Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interactions of thyrotropin releasing hormone, its metabolites and synthetic analogues with acute and chronic effects of endogenous and exogenous opiates have been described. The endogenous and exogenous opiates are represented by beta-endorphin and morphine, respectively. The pharmacological effects of opiates include analgesia, temperature effects, respiratory depression, catalepsy, locomotor activity, opiate receptor binding, tolerance, and physical dependence. Thyrotropin releasing hormone and related compounds appear to (a) antagonize hypothermia, respiratory depression, locomotor depression and catalepsy but not the analgesia induced by opiates, (b) inhibit the development of tolerance to the analgesic effect but not to the hypothermic effect of opiates, (c) inhibit the development of physical dependence on opiates as evidenced by the inhibition of development of certain withdrawal symptoms, and (d) suppress the abstinence syndrome in opiate dependent rodents. Thyrotropin releasing hormone does not interact with the opiate receptors in the brain. Potential therapeutic applications of thyrotropin releasing hormone and its synthetic analogues in counteracting some of the undesirable effects of opiates are discussed.
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PMID:Interactions of thyrotropin releasing hormone, its metabolites and analogues with endogenous and exogenous opiates. 614 Nov 21

Chlornaltrexamine (beta-CNA) a selective, long-acting irreversible opiate antagonist inhibited the analgesia, hypothermia, hypothermia tolerance and physical dependence produced by delta 9-tetrahydrocannabinol (THC) in rats. The results suggest that there are some common features between cannabis and opiates and some actions of THC may be mediated by opioid related mechanisms in the central nervous system.
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PMID:Antagonism by chlornaltrexamine of some effects of delta 9-tetrahydrocannabinol in rats. 626 44

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 development of ethanol tolerance as a function of daily treatment dosage was examined on two different test systems. Tolerance to the motor-impairment effect of ethanol, as measured by the tilting-plane test, failed to develop after daily administration of 1-3 g/kg, but developed to equal degrees after 4 or 5 g/kg daily. On the other hand, daily treatment with 2, 4 or 6 g/kg all produced significant tolerance to the hypothermic effect, and the extent of tolerance was proportional to the treatment dosage. Twenty-four hours after the termination of ethanol treatment, there was a significant hypothermia in the group treated with 6 g/kg, and at 32 hr hyperthermia occurred in both the 4 and 6 g/kg groups. These results indicate that treatment dosage is an important determinant of the extent of ethanol tolerance and physical dependence, but that the relationship is complex and varies with the test system used.
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PMID:Effect of treatment dose and test system on the development of ethanol tolerance and physical dependence. 654 77

A major goal of pharmacogenetic research on alcoholism remains the identification of some "marker" that could predict the liability of a particular individual for a genetic susceptibility to develop alcoholism. The present paper presents evidence that the severity of withdrawal from physical dependence on ethanol varies widely among inbred strains of mice, and that withdrawal severity is negatively genetically correlated with initial sensitivity and magnitude of tolerance to ethanol hypothermia. These correlations are supported by differences in hypothermic response between replicate lines of mice genetically selected for susceptibility and resistance to ethanol withdrawal seizures. The genetic relationships reported suggest that the effects of ethanol on thermoregulation in mice may offer a predictive marker for susceptibility to ethanol physical dependence.
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PMID:Genetic correlations with ethanol withdrawal severity. 668 10

The ability of chronic ethanol treatment to alter CNS membrane lipids was tested. Adult C57/BL6 mice were given a liquid diet containing ethanol for eight days. This regimen produced strong physical dependence as judged by withdrawal seizures, tremors and concomitant hypothermia. Analyses were performed on cholesterol, total phospholipid content and total phospholipid acyl composition of myelin, crude (P2), light and heavy synaptosomes as well as synaptosomal plasma membranes. Chronic ethanol treatment had no effect on total phospholipid levels nor phospholipid acyl composition in any of the above subcellular fractions. In ethanol dependent mice, significant increases in cholesterol content and cholesterol/phospholipid ratios were observed in synaptosomal plasma membranes.
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PMID:Alterations in brain lipid composition of mice made physically dependent to ethanol. 689 Jun 13

