobarbital narcosis and hypothermia in the rat. 407 Mar 26

Morphine 50 mg/kg i.p. produced a hypothermic effect in unrestrained guinea-pigs and this effect was potentiated when animals were restrained. The morphine-induced hypothermia was antagonized by dexamethasone treatment (1 mg/kg 24 hr and 0.5 mg/kg i.p. 2 hr before morphine). Treatment with the inhibitor of peptide biosynthesis cycloheximide (10 mg/kg i.p. 24 and 2 hr before morphine) also inhibited the hypothermic effect of morphine. ACTH injected intracerebroventricular produced no changes in body temperature. These results are consistent with the hypothesis that anterior pituitary peptide beta-endorphin may play a role in the hypothermic effect produced by morphine in the guinea-pig.
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PMID:Possible mechanisms implicated on the hypothermic effect induced by morphine in guinea-pig. 609 6


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