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)

Labetalol, an alpha- and beta- adrenoceptor antagonist was investigated for its central nervous system effects in rats and mice. A marked reduction in the spontaneous motor activity with no concomittant muscle weakness was produced. The drug caused closure of eyelids in rats. Labetalol caused hypothermia and prolonged the pentobarbitone-induced hyposis. In animals trained for conditioned avoidance response the drug blocked the SCR in all the animals and CAR in a few number of animals. The drug did not protect the animals against electroshock convulsions. From the results it appears that labetalol is a central nervous system depressant.
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PMID:Neuropharmacological actions of labetalol. 43 73

Rats pretreated daily with delta9-tetrahydrocannabinol (delta9-THC, 8 mg/kg) during 14 days showed tolerance to THC-induced hypothermia and depression of CAR acquisition in a shuttle-box. The noncontingent exposure of THC also produced tolerance to spontaneous (unlearned) behaviors as measured in a open-field test. The data suggest no essential role for learned tolerance in the sense that animals have to to learn to perform under the influence of THC for several of these behaviors.
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PMID:delta9-Tetrahydrocannabinol: tolerance after noncontingent exposure in rats. 63 25

Since nitric oxide (NO) has been implicated in nociceptive processing, the present study examined whether NO synthase inhibition with either Nw-nitro-L-arginine (L-NA) or its methyl ester (L-NAME) would alter antinociception elicited by either continuous (CCWS) or intermittent cold-water swims (ICWS) on the tail-flick and jump tests. Whereas CCWS antinociception on both tests was significantly potentiated by a dose range of L-NA (0.1-4 mg/kg IP) and L-NAME (1 mg/kg IP), ICWS antinociception was largely unaffected by these manipulations. In contrast, administration of the less active D isomer (D-NAME) failed to alter CCWS antinociception and reduced ICWS antinociception. The ability of NO synthase inhibition to potentiate CCWS antinociception could not be explained by changes in CCWS hypothermia. Since ICWS antinociception is mediated by mu-opioid manipulations and CCWS antinociception is sensitive to delta-opioid and nonopioid manipulations, this indicates that NO synthase inhibition may be acting upon a selective form of pain inhibition.
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PMID:Nitric oxide synthase inhibition selectively potentiates swim stress antinociception in rats. 751 79

The labile gas nitric oxide (NO) mediates a wide variety of thermoregulatory processes including vasomotor control, brown fat thermogenesis, and neuroendocrine regulation. Additionally, during endotoxemia, NO modulates the release of cytokines and hypothalamic peptides. To determine the role of NO in thermoregulation and fever, we intravenously injected the NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and measured its effects on body temperature during normal thermoregulation and endotoxemia in awake, unrestrained rats. L-NAME produced a stereoselective, dose-dependent hypothermia that lasted up to 4 h after bolus intravenous injection. Intravenous lipopolysaccharide (LPS) produced fever in a dose-dependent manner, which was preceded by hypothermia at higher doses alpha-LPS. NOS inhibition reduced the febrile response to LPS and produced marked hypothermia with a low dose of LPS. These findings indicate that NO may play an important role in thermoregulation and suggest that NO is required for the production of fever.
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PMID:Inhibition of nitric oxide synthase produces hypothermia and depresses lipopolysaccharide fever. 877 Jan 31

This study was undertaken to examine the possible role of nitric oxide (NO) on brown adipose tissue (BAT) thermogenesis in rats. The chronic administration of N omega-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) in drinking water given to rats decreased interscapular BAT (IBAT) weight as well as DNA content in a warm environment (25 +/- 1 degrees C; 2 and 4 weeks), and inhibited the cold-stimulated (5 +/- 1 degrees C; 2 weeks) increase in IBAT weight and DNA content. L-Arginine administration (4 weeks in a warm environment) increased the DNA content of IBAT. Chronic L-NAME administration (2 weeks in a warm environment) eliminated the NE-stimulated increase in in vivo oxygen consumption (VO2), caused hypothermia in acute cold exposure (0 degree C), and suppressed the NE-stimulated increase in in vitro IBAT VO2. In vitro incubation of native IBAT with L-NAME suppressed the basal and NE-stimulated increase in in vitro VO2. In vitro incubation of IBAT with methylene blue (soluble guanylate cyclase inhibitor and a scavenger of free NO) eliminated the NE-stimulated increase in in vitro IBAT VO2. These results suggest that the nitric oxide and NO-cGMP signaling systems are involved in the regulation of BAT cellularity and thermogenesis in rats.
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PMID:Effects of acute and chronic inhibition of nitric oxide synthase on brown adipose tissue thermogenesis. 904 15

Hypothermia is a response to hypoxia that occurs in organisms ranging from protozoans to mammals, but very little is known about the mechanisms involved. Recently, the NO pathway has been suggested to be involved in thermoregulation. In the present study, we assessed the participation of nitric oxide in hypoxia-induced hypothermia by means of NO synthase inhibition using NG-nitro-L-arginine methyl ester (L-NAME). The rectal temperature of awake, unrestrained rats was measured before and after hypoxia or L-NAME injection or both treatments together. Control animals received saline injections of the same volume. We observed a significant (P < 0.05) reduction in body temperature of 1.32 +/- 0.36 degrees C after hypoxia (7% inspired O2) and of 0.96 +/- 0.42 degree C after L-NAME (30 mg/kg body wt) injected intravenously. When the two treatments were combined, no significant difference in body temperature was observed. To assess the role of central thermo-regulatory mechanisms, a smaller dose of L-NAME (1 mg/kg) was injected into the third cerebral ventricle or intravenously. Intracerebroventricular injection of L-NAME caused an increase in body temperature, but when L-NAME was combined with hypoxia (7% inspired O2) no change in body temperature was observed. Intravenous injection of 1 mg/kg L-NAME had no effect. The data indicate that NO plays a major role in hypoxia-induced hypothermia at central rather than peripheral sites.
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PMID:Role of the nitric oxide pathway in hypoxia-induced hypothermia of rats. 932 75

