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)

When given a two-bottle choice between gradually increasing morphine concentrations (in 0.2% saccharin) and plain tap water, C57BL/6J mice consumed almost 90% of their daily fluid intake from the morphine-saccharin bottle, while the DBA/2J strain, in contrast, consumed 13% or less from the morphine-saccharin solution. The C57BL/6J strain consistently consumed mean daily doses of morphine sulfate in excess of 200 mg/kg, which was sufficient to induce an easily discernable withdrawal syndrome upon removal of the morphine solution, either with or without naloxone challenge. Hypothermia, tremor, wet dog shakes, jumping, and diarrhea were prominent withdrawal signs. In separate experiments, the saccharin was removed from the morphine-containing bottle, yet the C57BL/6J mice continued to prefer the morphine solution over tap water. In complete contrast to the above, mice of the DBA/2J strain rejected the morphine-saccharin solution at the lowest concentration employed, and at no time did their mean daily morphine dose exceed 20 mg/kg. Thus, morphine-saccharin preference is strongly genetically determined, and a high degree of physical dependence can result in the morphine-preferring strain. Palatability differences appear not to be the predominant explanation for these differences in morphine-saccharin consumption.
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PMID:Physical dependence induced by the voluntary consumption of morphine in inbred mice. 232 Jun 38

Cultured Chinese hamster V79 fibroblast cells at the transition from logarithmic to stationary growth have been shown to undergo apoptosis (programmed cell death) after cold shock [B. L. Soloff, W. A. Nagle, A. J. Moss, Jr., K. J. Henle, and J. T. Crawford, Biochem. Biophys. Res. Commun. 145, 876-883 (1987)]. In this report, we show that about 95% of the cell population was susceptible to cold-induced apoptosis, and the amount of cell killing was dependent on the duration of hypothermia. Cells treated for 0-90 min at 0 degrees C exhibited an exponential survival curve with a D0 of 32 min; thus, even short exposures to the cold (e.g., 5 min) produced measurable cell killing. The cold-induced injury was not produced by freezing, because similar results were observed at 6 degrees C, and cell killing was not influenced by the cryoprotective agent dimethyl sulfoxide. Cold-induced apoptosis was inhibited by rewarming at 23 degrees C, compared to 37 degrees C, by inhibitors of macromolecular synthesis, such as cycloheximide, and by 0.8 mM zinc sulfate. The results suggest that apoptosis represents a new manifestation of cell injury after brief exposure to 0-6 degrees C hypothermia.
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PMID:Cultured Chinese hamster cells undergo apoptosis after exposure to cold but nonfreezing temperatures. 239 28

The effects of morphine sulfate on rectal temperature and on Ca++-stimulated Mg++ATPase activity in crude synaptosomal fraction (P2) of cortex, hypothalamus and cerebellum were investigated in rat. Morphine (3-15 mg/kg, SC) produced hyperthermia at 30-120 min after the drug administration. The Ca++/Mg++ ATPase activity in hypothalamus and cortex was decreased while there was no change in Mg++ ATPase activity. The enzyme activity in cerebellum was not affected. The opiate antagonist naloxone hydrochloride (5 mg/kg, SC) antagonized the effect of morphine on rectal temperature and Ca++/Mg++ ATPase activity. The effects of different calcium channel antagonists (nimodipine 1 mg/kg, verapamil 2.5 mg/kg and diltiazem 10 mg/kg, SC) on the changes induced by morphine were also investigated. These antagonists not only antagonized morphine hyperthermia, but also the inhibitory effect of morphine on Ca++/Mg++ ATPase activity in hypothalamus. The calcium channel agonist BAY K8644 (3 mg/kg, SC) produced hypothermia and also stimulation of Ca++/Mg++ ATPase activity in hypothalamus. Naloxone failed to alter these effects of BAY K8644. These studies demonstrate that Ca++ transport in hypothalamus, as indicated by Ca++/Mg++ ATPase activity, plays an important role in thermoregulation and thermoregulatory changes induced by opiates.
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PMID:Opiate receptor mediated hyperthermic responses in rat following Ca++ channel antagonists. 243 Mar 6

The effect of a variety of morphine doses on thermoregulatory effector systems was examined in ambient temperatures of 27.0 degrees C and 4.0 degrees C. Rats were given saline or morphine sulfate (5, 15, or 25 mg/kg); their core temperature, oxygen consumption, and activity were monitored for 4 or 6 h post-injection. The results suggest two distinct actions of morphine, possibly mediated by two opiate receptors. Low doses of morphine produce hyperthermia that is the result of a direct activation of activity and whole body heat production. High doses produce effects dependent on ambient temperature: hypermetabolism and hyperthermia in the 27.0 degrees C environment; hypometabolism, vasodilation, and hypothermia in the 4.0 degrees C environment. The findings suggest limitations in current set-point theories of morphine's thermic actions.
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PMID:Effects of dose on effector mechanisms in morphine-induced hyperthermia and poikilothermia. 250 98

