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

The influence of opiate receptor antagonists: naloxone, naltrexone and diprenorphine, and of an agonist: morphine on ethanol-induced sleep, hypothermia and motor coordination impairment was investigated. Naloxone and naltrexone evidently antagonized the sleep and hypothermia, and improved the motor coordination impaired by ethanol. Naltrexone was the most, and diprenorphine the least potent ethanol antagonist. Morphine potentiated only ethanol-induced sleep, and this effect was opiate dependent (reversible by naloxone). The present results may partially support the hypothesis about participation of opioid system in ethanol action. However, ethanol effects were affected only by high doses of opiate antagonists, exceeding by far the doses antagonizing the morphine effects. Therefore the participation of additional, unspecific mechanisms, in addition to an opiate-mediated one, cannot be excluded.
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PMID:Ethanol-opioid interaction in mice. 609 96

Di-isopropyl phosphofluoridate (DFP, 0.1--1.5 mg/kg, s.c.) produced antinociception in rats as measured by the hot plate test. Naloxone reduced DFP-induced antinociception but did not affect the attenuated locomotor activity or hypothermia produced by DFP. Animals rendered tolerant to the antinociceptive action of morphine failed to exhibit cross tolerance to the antinociceptive action of DFP. Morphine- and DFP-induced antinociceptive states were antagonized by MR 2266 and GPA 1843, the (-)-isomers of 5,9 alpha-Diethyl-2-(3-furylmethyl)-2'-hydroxy-6, 7-benzomorphan and -2-allyl-2'-hydroxy-9 beta-methyl-5-phenyl-6, 7-benzomorphan hydrochloride, respectively; the corresponding (+)-isomers, MR 2267 and GPA 1847, did not antagonize the antinociceptive state produced by DFP or morphine. These results suggest that DFP-induced antinociception may be mediated via the release of endogenous opioids; however, this could occur at sites different from those concerned with morphine tolerance.
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PMID:Di-isopropyl phosphofluoridate-induced antinociception: possible role of endogenous opioids. 624 66

Morphine and delta 9-tetrahydrocannabinol (THC) have been shown to have certain pharmacologic characteristics in common. Among these are antinociception, hypothermia, and the suppression of precipitated abstinence in morphine-dependent rats. In the present study the effects of morphine were compared with the effects of THC and two synthetic cannabinoids, nantradol and nabilone, in both nondependent and morphine-dependent chronic spinal dogs. Single doses of THC, nantradol, and nabilone depressed the flexor and skin twitch reflexes and had a calming effect after intravenous infusion. These effects are similar to those of morphine. Morphine, nantradol, and nabilone, but not THC, depressed rectal temperature. Unlike morphine, however, the cannabinoids produced mydriasis and an increased startle response, and these effects were not antagonized by naltrexone. THC, nantradol, and nabilone suppressed withdrawal abstinence in 40-hour and maximally abstinent morphine-dependent chronic spinal dogs. The results suggest that THC, nantradol, and nabilone share some properties with morphine since they increased the latency of the skin twitch reflex and suppressed withdrawal abstinence. It is doubtful, however, that these actions of the cannabinoids are mediated through opioid receptors since they were not antagonized by naltrexone.
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PMID:A comparison of THC, nantradol, nabilone, and morphine in the chronic spinal dog. 627 35

The present study investigates the results of pretreatment with five prostaglandin (PG) synthetase inhibitors on effects of morphine on body temperature, pupillary diameter, body movement and production of exophthalmos in rat. Hyperthermia, induced by a low dose of morphine, was inhibited in animals pretreated with any of the PG synthetase inhibitors. However, PG synthetase inhibitors had no clear effect on hypothermia induced by higher doses of morphine. The duration of morphine-induced catalepsy was attenuated by pretreatment with the PG synthetase inhibitors in a dose-related manner. The exophthalmos induced by all doses of morphine was either shortened in duration or inhibited by sulindac, paracetamol or ibuprofen. Morphine-induced mydriasis was either attenuated or inhibited by paracetamol, ibuprofen or meclofenamic acid. The results suggest that endogenous PGs play a role in morphine-induced hyperthermia, catalepsy, exophthalmos and mydriasis whereas a physiological role for PGs in morphine-induced hypothermia was not indicated.
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PMID:Effect of prostaglandin synthetase inhibitors on non-analgesic actions of morphine. 640 56

p-Chlorophenylalanine (p-CPA) reduces brain 5-hydroxytryptamine (5-HT) without altering the dopamine and norepinephrine content. Morphine does not influence the 5-HT level, but partly reverses the depletion of 5-HT by p-CPA. Morphine analgesia and toxicity are not affected by p-CPA treatment. p-CPA also has no effect on acute morphine hypothermia, but after chronic treatment of 5-HT-deficient mice the dose--response curve is no longer parallel, which suggests that another mode of morphine hypothermia occurs. p-CPA diminishes morphine-induced running after acute as well as after chronic morphine administration. p-CPA treatment reduces the sensitivity to the naloxone-precipitated withdrawal reaction, but does not affect the development of physical dependence.
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PMID:The influence of p-chlorophenylalanine on different morphine effects. 644 58