Rats of 30, 45, 60 and 120 days of age, maternally exposed to methadone (5 mg/kg daily) during gestation and/or lactation, were evaluated on a variety of behavioral and physiological parameters related to drug withdrawal. Animals were tested before and after an acute injection of naloxone (10 mg/kg). Prior to naloxone injection, methadone-exposed rats were subnormal in body temperature at 30 days of age, hypoalgesic at 45 days, and weighed less than controls at 60 days. Additionally, and in contrast to control rats, methadone-exposed animals at most ages displayed head shake and wet-dog shake behaviors. After naloxone administration, methadone-exposed rats exhibited an increase in the mean number of head and wet-dog shakes over pre-injection levels. Although control rats injected with naloxone also demonstrated head shakes (at all ages) and wet-dog shakes (at 45 days), these behavior were usually not of the magnitude as noted for methadone-exposed offspring receiving naloxone. Perturbations in body weight and hypothermia during development, along with head shake and wet-dog shake behaviors which were exacerbated following naloxone administration, suggest a protracted state of physical dependence/withdrawal and/or permanent damage as a result of perinatal exposure to methadone.
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PMID:Withdrawal-like symptoms in young and adult rats maternally exposed to methadone. 719 96

1. The effect of naltrexone pellets containing either 10 or 30 mg of naltrexone base on the development of tolerance and physical dependence on morphine was assessed in male Sprague-Dawley rats. Tolerance-dependence on morphine was induced by s.c. implantation of six morphine pellets, each containing 75 mg morphine base for 7 days. 2. Naltrexone pellet implantation blocked the development of tolerance to the analgesic and hyperthermic effects of morphine. Similarly, naltrexone pellet implantation reversed morphine withdrawal-induced body weight loss. The effect of pellets containing 10 and 30 mg naltrexone did not differ. 3. The effect of naltrexone (10 mg) pellet implantation on various signs of naltrexone-precipitated withdrawal such as body weight loss, hypothermia and increases in urinary and fecal output was investigated. Naltrexone pellet implantation did not alter the naltrexone-precipitated withdrawal-induced body weight loss. Concurrent naltrexone pellet implantation blocked the naltrexone-precipitated withdrawal-induced hypothermia, increased fecal and urinary output in morphine-dependent rats. 4. These results indicate that a single pellet of 10 mg of naltrexone can effectively block morphine tolerance and physical dependence in the rat. Such a procedure may be useful in studying biochemical, endocrinological and immunological mechanisms involved in opioid addiction processes.
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PMID:Effects of naltrexone pellet implantation on morphine tolerance and physical dependence in the rat. 802

The function of the central cannabinoid receptor (CB1) was investigated by invalidating its gene. Mutant mice did not respond to cannabinoid drugs, demonstrating the exclusive role of the CB1 receptor in mediating analgesia, reinforcement, hypothermia, hypolocomotion, and hypotension. The acute effects of opiates were unaffected, but the reinforcing properties of morphine and the severity of the withdrawal syndrome were strongly reduced. These observations suggest that the CB1 receptor is involved in the motivational properties of opiates and in the development of physical dependence and extend the concept of an interconnected role of CB1 and opiate receptors in the brain areas mediating addictive behavior.
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PMID:Unresponsiveness to cannabinoids and reduced addictive effects of opiates in CB1 receptor knockout mice. 988 57

The role of metabolic polymorphism in the development of physical dependence to codeine was assessed in cytochrome P450 2D2 (CYP2D2) deficient Dark Agouti and CYP2D2 intact Sprague-Dawley rats by assessment of the severity of naloxone precipitated withdrawal after codeine and morphine administration. Plasma morphine concentrations after codeine were significantly higher (P<0.01) in Sprague-Dawley than in Dark Agouti rats with metabolic ratios of 0.71 +/- 0.27 and 0.07 +/- 0.04, respectively. Withdrawal after codeine resulted in significantly greater hypothermia (3.5-4 degrees C, P<0.0001) in Sprague-Dawley animals compared to the other groups. Body weight loss was similar for all groups ranging from 6.2 +/- 0.4 to 8.2 +/- 0.6 g. When strain and treatment data were combined, a relationship between body temperature and plasma morphine concentration could be described by the inverse Hill equation (r(2)=0.76, EC(50)=556 +/- 121 ng/ml, n=2.9 +/- 1.5). These data indicate that dependence and withdrawal after codeine administration are dependent on its bioconversion to morphine.
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PMID:Precipitated withdrawal following codeine administration is dependent on CYP genotype. 1151 33


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