A simple method allows rewarming severe accidental hypothermia patients by an extra-corporal veno-venous circuit. Blood is removed from the femoral vein and brought to infusion pump accelerator which sends it through a blood-rewarmer before reinjecting it into the terminal jugular or sub-clavian vein. This allows the heart to be rewarmed preferentially. The blood is heparinized upon entering the circuit and later neutralized with protamine sulfate upon leaving it. Five severely hypothermic patients (average temperature: 26.5 degrees C) were treated using this technique. Rapid improvement was obtained with disappearance of cardiovascular shock within one hour. Rectal temperature increased by 1.84 degrees C.h-1 and became normal in 6 hours. No complications were encountered. Particularly, there were no incidents of shock due to rapid rewarming and no secondary biological disturbances observed imputable to the extra-corporal circuit. It should be emphasized that the equipment used is readily available in most Emergency and Intensive Care Units.
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PMID:[Treatment of severe accidental hypothermia with a simple extracorporeal circuit]. 262 4

The mechanism of sodium fluoride (NaF) induced hypothermia was investigated on relations between the monoamine synthesis and metabolism in the rabbit brain. Five male rabbits per a group, weighing about 2.5kg and having rectal temperatures of 38.4 to 39.3 degrees C, were used in this experiment. The rectal temperature measurements were made by means of an electric thermometer for 5 hours at intervals of 15 or 30 minutes. Through this experiment, animals were housed in a room kept at 22 to 23 degrees C. The following drugs were used in this experiment: NaF (40 mg/kg i.v.), barbital sodium (0.1 g/kg s.c.), hexamethonium bromide (C6, 10 mg/kg i.v.), ergotamine tartrate (30 mg/kg s.c.), phenoxybenzamine hydrochloride (15 mg/kg i.v.), propranolol hydrochloride (5 mg/kg s.c.), pindolol (0.3 mg/kg s.c.), atropine sulfate (30 mg/kg s.c.), 2, 4-dinitrophenol (DNP, 20 mg/kg i.v.), l-DOPA (20 mg/kg i.v.), 5-HTP (20 mg/kg i.v.) Results 1. Intravenous injection of 30 mg/kg of NaF induced a drop of 0.66 degrees C in rectal temperature. 2. Pretreatment with 0.1 mg/kg of barbital sodium or 10 mg/kg of C6 prominently inhibited the NaF-induced hypothermia. 3. The alpha-blockade caused by ergotamine tartrate and phenoxybenzamine or the beta blockade by propranolol hydrochloride and pindolol resulted in an approximate 50% inhibition of maximum drop in body temperature induced by NaF administration. Both alpha- and beta-blockades caused by ergotamine tartrate and propranolol or by phenoxybenzamine and pindolol, however, made a remarkable inhibition of the NaF effect. Cholinergic blockade brought on by atropine sulfate, on the other hand, had no effect against NaF-induced hypothermia. 4. Bilateral splanchnicotomy completely inhibited drops in rectal temperature. 5. Intravenous injection of NaF 40 mg/kg failed to counteract the rise of rectal temperature caused by DNP 20 mg/kg. 6. Pretreatment with l-DOPA made a prominent inhibition of NaF-induced hypothermia. The inhibiting effects of 5-HTP, however, were slight. 7. Administration of NaF made a significant decrease in norepinephrine levels in the rabbit hypothalamus, but had no effect on 5-HT levels.
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PMID:[The rabbit thermo-regulatory system. Effects of high dose of sodium fluoride]. 262 92

We studied the effects of two ovarian steroid treatments that induce proestrous-like surges in LH secretion on responsiveness to morphine sulfate (MS), as measured by induced hypothermic, antinociceptive, behavioral, and LH secretory changes. Ovariectomized rats received no steroids (OVX), 7.5 micrograms estradiol benzoate 2 days before the experiment (EB), or EB and then 5 mg progesterone 48 h later (EBP). MS administration coincided with the steroid-induced LH hypersecretion that occurs in the EB and EBP rats at 1530-1630 h. Serum LH concentrations were determined 30 min after administration of MS. In OVX and EB rats, MS caused a dose-dependent decrease in serum LH, but even 20 mg/kg MS did not alter serum LH during the EBP-induced LH surge. Brain-mediated morphine-induced analgesia was evaluated in the three steroid treatment groups from measurement of latency to pawlick on a hot plate. EB and EBP rats were less responsive than OVX rats to MS-induced antinociception. EB and EBP rats were also less responsive than OVX animals to the spinal cord-mediated analgesia due to MS, as calculated by tail-flick latency. MS-induced hypothermia revealed a responsiveness order of OVX greater than EB greater than EBP. Whereas MS caused a dose-dependent reduction in locomotor activity in OVX and EB rats, EBP rats showed marked hyperactivity at low MS doses and were less responsive to the suppression of locomotor activity at higher doses. These marked steroid-induced changes in MS responsiveness could not be explained by altered pharmacokinetic disposition of morphine. These data indicate that treatment with EBP, which stimulates a preovulatory-like LH surge, decreases the ability of MS to induce hypothermic, antinociceptive, and behavioral responses and abolishes its capacity to suppress LH release. These effects of gonadal steroids were not observed before the LH surge, which suggests that this surge is linked to the decline in MS sensitivity. Further, the diminished response to MS appears to be a function of the magnitude of the LH surge.
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PMID:Desensitization of brain opiate receptor mechanisms by gonadal steroid treatments that stimulate luteinizing hormone secretion. 283 73

