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)

Antagonism of the H-2 receptor with cimetidine and other histaminergic receptor antagonists has been used to differentiate nonopioid and opioid forms of footshock analgesia which are mediated by neural mechanisms. Cimetidine reduces nonopioid footshock analgesia while potentiating an opioid form of this analgesia. The present study examined whether cimetidine altered the nonopioid, neurohormonal analgesia induced by either continuous cold-water swims (CCWS: 2 degrees C for 3.5 min) or the opioid analgesia induced by intermittent cold-water swims (ICWS: 2 degrees C, 18 10-sec swims, 18 10-sec recovery periods). Vehicle or cimetidine (10, 50, 100 mg/kg) injections were administered alone or paired with either CCWS or ICWS; tail-flick latencies, jump thresholds and core body temperatures were then measured. Cimetidine (100 mg/kg) significantly potentiated CCWS and ICWS analgesia and hypothermia, while having minimal effects upon basal thresholds. Lower cimetidine doses produced transitory effects on these measures. These data demonstrate dissociations between neural and neurohormonal forms of nonopioid analgesia following cimetidine treatment. The latter effect may be attributed to changes in stress responsiveness or thermoregulation rather than pain inhibition.
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PMID:Potentiation of opioid and nonopioid forms of swim analgesia by cimetidine. 285 66

Prostacyclin (PGI2) administered i.c.v. into the lateral rat brain ventricle in a dose of 1 and 10 micrograms causes hypothermia, catalepsy as well as a mild analgesic effect. Joint administration of PGI2 along with chloropromazine or morphine produces a greater cataleptic effect than that observed after application of neuroleptics and morphine alone. Cimetidine (CMT) (2 g/kg p.o.) administered 60 min before intraventricular PGI2 injection inhibits hypothermic and cataleptogenic action of the investigated prostaglandin. CMT blocks cataleptogenic effect of chloropromazine and morphine as well as the combination of these two substances with PGI2. CMT inhibits the cataleptogenic effect of haloperidol, but it does not block the catalepsy induced by joint administration of haloperidol and PGI2. CMT does not modify the analgesic action of PGI2. The results indicate that H2 receptors take part in some central pharmacological effects of PGI2 in rats.
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PMID:Effect of H2 receptor blockade upon hypothermic, cataleptogenic and antinociceptive action of prostacyclin (PGI)2 administered into the lateral rat brain ventricle. 286 62

Prostacyclin (PGI2) administered icv into the lateral rat brain ventricle in a dose of 1 and 10 micrograms caused hypothermia and catalepsy. Joint administration of PGI2 and chlorpromazine produced a greater cataleptic effect than that observed after the neuroleptic alone. Cimetidine (CMT) 2 g/kg po administered 60 min before PGI2 icv injection inhibited hypothermic and cataleptogenic action of PGI2. CMT blocked the cataleptogenic effect of chlorpromazine as well as combination of it with PGI2. CMT inhibited cataleptogenic effect of haloperidol, but it did not block the catalepsy induced by joint administration of haloperidol and PGI2. PGI2 did not change concentration of noradrenaline and dopamine in different brain areas. The results indicate that H2 receptors take part in some central pharmacological effects of PGI2 in rats.
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PMID:Influence of H2 receptors blockade upon some central effects of prostacyclin in rats. 287 Apr 86

To characterize the transport system of cimetidine, an organic cation, in the blood-cerebrospinal fluid barrier, the accumulation of cimetidine by the isolated rat choroid plexus was examined. Accumulation of cimetidine was against a concentration gradient via a saturable process (Km = 53 microM, Vmax = 12 nmol/ml/min) that was inhibited by sulfhydryl reagents (p-hydroxymercuribenzoate), metabolic inhibitors (KCN and 2,4-dinitrophenol) and hypothermia (Q10 = 4.5), but did not require inward Na+ gradient. Organic cations such as 1N-methylnicotinamide, tetraethylammonium, choline, histamine and creatinine did not affect the accumulation of cimetidine at the concentration of 1 mM. Cimetidine did not affect the accumulation of tetraethylammonium. More lipophilic cations such as quinidine and quinine inhibited not only the accumulation of cimetidine but also that of an organic anion, benzylpenicillin, although the inhibitory mechanisms are not known. One millimolar of organic anions, such as 5-hydroxyindoleacetic acid, p-aminohippuric acid, homovanillic acid, salicylic acid and benzylpenicillin, inhibited the accumulation of cimetidine. Furthermore, the accumulation of organic anions (benzylpenicillin and salicylic acid) showed saturability and was inhibited by cimetidine. Cimetidine and the organic anions thus showed a mutual inhibition. Oligopeptides also inhibited the accumulation of cimetidine. These findings suggested that cimetidine transport in the choroid plexus is via carrier-mediated active transport process, but does not require inward Na+ gradient. This transport is inhibited by several compounds with different properties like oligopeptides, lipophilic cations and organic anions, although the inhibitory mechanism is not known.
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PMID:Transport of cimetidine by the rat choroid plexus in vitro. 379 52

