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

The effects of the atypical antidepressant and serotonin antagonist mianserin on the expression of opiate withdrawal was examined using an acute and a chronic model of morphine dependence. In the first experiment, rats, trained to perform a food-reinforced, autoshaped lever touch response, were injected with naloxone (5 mg/kg) 4 hr after treatment with a single moderate dose of morphine (15 mg/kg). Mianserin (0.25, 1.0 and 2.5 mg/kg) attenuated the naloxone-induced suppression of autoshaped responding. Colonic temperatures were also monitored. Morphine treatment resulted in significant hyperthermia, while precipitation of withdrawal by naloxone produced hypothermia. Mianserin also attenuated the naloxone-induced hypothermia. In the second experiment, rats were implanted s.c. with a single 75-mg morphine or placebo pellet. Withdrawal was precipitated with naloxone (5 mg/kg) 24, 48 and 120 hr post implantation. Mianserin (2.5 mg/kg) blocked or attenuated signs of withdrawal precipitated by naloxone. Naloxone-precipitated weight loss was also attenuated 48 and 120 hr post implantation. At 120 hr post implantation, rats were decapitated 1 hr after the administration of naloxone and trunk blood was collected. Mianserin did not block the naloxone-induced rise in plasma corticosterone levels. Thus, several signs of withdrawal (e.g., behavioral effects, weight loss and hypothermia) seem to involve serotonergic mediation and can be blocked by mianserin, while others (e.g., rise in plasma corticosterone), which may be unaffected by mianserin, may be a reflection of a compensatory response to withdrawal stress, rather than a mediator of maladaptive consequences of withdrawal that are not mediated by serotonin.
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PMID:Mianserin attenuates naloxone-precipitated withdrawal signs in rats acutely or chronically dependent upon morphine. 300 Dec 81

The effect of the opiate antagonists naloxone and MR2266 on ethanol-induced hypothermia and changes in Ca2+-stimulated Mg2+-ATPase activity in brain regions were investigated in the present study. Administration of different doses of ethanol (0.5-2 g/kg, IP) produced a dose-dependent hypothermia. Ca2+/Mg2+-ATPase activity in the hypothalamus was stimulated at 30 min and 2 hr after ethanol (2 g/kg, IP) treatment. In cortex, enzyme activity was inhibited by ethanol at 30 min with no change seen at 2 hr. Naloxone (7.5 mg/kg, SC) at a dose which did not affect body temperature or enzyme activity, partially inhibited ethanol-induced hypothermia and enzyme activity at the earliest time (30 min) but not at 2 hours. The opiate Kappa antagonist MR2266 (5 mg/kg, SC), however, significantly protected against ethanol hypothermia and enzyme activation measured at 30-120 min. This evidence suggests that ethanol-induced hypothermia and subsequent activation changes of Ca2+/Mg2+-ATPase in the hypothalamus may be regulated by opiate Kappa receptors, and that Ca2+ ions play an important role in mediating the effects of ethanol.
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PMID:Ethanol-induced hypothermia in rats: possible involvement of opiate kappa receptors. 301 66

Administration of the opiate U-50,488H (3-20 mg/kg s.c.), a selective kappa receptor agonist, produced a dose-dependent decrease of rectal temperature in rats. This hypothermic effect of U-50,488H was accompanied by an enhanced activity of Ca2+/Mg2+ ATPase in crude synaptosomal (P2) fractions obtained from hypothalamus but not from cortex or cerebellum. Mg2+ ATPase activity in these regions was not altered by U-50,488H (15 mg/kg s.c.). Naloxone (5 mg/kg) partially and MR2266 (5 mg/kg) completely reversed the temperature and enzyme changes. Pretreatment with the calcium channel blockers nimodipine (1 mg/kg s.c.), diltiazem (10 mg/kg s.c.) and verapamil (2.5 mg/kg s.c.) potentiated the hypothermic effect of U-50,488H as well as the stimulation of Ca2+/Mg2+ ATPase in hypothalamus. These observations suggest that kappa agonists may produce opiate receptor mediated hypothermia through changes in intracellular Ca2+ levels in the hypothalamus.
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PMID:Interaction of kappa receptor agonists with Ca2+ channel antagonists in the modulation of hypothermia. 302 38

Subcutaneous administration of the enkephalin analogue FK33-824 (FK) elicited a dose-related decrease in rectal temperature and respiratory rate in male ddY strain mice. Naloxone and 3 days' implantation of morphine pellet decreased the effects of FK, suggesting the involvement of opioid receptors and cross-tolerance with morphine to both effects of FK. A positive correlation was found between the FK-induced decrease in rectal temperature and that in respiratory rate among the 6 strains of inbred mice including BALB/c, C3H, A/J, CBA, C57BL/6 and DBA/2. The degree of hypothermia elicited by FK was different among strains, whereas marginal strain difference was seen in the respiratory depression induced by FK. The strain difference in the FK responses may be due to the difference in the opioid receptor subtypes in the brain.
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PMID:Effects of the enkephalin analogue FK33-824 on rectal temperature and respiratory rate in male mice. 322 53