Neurotensin (NT) differentially altered ethanol-induced anesthesia as measured by duration of loss of righting response or by blood ethanol levels producing loss of righting response in mice (LS and SS) which were selectively bred for differences in response to ethanol. At doses of 5-500 ng i.c.v., NT increased ethanol sensitivity in SS mice, but not in LS mice, as measured by blood ethanol concentrations at loss of righting response. At higher doses, 0.5-10 micrograms i.c.v., NT enhanced the sensitivity of both SS and LS mice to ethanol-induced anesthesia. The hypothermic effect of ethanol determined at loss of righting response was not altered in either LS or SS mice at low doses of NT, but at higher doses NT enhanced ethanol-induced hypothermia in both lines of mice. The altered anesthetic sensitivity was specific for ethanol in that NT did not alter pentobarbital-induced sleep time in either LS or SS mice and halothane anesthesia was altered slightly only in LS mice. NT analogues, N-acetyl-NT8-13, and [D-Trp11]-NT but not NT1-8 enhanced the anesthetic action of ethanol in SS mice. Bombesin, cholecystokinin sulfate, substance P, [D-Trp8, D-Cys14]-somatostatin and corticotropin releasing hormone (CRF) were not effective in enhancing ethanol-induced anesthesia in LS or SS mice. CRF appeared to decrease ethanol sensitivity in LS but not in SS mice. Beta-Endorphin (beta-END) markedly increased the ethanol sensitivity of SS and to a lesser extent of LS mice at relatively high doses, e.g. 0.5-1.0 micrograms i.c.v. The results of the present study indicate that differences in brain sensitivity of LS and SS mice to ethanol may be mediated by genetic differences in NT systems. Likewise, NT, and probably beta-endorphin, may interact with other neurochemical processes that are involved in the mechanism of ethanol-induced anesthesia and that differ genetically in LS and SS mice.
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PMID:Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice. 294 96

The effects of shivering on hemodynamics and systemic oxygenation, as well as the effectiveness of therapeutic interventions in decreasing shivering and increasing mixed venous oxygen saturation, were studied. Thirty adult patients undergoing cardiopulmonary bypass with systemic hypothermia were observed for 1 1/2 to 5 hours postoperatively for signs of shivering associated with a simultaneous decrease in oxygen transport. Systemic and pulmonary hemodynamic measurements were made, blood temperature and mixed venous oxygen saturation were monitored via the pulmonary arterial catheter, and oxygen consumption and delivery were calculated. Shivering was graded by a single investigator on scale of 0 to 4, with 0 = no shivering and 4 = continuous violent muscle activity. Therapy was instituted when shivering reached grade 4 or when SvO2 decreased to less than two thirds of its value on arrival in the intensive care unit (ICU). Patients were randomly assigned to receive either morphine sulfate, 5 to 10 mg, or meperidine, 25 to 50 mg intravenously (IV), followed by the other narcotic if the initial drug failed to improve SvO2 or decrease shivering within ten minutes. The end-point for successful treatment was a return of SvO2 to within 5% to 10% of its value upon arrival in the ICU or a cessation of shivering that did not recur within 45 minutes. Twenty of the thirty patients shivered sufficiently to decrease SvO2 by more than one third of its initial value, thus requiring pharmacologic therapy. As shivering increased from a score of 0.8 +/- 1.1 to 3.4 +/- 0.9, SvO2 decreased from 74 +/- 6% to 57 +/- 12%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Shivering following cardiac surgery: hemodynamic changes and reversal. 297 67

In a set of experiments designed to examine learned associations between drug states, atropine sulfate (10 mg/kg) elicited a conditional hyperthermia in rats following ten treatment sessions in which the drug was paired with either chlorpromazine hydrochloride (10 mg/kg) or ethanol (2.3 g/kg), both hypothermia-inducing agents. Atropine methyl nitrate, a quaternary analogue with similar peripheral effects but little central action, was ineffective as a cue in this situation. These experiments demonstrated that a sequential pairing of drug states can yield a change in an organism's response to the cue drug (the first drug in the sequence).
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PMID:Conditional hyperthermia in response to atropine associated with a hypothermic drug. 309 19


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