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

The mechanism of the hypothermia produced in mice by the naturally occurring cannabinoids, delta9-tetrahydrocannabinol, cannabinol, and cannabidiol, was investigated by evaluating the direct effect of these drugs on the oxygen consumption of tissue homogenates and isolated mitochondria. The tissues studied were brain, liver, skeletal muscle, and heart; the mitochondrial preparations were limited to brain and skeletal muscle. The in-vitro studies included a description of the influence of various cannabinoid vehicles containing Tween 80, ethanol, Pluronic F68, and albumin on the oxygen consumption of tissue preparations. Of these vehicles, only albumin was without effect on all tissues. The other vehicles produced diverse responses, including some that were qualitatively different; the data illustrate that the influence of each vehicle on oxygen consumption must be defined for each tissue employed. In spite of the different vehicle effects, delta9-tetrahydrocannabinol generally reduced oxygen consumption of all tissue preparations; however, the vehicles were capable of modifying the dose-effect relationship. The results of all three drugs prepared in Pluronic F68 on brain and skeletal muscle indicated that the cannabinoids generally cause a dose-related depression of oxygen consumption. The findings demonstrate that the cannabinoids can directly decrease oxidative metabolism of tissue and isolated mitochondria and that a marked response occurs in the concentration range of 1 X 10(-5) to 1 X 10(-4) M. Because these concentrations can exist in tissues following the in-vivo administration of delta9-tetrahydrocannabinol, the results suggest that the depressant effect of the cannabinoids on metabolic rate may contribute to the mechanism of the hypothermia produced by the drugs.
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PMID:The influence of delta9-tetrahydrocannabinol, cannabinol and cannabidiol on tissue oxygen consumption. 119 14

These studies were designed to determine several, possibly related, physiological correlates of an acute dose of ethanol. Male rats were injected with 0.5, 1.0, or 2.5 g/kg of ethanol intraperitoneally, and the accumulation of newly synthesized labeled norepinephrine (from 3H-tyrosine) and of labeled norepinephrine metabolites was examined in several brain regions. Ethanol treatment increased labeled norepinephrine and decreased norepinephrine metabolities in the hypothalamus, brain stem plus midbrain, and telencephalon, without altering endogenous norepinephrine levels. A time course, selected on the basis of previous behavioral studies (Jaffe and Pohorecky, submitted manuscript) on the effects of ethanol on central noradrenergic neurons, disclosed that the accumulation of labeled norepinephrine metabolites was higher than that in saline-injected controls from 30-60 minutes after ethanol injection in the brainstem plus midbrain area, while between 5 and 35 minutes levels were lower than those in control animals. Plasma corticosterone levels were highest 30 minutes after saline injection, while in the ethanol group (1 g/kg) steroids were highest 60 minutes after the injection. Body temperature was significantly decreased only by the 2.5 g/kg dose of ethanol; the hypothermia became evident 50 minutes after an injection of this dosage. We conclude that the brief hypermotile stage produced by a 1 g/kg dose of ethanol (Jaffe and Pohorecky, submitted manuscript) is possibly related to the increased synthesis and release of norepinephrine from central noradrenergic neurons.
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PMID:Noradrenergic involvement in the acute effects of ethanol. 119 25

This report updates the bidirectional selective breeding of taste aversion (TA) prone (TAP) and TA resistant (TAR) rat lines from the 8th through the 22nd generations. A palatable saccharin solution and the aversive consequences of a cyclophosphamide injection are the respective conditioned stimulus (CS) and unconditioned stimulus (US) of line development. Nonsibling matings within each of the two extremes of TA conditionability have produced TAP and TAR lines having markedly different TA propensities. As previously reported, the substitution of a rotational (i.e., motion sickness) US for cyclophosphamide during TA conditioning also produced characteristic line differences in conditioned taste aversion acquisition. The present report extends the effective line separating USs to include injections of lithium chloride, emetine hydrochloride, and EtOH. A range of EtOH dose levels produced dose-dependent TAs within TAP rats but failed to induce TAs in TAR rats. Following the conclusion of TA testing, the administration of a hypnotic EtOH dose produced equivalent loss of righting capability and equivalent hypothermia in both TAP and TAR rats. The line differences in EtOH induced TA conditionability therefore do not reflect general line differences in EtOH sensitivity. The lines may be useful within studies of biological bases of TA conditionability and animal analog studies of prevention and treatment of alcohol dependence.
Alcohol Clin Exp Res 1992 Oct
PMID:Continued development and unconditioned stimulus characterization of selectively bred lines of taste aversion prone and resistant rats. 133 25