The effects of various psychoactive drugs were studied in rats exposed for 45 min in a circularly polarized, pulsed microwave field (2450 MHz; SAR 0.6 W/kg; 2-microseconds pulses, 500 pps). Apomorphine-induced hypothermia and stereotypy were enhanced by irradiation. Amphetamine-induced hyperthermia was attenuated while stereotypy was unaffected. Morphine-induced catalepsy and lethality were enhanced by irradiation at certain dosages of the drug. Since these drugs have different modes of action on central neural mechanisms and the effects of microwaves depend on the particular drug studied, these results show the complex nature of the effect of microwave irradiation on brain functions.
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PMID:Psychoactive-drug response is affected by acute low-level microwave irradiation. 662 72

Previous experiments in our laboratory demonstrated that morphine, at doses which produced pronounced hypothermia in normal rats, not only failed to decrease but instead increased body temperature in thyroxine-treated animals. The present studies were undertaken to further investigate these initial findings. In animals treated chronically with subcutaneous thyroxine, basal body temperatures were elevated and morphine induced only hyperthermia whether given subcutaneously (10 mg/kg) or centrally (30 micrograms) into the anterior hypothalamus. Basal oxygen consumption, which reflects metabolic heat production, was significantly elevated when compared to controls. In response to morphine, control animals showed decreased oxygen consumption while thyroxine-treated animals showed a slight increase. In both groups of animals, changes in core temperatures reflected changes in oxygen consumption. These results indicate that hyperthyroid animals fail to decrease body temperature in response to morphine because they are unable to decrease metabolic heat production. Morphine, acting at central hypothalamic sites, reduces heat production in normal animals, but in thyroxine-treated animals morphine cannot overcome the increased thermogenesis.
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PMID:Thermoregulation in hyperthyroid rats: mechanism underlying the lack of hypothermic response to morphine in hyperthyroid animals. 664 81

Thermoregulatory reactions to warm exposure and naloxone treatment, as well as behavioral reactions to morphine withdrawal, were recorded in morphine tolerant rats after capsaicin pretreatment. Enhanced behavioural reactions to morphine withdrawal were found in capsaicin pretreated rats, although no differences in degree of withdrawal hypothermia were seen. Morphine tolerant rats displayed increased thermal tolerance; this was partially prevented by capsaicin pretreatment. The results provide further evidence concerning the interference of neural mechanisms sensitive to capsaicin and opiates.
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PMID:Morphine tolerance and withdrawal in capsaicin--pretreated rats. 668 33

Intraventricular administration of kainic acid at the dose of 0.1 microgram induces a significant depression of rectal temperature followed rapidly by its slight elevation. Morphine (40.0 mg.kg-1 IP), which by itself elicited biphasic effect on the body temperature of rats--initially hypothermia followed by hyperthermia--slightly increased the kainic acid-induced hypothermia. Kainic acid did not cause any changes in the hyperthermic effect of low doses of morphine (10.0 mg.kg-1). Pretreatment of rats with nalorphine enhanced the kainic acid-induced hypothermia. On the contrary, nalorphine reversed the hypothermic effect produced by morphine at the dose of 40.0 mg.kg-1. The results suggest that morphine and kainic acid-induced hypothermia are not mediated by the influence on the same type of receptors.
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PMID:Effects of morphine and nalorphine on kainic acid-induced hypothermia in rats. 678 14

Morphine and a number of opioid agonists and agonist-antagonists were injected into rats to examine their effects on body temperature after acute systemic administration. Dose- and time-response curves were constructed for each drug alone and in the presence of the antagonist naloxone. Based on these data, the opioids could be subdivided into several groups. The first group, made up of morphine, heroin, l-methadone, etorphine, fentanyl and levorphanol, caused hyperthermia at lower doses and hypothermia at higher ones. Both effects could be blocked by naloxone. A second group, consisting of buprenorphine, nalbuphine and l-pentazocine, produced only a naloxone-sensitive increase in body temperature, whereas the group comprising ethylketazocine, ketazocine, l-cyclazocine and normeperidine caused only a decrease. This fall in temperature was relatively less sensitive to naloxone blockade. Still another group of drugs (meperidine, normorphine and d-pentazocine) had little effect themselves but, in combination with naloxone, induced hypothermia. The fifth group (N-allylnormetazocine, d-cyclazocine, dextrorphan and d-methadone) had no effect whether alone or in the presence of the antagonist. These findings can be explained in terms of a two-receptor model by ascribing distinct thermoregulatory functions to each receptor type.
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PMID:Subclasses of opioids based on body temperature change in rats: acute subcutaneous administration. 684 2


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