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

The effects of morphine on body temperature have been shown to be altered by restraint. The purpose of this study was to determine how the type of restraint alters body temperature measurements and whether restraint alters the effects of morphine on body temperature by interfering with the ability of the rats to adjust their posture. The thermic effects of 5 doses of morphine (3.8 to 45 mg/kg) were compared in two types of restraint and confinement to a 13 X 20 X 20 cm pan without restraint. In unrestrained rats, morphine caused predominantly hyperthermia, but with restraint morphine caused hyperthermia at low doses and hypothermia at higher doses. Morphine hypothermia was greater in rats restrained in a wire-mesh restrainer which prevented heat and humidity build-up than in the commonly used plastic restrainer. In the unrestrained rats, morphine treatment was associated with a posture characterized by exophthalmos, immobility, a hunched position and increased muscle tone. Restrained rats could not assume a compact posture. These results suggest that restraint alters the thermic effect of morphine mainly by interfering with postural mechanisms which reduce heat loss.
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PMID:Restraint alters the thermic response to morphine by postural interference. 686 55

Neurotensin or morphine can each cause hypothermia and an antinocisponsive effect when administered into the liquor spaces of the rat brain. These actions of neurotensin are not blocked by naloxone whereas those of morphine are. The present experiments were carried out to examine the action of each substance following its injection into the subarachnoid space of the spinal cord. Given intrathecally, neurotensin evoked a dose-related fall in the rectal temperature of the rat without exerting an antinocisponsive action. Morphine on the other hand evoked hyperthermia and a dose-related antinocisponsive action. Since neurotensin exerted an effect on rectal temperature opposite to that of morphine and failed to exert an antinocisponsive effect, the data provide further evidence to suggest that neurotensin and morphine exert their effect via different mechanisms. Furthermore, the results also suggest that neurotensin exerts its antinocisponsive action via a supraspinal site.
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PMID:Differences in the pharmacological actions of intrathecally administered neurotensin and morphine. 689 46

We have previously shown in mice that opiate agonists produce either hypothermia or hyperthermia or both, depending on the dose used and the ambient temperature. We have also shown that both temperature effects are blocked by the antagonists, naloxone and naltrexone. In order to confirm that these are specific opiate effects, the present studies to explore the development of tolerance to both temperature effects were undertaken. Mice were treated chronically with twice-daily injections of 2.5, 10, 40 or 160 mg/kg of morphine sulfate. Rectal temperature changes were monitored at 20 degrees, 25 degrees or 30 degrees C ambient temperature after the initial injection and at weekly intervals thereafter. At 20 degrees and 25 degrees C, the initial hypothermic response was replaced by hyperthermia after 7 weeks of twice-daily injections. At 30 degrees C, the initial hyperthermia became more pronounced and no evidence of tolerance was seen at any dose. A challenge dose of 160 mg/kg was given to all animals at 20 degrees C ambient temperature after 9 weeks of injections. There was a diminution of the hypothermic response inversely related to the chronically administered dose. At 30 degrees C, the 160 mg/kg challenge dose at 9 weeks showed little evidence of tolerance to the hyperthermia. Morphine-base pellet implantation, however, resulted in profound tolerance to both the hypo- and hyperthermic response within 1 day after implantation, peaking at 4 days and somewhat reduced by 1 week. Tolerance to the hypothermic effects induced by chronic administration of levorphanol and morphine-levorphanol cross-tolerance was also observed. It appears that both the hypo- and hyperthermia induced by the opiate and opioid agonists are opiate receptor effects because both effects can be blocked by the opiate antagonists and tolerance and cross-tolerance can be developed to both effects as well.
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PMID:Opiates and thermoregulation in mice. IV. Tolerance and cross-tolerance. 714 33

