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

Hypothermia results in diminished voluntary muscle activity, and is frequently used as a means of providing deep anesthesia to ectotherms and some mammals. In ectotherms, however, it is unclear if hypothermia produces true pain insensation. A needle-probe thermometer was used to demonstrate in frogs (Rana pipiens) that local hypothermia (9 degrees C) could be induced by placement of a tourniqueted leg into ice water (6 degrees C) for 10 min in contrast to the contralateral nontourniqueted leg (21.8 degrees C) kept out of ice water. Analgesia was tested by placement of dilutions of acetic acid on the rear leg. Further tests using groups of 10 frogs demonstrated that frogs with local hypothermia tolerated greater concentrations of acetic acid (mean acetic acid test score = 11) than morphine (10 mg/kg)-treated (9.6) or nontreated (5.8) frogs. Additional studies showed that morphine analgesia was blocked with naloxone doses as low as 0.01 mg/kg and hypothermia-induced analgesia at 10 mg/kg. Naltrexone blocked morphine analgesia at dosages as low as 0.01 mg/kg and hypothermia-induced analgesia at 0.10 mg/kg. In summary, this study demonstrates that hypothermia induces significant analgesia in an amphibian, and that this analgesia is partially blocked by naloxone and naltrexone, suggesting that the effect is mediated at least partially by opioid receptors.
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PMID:Evaluation of hypothermia-induced analgesia and influence of opioid antagonists in leopard frogs (Rana pipiens). 1034 May 22

The present study examined the effects of ethanol and naltrexone hydrochloride (a nonselective opiate receptor antagonist) on flash-evoked potentials recorded from both the visual cortex (VC) and the superior colliculus (SC) of chronically implanted hooded rats. There were four treatment conditions administered on separate days: Either saline or naltrexone (10 mg/kg; volume of 1.0 ml/kg) was given 10 min before either saline or ethanol (2.0 g/kg; 20% ethanol solution in a volume of 1.26 ml/100 g). Evoked potentials were recorded 15 min after the intraperitoneal injections were completed. Animals were tested at 23.1 degrees C room temperature. In the VC, ethanol significantly decreased the amplitude of components N1, P3, and N3, whereas it increased the amplitude of P2. Components P1 and N2 were unaffected by ethanol treatment. The SC components P3 and N4 were reduced in amplitude by ethanol, but component P1 was not altered. Latencies of all components in both structures were increased by ethanol. Naltrexone alone did not significantly affect the potentials, nor did naltrexone pretreatment significantly alter the effects of ethanol on the potentials. Naltrexone produced a modest hypothermia of about 0.25 degrees C, whereas ethanol resulted in hypothermia of about 1.0 degrees C. Ethanol, either alone or in combination with naltrexone, significantly reduced body movement during the evoked-potential recording sessions. The results indicate that endogenous opioid systems do not play a major role in the acute effects of ethanol on flash-evoked potentials recorded from primary areas of the visual system.
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PMID:Effects of ethanol on flash-evoked potentials of rats: lack of antagonism by naltrexone. 1166 14

Despite insights into an increasingly significant role for delta opioid receptors in thermoregulation, it is unclear whether delta receptors located in the brain or periphery play the more critical role in body temperature regulation. Moreover, it is not entirely clear which delta receptor phenotype, delta1 or delta2, mediates the hypothermic actions of delta agonists. Because SNC-80 distributes into central and peripheral compartments and produces rapid hypothermia following systemic injection, the nonpeptide delta agonist is particularly useful in discriminating the site of action of delta receptor-mediated hypothermia. To determine the locus and phenotype of delta receptor which mediates SNC-80-induced hypothermia, we injected SNC-80 and phenotype selective delta antagonists to male Sprague-Dawley rats. SNC-80 (10-50 mg/kg, im) evoked hypothermia that peaked 30 min post-injection. Naltrexone (5 mg/kg, sc), an opioid antagonist, or naltrindole (5 mg/kg, sc), a delta antagonist, blocked the hypothermic response to SNC-80 (35 mg/kg, im). The hypothermia caused by SNC-80 (35 mg/kg, im) was blocked by a delta2 antagonist, naltriben (2.5 mg/kg, sc), but was not affected by BNTX (5 and 10 mg/kg, sc), a delta1 antagonist. The administration of naltriben (10 microg/rat, icv) 30 min before SNC-80 (35 mg/kg, im) prevented SNC-80-evoked hypothermia. In contrast, methylnaltrexone (5 mg/kg, sc), a peripherally restricted opioid antagonist, did not affect the hypothermia caused by SNC-80. The present data demonstrate that selective activation of brain delta2 receptors is a major mechanism of SNC-80-evoked hypothermia in rats.
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PMID:Brain delta2 opioid receptors mediate SNC-80-evoked hypothermia in rats. 1593


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