Impromidine, a highly potent histamine H2-receptor agonist, given i.v. at doses of 3.1-62 nmole, induced a dose-dependent hypothermia in the rat with a maximal effect after 15 min. Cimetidine, an H2-receptor antagonist, having no effect when administered alone, antagonized the hypothermic action of impromidine. Two antiserotoninergic agents, p-chlorophenylalanine and metergoline, and chronic treatment with an antidepressant mianserine reduced the impromidine-induced hypothermia. It is suggested that the impromidine-induced hypothermia is an H2-receptor-mediated phenomenon, and the antagonizing effect of mianserine is related to serotonin receptor blocking activity of the drug rather than to its direct H2-receptor antagonism.
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PMID:Impromidine-induced hypothermia in rats: effect of cimetidine and mianserine. 628 72

Cimetidine, a drug in widespread use in the treatment of peptic ulcer disease, is eliminated primarily via urinary excretion. We examined cimetidine transport by rabbit proximal straight tubules perfused in vitro. [3H]Cimetidine in the bath was actively secreted into the tubule lumen. There was a curvilinear relationship between the rate of cimetidine secretion and the concentration of bath cimetidine. Cimetidine secretion was inhibited by hypothermia and ouabain. Quinine, tolazoline, probenecid, phloridzin, creatinine, p-aminohippurate, and cimetidine sulfoxide inhibited cimetidine secretion in a dose-related manner. At low cimetidine concentrations lumen-to-bath transport rates were only 11-18% of bath-to-lumen secretory rates. High performance liquid chromatographic analysis of collected tubular fluid showed a predominance of cimetidine and a small amount of cimetidine sulfoxide in ratios similar to those of the bath. These studies show that cimetidine is actively secreted into the lumen of rabbit proximal straight tubules in vitro. Secretion probably occurs via the organic base and to a lesser extent the acid transport systems.
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PMID:Cimetidine secretion by rabbit renal tubules in vitro. 724 76

Since pretreatment with cimetidine results in the prevention of scald injury on the peritoneo-serosal surface caused by intraperitoneal hyperthermic perfusion (IPHP) for advanced gastric cancer, the diverse influence of IPHP on patients who were either given or not given cimetidine was studied both during and after IPHP treatment. Cimetidine 50 mg/kg was injected intravenously into 12 patients immediately prior to IPHP. There were no statistical background differences between the cimetidine and control groups (those not given cimetidine). The inflow and outflow temperatures of the hyperthermic perfusate in the control and cimetidine groups were 46.1 +/- 0.1 degree C and 44.1 +/- 0.1 degree C and 46.3 +/- 0.1 degree C and 44.2 +/- 0.04 degree C, respectively. Either the pre-IPHP hypothermia or IPHP in the control group resulted in a considerable increase in serum noradrenaline and adrenaline. The intravenous administration of cimetidine led to a stransient but moderate drop in the mean blood pressure as well as a delayed appearance of high concentrations of noradrenaline and adrenaline, induced by high concentrations of circulating histamine released with cimetidine. These results suggest that the sympathetic nervous responses were activated either by hypothermia or hyperthermia. The transient hypotension and delayed increases of both serum catecholamines were attributed to a marked increase in circulating histamine, released with the intravenous cimetidine.
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PMID:Metabolic changes in cimetidine treatment for scald injury on the peritoneo-serosal surface in far-advanced gastric cancer patients treated by intraperitoneal hyperthermic perfusion. 832 32

The effects of histamine antagonists on naloxone-precipitated withdrawal symptoms were studied in morphine-dependent mice. Chlorpheniramine (0.5-10 mg/kg), a H1-blocker, given 1P 30 min before naloxone challenge produced a dose-dependent potentiation of withdrawal body weight loss, burrowing, and hypothermia, but did not influence either jumping or wet-dog shakes. On the other hand, cimetidine (10-100 mg/kg), a H2-blocker, produced dose-dependent potentiation of withdrawal hypothermia and jumping. Cimetidine was without effect on wet-dog shakes, burrowing, and body weight loss. The effect of chlorpheniramine was investigated in mice injected with 6-hydroxydopamine (6-OHDA) intracerebrally to examine whether histamine-mediated effects are some-how linked to noradrenergic pathways. Intracerebral injection of 6-OHDA in 5-day-old mice pups resulted in hyperlocomotion by the end of 30 days before initiation of morphine dependence. Mice pretreated with 6-OHDA developed a higher degree of naloxone-induced withdrawal jumping than nontreated mice. 6-OHDA (50 micrograms) lesions completely blocked the potentiating effect of chlorpheniramine on burrowing, hypothermia, and even reversed the effect on body weight loss. These findings suggest that both histamine H1- and H2-receptors may be involved in the expression of precipitated withdrawal in morphine-dependent mice and histamine receptors function as modulators of noradrenergic neurotransmission.
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PMID:The role of histaminergic-noradrenergic axis in naloxone-induced withdrawal symptoms in mice. 887 37