The role of nitric oxide (NO) in the development of cannabinoid tolerance was examined by using N(omega)-nitro-L-arginine methyl ester (L-NAME) as an inhibitor of NO synthase. R(+)-[2,3-Dihydro-5-methyl-3 [(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl]-(1-napht halenyl)methanone mesylate (WIN 55,212-2), a cannabinoid receptor agonist, or L-NAME plus WIN 55,212-2 was acutely or chronically injected i.p. to mice and analgesia, body temperature and immobility were measured. A single injection of WIN 55,212-2 induced time- and dose-dependent analgesia, hypothermia and catalepsy. L-NAME (50 mg/kg), which per se was ineffective, administered 20 min before WIN 55,212-2 did not modify the analgesic, hypothermic and cataleptic responses to the cannabinoid. When WIN 55,212-2 was administered once a day, the animals became completely tolerant to the analgesic, hypothermic and cataleptic effects within five, seven and nine days respectively. L-NAME injected once daily 20 min before WIN 55,212-2 inhibited the development of tolerance to the hypothermic and cataleptic actions but not to the analgesic action of WIN 55,212-2. Since L-NAME given chronically by itself did not modify the analgesia, hypothermia and catalepsy induced by acute administration of WIN 55,212-2, our findings suggest L-NAME acts with some selectivity on the mechanisms involved in cannabinoid tolerance.
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PMID:A role of nitric oxide in WIN 55,212-2 tolerance in mice. 957 Apr 63

The striatum is rich in nitric oxide synthase (NOS). It is present in a dense fiber network and in a few medium-sized non-spiny interneurons. Previous work showed chronic overexpression of NOS in the rat striatum after a severe perinatal asphyctic (SPA) insult. This was prevented by hypothermia. We investigated whether the overexpression of NOS was accompanied by increased NOS activity. As nitric oxide (NO) is a potent activator of the soluble isoform of guanylyl cyclase, we measured striatal 3',5'-cyclic monophosphate (cyclic GMP) synthesis in 10-day-old (P10) rat pups that were subjected to SPA during normothermia or hypothermia during or after the insult. Cyclic GMP levels in striatal tissue from control pups were approximately 25.8 pmol/mg protein and in the SPA group approximately 38.1 pmol/mg protein (p<0.01). Hypothermia, during as well as after insult, prevented this increase of cyclic GMP. Nomega-nitro-L-arginine (L-NAME) (0.1 mM) decreased cyclic GMP levels in control, SPA and hypothermia treated pups to similar low levels (approximately 8% of level without L-NAME). Sodium nitroprusside (SNP) stimulated cyclic GMP showed no differences between the four groups. This indicates that high cyclic GMP levels in the striatum of rats subjected to SPA are caused by increased NOS activity. Hypothermia after an asphyctic insult could be a promising treatment.
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PMID:Hypothermia during or after severe perinatal asphyxia prevents increase in cyclic GMP-related nitric oxide levels in the newborn rat striatum. 959 57

This study was performed to examine the roles of body temperature, NMDA receptors and nitric oxide (NO) synthase in post-ischemic retinal injury in rats. Cell loss in the ganglion cell layer and thinning of the inner plexiform layer were observed 7 days after ischemia. Cell loss in the ganglion cell layer but not thinning of the inner plexiform layer was reduced by hypothermia during ischemia. Intravenous injection of dizocilpine (MK-801) or Nomega-nitro-L-arginine methyl ester (L-NAME) prior to ischemia ameliorated retinal injury. These results suggest that activation of NO synthase following NMDA receptor stimulation is involved in ischemia-induced retinal injury.
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PMID:Inhibition of NMDA receptors and nitric oxide synthase reduces ischemic injury of the retina. 968 14

It has been reported that arginine vasopressin (AVP) plays a thermoregulatory action, but very little is known about the mechanisms involved. In the present study, we tested the hypothesis that nitric oxide (NO) plays a role in systemic AVP-induced hypothermia. Rectal temperature was measured before and after AVP, AVP blocker, or NG-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) injection. Control animals received saline injections of the same volume. The basal body temperature (Tb) measured in control animals was 36.53 +/- 0.08 degreesC. We observed a significant (P < 0.05) reduction in Tb to 35.44 +/- 0.19 degreesC after intravenous injection of AVP (2 micrograms/kg) and to 35.74 +/- 0. 10 degreesC after intravenous injection of L-NAME (30 mg/kg). The systemic injection of the AVP blocker [beta-mercapto-beta, beta-cyclopentamethylenepropionyl1,O-Et-Tyr2,Val4,Arg8]vasopressin (10 micrograms/kg) caused a significant increase in Tb to 37.33 +/- 0.23 degreesC, indicating that AVP plays a tonic role by reducing Tb. When the treatments with AVP and L-NAME were combined, systemically injected L-NAME blunted AVP-induced hypothermia. To assess the role of central thermoregulatory mechanisms, a smaller dose of L-NAME (1 mg/kg) was injected into the third cerebral ventricle. Intracerebroventricular injection of L-NAME caused an increase in Tb, but when intracerebroventricular L-NAME was combined with systemic AVP injection (2 micrograms/kg), no change in Tb was observed. The data indicate that central NO plays a major role mediating systemic AVP-induced hypothermia.
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PMID:Role of nitric oxide in systemic vasopressin-induced hypothermia. 975 20


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