Alcohol preference and manifestation of alcoholism are thought by many to be associated with serotonin (5-HT) dysfunction in the brain. Thus, experiments were performed to determine the effect of acute and subchronic administration of (+/-) 3,4-methylenedioxymethamphetamine (MDMA), an amphetamine analog that stimulates 5-HT release, on alcohol preference in two strains of alcohol-preferring rats, the Fawn-Hooded (FH) and alcohol-preferring (P) rats. Rats were individually housed and provided free access to a solution of 10% ethanol, food, and water. Ethanol, food, and water intakes were measured daily. After establishing a stable baseline for ethanol and water intake, each rat was injected SC with a dose of 5.0 mg/kg MDMA or an equal volume of saline for 1 or 3 consecutive days. Body temperature was recorded immediately before and 120, 240, and 360 min after MDMA treatment. Ethanol, food, and water intake were measured for the preceding 24 h. Further, to determine the effect of MDMA on alcohol metabolism rats were injected with 5.0 mg/kg MDMA or saline and 15 min later with 2.5 g/kg alcohol. Then, blood alcohol levels were determined at 1, 3, and 5 h after alcohol administration. Our results show that a single administration of 5.0 mg/kg MDMA significantly decreased ethanol intake in both FH and P rats and increased water intake. Subchronic administration of 5.0 mg/kg MDMA for 3 consecutive days significantly attenuated alcohol intake in both strains but only increased water intake in P rats. Administration of MDMA induced hyper- and hypothermia in FH and P rats, respectively. This drug failed to exert any significant effect on the pharmacokinetics of alcohol, indicating a central effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Attenuation of alcohol consumption by MDMA (ecstasy) in two strains of alcohol-preferring rats. 135 75

The present study tested the hypothesis that the attenuation by oxytocin of tolerance to ethanol-induced hypothermia relies upon an impairment of the putative conditioning processes underlying environment-specific tolerance. According to the conditioning model of tolerance, such tolerance occurs because an opposite compensatory response conditioned to ethanol-paired cues attenuates ethanol's effects. Tolerance to ethanol-induced hypothermia was established to a particular environment over 4 days by injecting mice (daily) with oxytocin 2 h before ethanol, outside the colony room. As controls, other mice were injected similarly but following testing in the animal room. We found that oxytocin suppressed the conditioned compensatory response, revealed by injecting saline to every group in the tolerance-associated environment. These results suggest that oxytocin acted, at least partly, via an inhibition of the associative learning processes that facilitate tolerance development.
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PMID:Oxytocin blocks the environmentally conditioned compensatory response present after tolerance to ethanol-induced hypothermia in mice. 136 94

It was shown that intracerebroventricular (icv) administration of 2 micrograms neuropeptide Y (NPY) increased the rectal temperature in rats 2.5 hours postinjection. During 5 days we analysed dynamics of the effect of NPY on alcohol-induced hypothermia in this particular interval. 2 micrograms of NPY were given daily 30 min prior to 25% solution of ethanol (3 g/kg weight rat) intraperitoneal injection. It was found that NPY can prevent the attenuation of alcohol hypothermia on the 3-d and 4-th injection day. It was supposed that the inhibitory effect of NPY on the development of alcohol tolerance may be due to the capacity of NPY to increase food behavior. So it's known that activation of other competitor motivation may inhibit the development of alcoholism.
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PMID:[Effects of neuropeptide Y on rat body temperature in normal conditions and after ethanol administration]. 139 83