Continuous cold-water swims (CCWS) and intermittent cold-water swims (ICWS) elicit respective nonopioid and opioid analgesic responses in adult male rats. The present experiment evaluated whether gender differences were observed in naloxone's (14 mg/kg, SC) ability to alter differentially CCWS and ICWS analgesia on the tail-flick and jump tests in age-matched and weight-matched intact rats and in gonadectomized rats. CCWS analgesia was unaffected by naloxone on either test in age-matched males and females. Naloxone significantly reduced ICWS analgesia on the tail-flick (45%) and jump (37%) tests in intact males, but not age-matched females. Naloxone significantly reversed ICWS analgesia in weight-matched males on the tail-flick (1-14 mg/kg, 30-32%) and jump (14 mg/kg, 31%) tests. Naloxone also significantly reduced ICWS analgesia on the tail-flick (32%) and jump (41%) tests in castrated males, but not ovariectomized females. Changes in swim hypothermia could not account for the above effects. These data indicate gender differences in naloxone's differential modulation of swim analgesia, and reflect further differences in pain-inhibitory responses as a function of gender.
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PMID:Gender determinants of opioid mediation of swim analgesia in rats. 341 98

Accumulated evidence suggests that increased endogenous opioid activities may facilitate the onset of hibernation. The present study investigated the change in thermoregulatory responses following ICV infusion of morphine or [D-Ala2]-Met enkephalinamide (EK) in unanesthetized, unrestrained Columbian ground squirrels (Spermophilus columbianus) during its annual hibernation cycle. In the nonhibernating phase, low doses of either morphine (less than 160 micrograms) or EK (less than 400 micrograms) elicited a dose-related hyperthermia and an increase in heat production, whereas a higher dose of opiates caused hypothermia and a decrease in metabolic rate. Naloxone (5 mg/kg, SC) pretreatment reduced or reversed both the hyper- and hypothermic responses to opiates. Lower ambient temperature (5 degrees C) enhanced the hypothermic response and attenuated the hyperthermic response. In the hibernating phase, euthermic ground squirrels exhibited a reduced responsiveness to exogenous opiates: the hyperthermic response to low dose of morphine (10 micrograms) was significantly reduced and hyperthermia, rather than hypothermia was observed at the highest dose of morphine (160 micrograms). The reduced responsiveness to opiates observed during the hibernating phase seems to suggest a reduction in opiate receptor efficacy which is in agreement with the contention that an increase in endogenous opioid activities may be incumbent with the commencement of hibernation.
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PMID:Seasonal difference in thermoregulatory responses to opiates in a mammalian hibernator. 357 72

Dermorphin, administered into the third ventricle of conscious rabbits, induces an increase of the total power density spectrum of the cortex and a decrease of the total power of the hippocampus. The electrocortical pattern is similar to that found with other opiates and reported as specific of mu agonists. Simultaneously the peptide causes respiratory depression, bradycardia and hypothermia. Naloxone (0.5 mg/kg IV) quickly and completely inverts all these effects. The activity of serotoninergic, Gabaergic, catecholaminergic and cholinergic systems does not seem to be required for these dermorphin actions. Thus, the hypothesis that dermorphin acts directly in modifying cerebral electrical activity is put forward.
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PMID:Electroencephalographic and autonomic effects of centrally administered dermorphin in rabbits. 383 58

In this study we have examined the effect and the possible interaction of ICV injection of Leu8phyllolitorin and SC injection of naloxone on thermoregulation in fasted and fed rats at cold (4 degrees C) and ambient (22 degrees C) temperature. Central injection of Leu8phyllolitorin have been shown to produce hypothermia in animals exposed to a cold environment, but not in animals maintained at 22 degrees C. This suggests that the stressful situation of a cold temperature is an important factor in causing peptide hypothermia. Naloxone enhanced the hypothermic effect of Leu8phyllolitorin at 4 degrees C and 22 degrees C both in fasted and in fed rats, reflecting an opiate receptor interaction for this response.
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PMID:The effect of a new amphibian peptide, Leu8phyllolitorin, on thermoregulation in the rat. 383 74

The authors have studied the protection against ischemic damage to rabbit spinal cord by pretreatment with agents that block neuronal activity and directly or indirectly reduce tissue metabolism. Hypothermia, thiopental, magnesium, lidocaine, and naloxone were used to pretreat the spinal cord prior to ischemia. Hypothermia and thiopental provided comparable protection: they each increased the duration of ischemia required to produce neurological deficits in 50% of the animals from 26 to 41 minutes. They also increased from 10 to 30 minutes the time that the postsynaptic waves of the spinal somatosensory evoked potential (SSEP) could be absent and the animal still have neurological recovery. Hypothermia and thiopental, when used together, increased the duration of ischemia required to produce neurological deficits to 57 minutes in 50% of the animals. Naloxone increased the duration of ischemia required to produce neurological deficits to 36 minutes in 50% of the animals, and increased to 20 minutes the time that the postsynaptic waves of the SSEP could be absent and the animal still have neurological recovery. Magnesium pretreatment improved neurological outcome, possibly by improving collateral circulation as the SSEP did not fail completely during aortic occlusion in all animals. Lidocaine was not beneficial, perhaps because of the prolonged hypotension that resulted.
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PMID:Protection against experimental ischemic spinal cord injury. 395 Jul 46

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


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