Systemically administered beta-endorphin was tested in rats for its ability to modify the hypothermia and hypermotility induced by d-amphetamine. Colonic temperature and motor activity were measured in a cold (4 degrees C) ambient temperature in animals given IP injections of beta-endorphin (0.1, 1.0 or 3.0 mg/kg), naloxone (10 mg/kg), or morphine (30 mg/kg). The same measurements were taken in animals given beta-endorphin (1.0 mg/kg) in combination with naloxone or saline pretreatment and d-amphetamine (15 mg/kg) or saline post-treatment. Morphine alone had a biphasic effect on thermoregulation, but did not affect d-amphetamine-induced hypothermia. Activity scores were decreased by morphine, in both d-amphetamine and saline treated animals. The thermal response of rats to beta-endorphin alone was variable, depending on dosage, but all 3 dosages partially blocked the hypothermic effect of d-amphetamine. Naloxone blocked the thermal effects of both beta-endorphin and d-amphetamine. Motor activity tended to be decreased by naloxone, regardless of amphetamine treatment, but beta-endorphin tended to increase activity in amphetamine-treated animals and reduce it in saline-treated controls. In their action on both thermoregulation and activity, naloxone and beta-endorphin appeared to interact independently with d-amphetamine, often producing effects in the same direction, but in combination, they tended to be mutually inhibitory.
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PMID:D-Amphetamine-induced hypothermia and hypermotility in rats: changes after systemic administration of beta-endorphin. 724 18

mu-Opiate receptor binding and function were examined in mice selectively bred for sensitivity (COLD) and resistance (HOT) to ethanol-induced hypothermia. These mice also have differential hypothermic sensitivity to mu-opiates. mu-Opiate receptor density was higher in the frontal cortex of HOT mice compared with COLD mice, but was the same in other brain areas. In addition, there were no line differences in Kd values. Basal adenylate cyclase (AC) activity was similar in both lines, as was the response to forskolin (FS) stimulation. Morphine was more effective at inhibiting FS-AC activity in the hypothalamus of HOT mice compared with COLD mice but was equally effective in the frontal and parietal cortex. There were no differences between lines in basal Ca2+, Mg2+, or Ca2+/Mg(2+)-ATPase activity. Further, 30 min after treatment ATPase activities were not altered in ethanol- or levorphanol-treated mice. These results suggests that mu-opiate biochemical pathways, but not ATPase enzyme systems, may be involved in mediating differential hypothermic sensitivity observed in HOT and COLD mice.
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PMID:Mu-opiate receptor binding and function in HOT and COLD selected lines of mice. 827 28

The influence of pregnancy and lactation on morphine-induced hypothermia and hyperactivity was investigated in Rockland-Swiss mice. Pregnant mice were slower to recover from the hypothermic effect of morphine than nonpregnant controls. The greatest hypothermic response was seen in mice at day 18, the day before parturition. On the day after parturition, mice recovered faster from morphine-induced hypothermia than controls. During lactation, mice were again slower to recover from the morphine-induced hypothermia. Morphine-induced locomotor activity, however, was attenuated by both pregnancy and lactation. A further experiment compared the hypothermic effect of morphine in postpartum mice that were allowed to remain with pups and mice that were separated from pups. The enhanced hypothermia in the postpartum period was abolished by removing pups. This indicates that the altered response to morphine in the postpartum period was an effect of lactation rather than an aftereffect of pregnancy or parturition.
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PMID:Effect of morphine during pregnancy and lactation in mice. 832 45