The anesthetic potency of many agents, including alcohols, barbiturates and other sedative-hypnotic drugs, is influenced by lipid solubility. Previous studies from our laboratory, however, have demonstrated that genetic factors influence this relationship. We have reported that mouse lines selectively bred for differences in duration of ethanol-induced anesthesia, the long-sleep (LS) and short-sleep (SS) mice, differ in sleep-time response to water-soluble, but not lipid-soluble, sedative-hypnotic drugs. The studies described here sought to determine whether this same relationship exists for the hypothermic response produced by 17 sedative-hypnotic drugs in the LS and SS mice. Dose-response and time course relationships for hypothermic actions were determined and were compared with the dose-related anesthetic effects of the drugs. Hypothermic potencies increased along with lipid solubility for both the LS and SS mouse lines, but the rate of change differed for the two mouse lines. LS mice were more responsive to ethanol and other water-soluble drugs whereas the SS were more responsive to lipid-soluble drugs; significant correlations were obtained between lipid solubility (log P-octanol-water partition coefficient) and relative LS-SS responsiveness to both the hypothermic and hypnotic actions of the 17 test drugs. Thus, both hypnotic and hypothermic actions of sedative-hypnotic drugs are correlated with lipid solubility. Possible explanation for these correlations include greater LS central nervous system sensitivity to water-soluble drugs and LS-SS differences in distribution of lipid-soluble drugs.
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PMID:Lipid solubility of sedative-hypnotic drugs influences hypothermic and hypnotic responses of long-sleep and short-sleep mice. 140 88

C57BL/6J mice were given 5 weeks of voluntary wheel running and then studied for ethanol (EtOH) sensitivity as indicated by EtOH-induced hypothermia and loss of righting response (LORR) after 3.8 g/kg EtOH (20% w/v). Mice were assigned to wheel (free access to a running wheel in the home cage) or no wheel conditions, and wheel counts were monitored by a computer at 5-min intervals around the clock. In Experiment 1, duration of EtOH-induced LORR was assessed as amount of time required for the animal to right itself three times in a 30-s period, and body temperature was assessed by rectal probe. Wheel animals showed significantly shorter LORR and significantly less hypothermia at regaining the righting response than no wheel controls. In Experiment 2, temperature was assessed at 45 and 90 min after EtOH challenge. Baseline temperatures for wheel and no wheel animals did not differ, but wheel animals showed dramatic resistance to EtOH-induced hypothermia at both time points. Together with our earlier work, these results provide evidence that prior exercise can offset the effects of EtOH intoxication in several domains of EtOH sensitivity.
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PMID:Effects of exercise on ethanol-induced hypothermia and loss of righting response in C57BL/6J mice. 140 13

Microinjections of acetylcholine (ACh) and carbachol were made into discrete forebrain loci in goldfish (Carassius auratus) to evaluate the importance of cholinergic mechanisms for behavioral thermoregulation. Injections of 5, 10, 25, and 50 micrograms ACh into the far anterior nucleus preopticus periventricularis (NPP) (R. Peter and V. Gill. J. Comp. Neurol. 159: 69-102, 1975) and immediately adjacent ventral telencephalon led to consistent dose-dependent decrease in selected temperature. No effect was observed following injections of 2 micrograms ACh or 0.7% NaCl. Injections of ACh into a different portion of the ventral telencephalon led to increases in the selected temperature. Lower doses of carbachol (0.5 and 1.0 micrograms) injected into the NPP produced decreases in selected temperature similar to the highest doses of ACh. Injections of ACh into loci other than those mentioned above either had no thermoregulatory effect or had lesser thermoregulatory effects which, in comparison with injections into the most effective sites, were inconsistent and required larger doses to obtain. The site where cholinergic stimulation led to decreases in the selected temperature exactly overlapped the effective site of ethanol hypothermia in the goldfish.
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PMID:Effective loci and roles of acetylcholine in temperature regulation of goldfish. 141 47

This study shows inhibition of the increase in locomotor activity induced by ethanol (2 g/kg i.p.) in mice by a low dose (0.1 mg/kg i.p.) of the non-opioid beta-endorphin fragment ORG 5878 (des-enkephalin-gamma-endorphin). ORG 5878 (0.1 mg/kg i.p.) also significantly antagonised the large increase in electroshock seizure threshold produced by ethanol (1.5 g/kg i.p.). In contrast, the hypothermia induced by ethanol (2 g/kg i.p.) was not altered by ORG 5878 (0.1 mg/kg i.p.). The effects of ORG 5878 showed an abnormal dose-response relationship, in that a high dose (1 mg/kg i.p.) did not significantly suppress any of the behavioural effects of ethanol examined although there was some indication that it attenuated the stimulant action of ethanol. ORG 5878 (0.1, 1 mg/kg i.p.) did not have any intrinsic effects on locomotion, seizure threshold or body temperature in mice. These results are the first demonstration that ORG 5878 may act as an ethanol antagonist in some paradigms.
Alcohol Alcohol 1992 Jul
PMID:Attenuation of the behavioural effects of ethanol in mice by des-enkephalin-gamma-endorphin (ORG 5878). 141 12


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