Female OF1 mice were fed on a diet deficient in alpha-linolenic acid or on a control diet 3 weeks before mating and throughout pregnancy and lactation. Pups fed on the same diet as their mothers were used for experiments. The effects of dietary alpha-linolenic acid deficiency were studied in a model of learning, the Morris water maze, and on the following effects of morphine: increase in locomotor activity, modifications of rectal temperature and analgesia. In the place and in the cue versions of the Morris water maze, learning occurred at the same speed in the two diet groups; however, in the place version of the test, the level of the performance was significantly lower in the deficient mice. The probe trial and the extinction procedure did not show any difference between the two diet groups. The morphine-induced increase in locomotor activity occurred significantly earlier and was greater in the deficient diet group. Morphine induced an early hypothermia followed by a late hyperthermia; the hypothermia was significantly greater and the hyperthermia significantly smaller in the deficient mice. The pain thresholds and the morphine-induced analgesia were unmodified by the dietary deficiency. The plasma levels of morphine were similar in the two diet groups.
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PMID:Influence of a dietary alpha-linolenic acid deficiency on learning in the Morris water maze and on the effects of morphine. 884 19

1. The influence of isolation of three durations 8, 15 and 30 days has been examined in mice on the effects of morphine on rectal temperature and on locomotor activity. Isolated mice were compared to non isolated mice with the same age. 2. Morphine (20 mg/kg ip) induced in mice an early hypothermia followed by a late hyperthermia. The hypothermic effect was significantly reduced following isolation, but the duration of isolation (8, 15, 30 days) had no influence. Isolation did not modify the hyperthermic effect of morphine. 3. Morphine (40 mg/kg ip) induced in mice an increase in locomotor activity called "running". The running activity was significantly increased following isolation. The duration of isolation (8, 15, 30 days) did not seem to influence this effect. 4. These results show that isolation does not modify in the same way every effects of morphine, they suggest that isolation alters the mechanism involved in the running activity and in the hypothermic effect. The nature of these mechanisms is discussed.
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PMID:Effect of isolation on morphine-induced running and changes in body temperature. 887 67

Central hemodynamics was studied by thermodilution in 16 patients with acquired mitral defect during surgery under conditions of hypothermia without perfusion. Cooling and surgical correction were carried out under superficial ether anesthesia with morphine and droperidol. A 28% decrease of the minute circulation volume is observed as early as under general anesthesia and at the very beginning of cooling (10.8% more); this decrease is caused by rarer heart contractions and increase of the total peripheral vascular resistance as a result of body response to cool exposure. An almost 10 degrees C drop of body temperature (to 27.2 +/- 0.2 degrees C) involves a just 13% decrease of the cardiac index in comparison with the value at the beginning of cooling. Injection of droperidol before cooling blocks the increase of the total peripheral resistance in a dose-dependent mode (about 0.13 mg/kg of droperidol is needed for sufficiently complete prevention of the increase of total peripheral resistance), and thus maintains the stroke and cardiac indexes at a sufficiently high level. Morphine (in doses of up to 2.3 mg/kg) did not bring about such an effect.
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PMID:[Components of anesthesiological provision and central hemodynamics in hypothermia without perfusion]. 922 80

Postnatal day-14 (P14) infant rats remained naive or were implanted with osmotic minipumps infusing saline or fentanyl (50 microg kg(-1) h(-1)). Fentanyl was administered 72 h later for measurement of antinociception in the tail-flick test. The potency of fentanyl was 3.0-fold lower in fentanyl-infused compared to saline-infused P17 rats. Fentanyl-infused P17 rats injected with naloxone underwent withdrawal characterized by increases in spontaneous activity, wall climbing, diarrhea, abdominal stretching, forepaw treading/tremors, wet-dog shakes, jumping, ptosis, rhinorrhea and hypothermia. Other naive, saline-infused and fentanyl-infused P17 rats not challenged with fentanyl or naloxone were housed until maturing into P42 juveniles. Fentanyl's potency was equal among each treatment group. However, morphine's potency was reduced in juveniles tolerant to fentanyl as infants. Morphine was also less potent in P90 adults tolerant to fentanyl as infants. Thus, chronic opiate exposure during infancy may affect the developing central nervous system, and desensitize animals and humans to opiate analgesia throughout life.
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PMID:Long-term alterations in opiate antinociception resulting from infant fentanyl tolerance and dependence. 988 76


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