Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Naltrexone, in relatively high doses, has been reported to cause a fall in body temperature in human ex-heroin addicts who had been abstinent for at least 6 weeks. The underlying mechanism of this hypothermic effect has been investigated in rats. The first consideration was that the temperature change was a reflection of delayed withdrawal but rats implanted with a morphine pellet 45 days earlier showed no significant change in temperature after a dose of naltrexone that caused marked withdrawal hypothermia in dependent rats implanted 3 days previously. A fall in core temperature was only induced in rats after doses of 80 and 160 mg/kg i.p. of naltrexone. Behavioral thermoregulatory studies revealed that the animals correct the falling body temperature by increased exposure to a radiant heat source indicating that the central thermostats had not been significantly affected by the drug. These data suggest that the major component in the hypothermic effect of naltrexone is activation of efferent heat loss pathways or peripheral heat loss mechanisms. Due to current suggestions that opiate receptors might represent the receptors for an endogenous transmitter the results are discussed in relation to this consideration. When compared to the sites and mechanism of action of opiates on thermoregulation the results with naltrexone lend little support to the hypothesis that the fall in temperature is due to displacement of an endogenous substance from central opiate receptors.
 ...
PMID:Naltrexone-induced hypothermia in the rat. 18 61

The etiology of the Rett syndrome (RS) is unknown. Reduced function of biogenic amines has been described. Symptoms of central apnea, hyperventilation, hypothermia, peripheral analgesia, muscle rigidity, myoclonic jerks, hand stereotypy and seizures occur in RS and have been suggested as a result of elevated central beta-endorphins. It was hypothesized that a dysfunctional modulation of endogenous opiate systems and biogenic amines may be present. Cerebrospinal fluid (CSF) from 12 girls with RS was studied for beta-endorphin immunoreactivity, and biogenic amines. Lactates and pyruvate levels were measured. Eleven of the 12 girls had elevated beta-endorphin immunoreactivity in CSF, 4 girls had reduced biogenic amines and 6 girls had elevated pyruvate and lactate levels. Whether the elevated beta-endorphin immunoreactivity is a primary disorder or is a result of secondary feedback mechanisms is unknown. Naltrexone, an antiopioid drug, may reduce symptoms.
 ...
PMID:Cerebrospinal fluid studies in the Rett syndrome: biogenic amines and beta-endorphins. 169 44

Morphine slows hepatobiliary elimination of sulfobromophthalein in rodents, raising dye levels in plasma and liver. Earlier studies showed these effects to be independent of other opiate effects such as bile duct spasm, hypothermia or blood gas changes resulting from respiratory depression. Because opiate receptors are distributed throughout the body, within the central nervous system and at peripheral sites including the gastrointestinal tract, experiments were performed to ascertain whether central or peripheral sites mediate the hepatobiliary effects of morphine. Sulfobromophthalein was administered intravenously to mice and its levels were measured in plasma and liver. Tail-flick latency indicated centrally mediated analgesia. Inhibited intestinal transit of India ink reflected an opiate effect with a significant peripheral component. When injected into a cerebral ventricle morphine was much more potent in producing analgesia and raising sulfobromophthalein levels than when administered intravenously or intraperitoneally. An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing. Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing. The polar opiate agonist N-methylmorphine did not cause analgesia or raise sulfobromophthalein levels at peripheral intraperitoneal doses to 100 mg/kg. When given in a central ventricle at 4 x 10(-3) mg/kg, this agent produced analgesia and raised sulfobromophthalein but did not slow intestinal transit. After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice. These experiments demonstrate parallel opiate effects on analgesia and on BSP disposition but not on intestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hepatobiliary effects of morphine are mediated in the brain. 217 93

We studied the ability of opioid antagonists: naloxone, naltrexone and diprenorphine and an opioid agonist morphine to influence the effects of ethanol on hypothermia, sleeping time and impairment of aerial righting reflex. Naltrexone (2-16 mg/kg) and naloxone (2-16 mg/kg) were not able to attenuate effects of ethanol, while diprenorphine decreased ethanol sleeping time (4 microgram/kg) and antagonized the ethanol hypothermia (8 microgram/kg). Naltrexone in a dose of 8 mg/kg sc antagonized the ethanol impairment of aerial righting reflex. The present behavioral studies did not provide any evidence for the participation of the opioid system in the mediation of acute ethanol effects in rats.
 ...
PMID:The lack of effect of opioid agonists and antagonists on some acute effects of ethanol. 227 71

The reported studies on the development of tolerance to the analgesic effects of stress have been mostly concerned with the involvement of opioid or non-opioid substances in stress-induced analgesia (SIA). To further investigate the processes involved in SIA tolerance, rats were exposed to forced intermittent cold water swim (ICWS, 18 exposures, 3/min, 10 sec each) on 16 consecutive days. On days 15 and 16, they were injected prior to swim with saline and naltrexone (10 mg/kg), respectively. During swim, three types of readily identifiable behaviors were observed. They may be characterized by immobility and horizontal floating (Type I), intensive activity and escape attempts (Type II), and passivity and "behavioral despair" (Type III). In the acute condition, only Type II and Type III appear in sequence. In the chronic condition, the sequence of behaviors is: Type I, Type II, and Type III. Thirty minutes after swim, analgesia, core temperature, and degree of inactivity were measured. With chronic exposure, tolerance developed to the analgesia, core hypothermia and hypoactivity induced by the ICWS. Type I behavior appeared on day 3 or 4 and persisted throughout the chronic treatment. Type II behavior did not adapt. Naltrexone (10 mg/kg) antagonized the adaptive aspect of all those variables where adaptation or tolerance were found (analgesia, hypoactivity, core hypothermia, and Type I behavior) but had no effect on Type II behavior where no adaptation was observed. It is suggested that the endorphins have a functional role in the behavioral and and physiological adaptation to aversive stressful environmental situations.
 ...
PMID:Naltrexone antagonizes the biobehavioral adaptation to cold water stress in rats. 404 Feb 46

Morphine injected intraseptally in the amounts of 35 and 70 nmol prolonged pentobarbital-induced narcosis in the rat. Pentobarbital-induced hypothermia was also potentiated by intraseptal injection of 70 nmol of morphine. These effects were antagonized when morphine was injected together with naltrexone (29 nmol). Naltrexone injected by itself into the septum did not significantly affect pentobarbital-narcosis and hypothermia. It is concluded that activation of mu opioid receptors in the septal region could affect the actions of pentobarbital.
 ...
PMID:Intraseptal morphine potentiates pentobarbital narcosis and hypothermia in the rat. 407 Mar 26

The influence of opiate receptor antagonists: naloxone, naltrexone and diprenorphine, and of an agonist: morphine on ethanol-induced sleep, hypothermia and motor coordination impairment was investigated. Naloxone and naltrexone evidently antagonized the sleep and hypothermia, and improved the motor coordination impaired by ethanol. Naltrexone was the most, and diprenorphine the least potent ethanol antagonist. Morphine potentiated only ethanol-induced sleep, and this effect was opiate dependent (reversible by naloxone). The present results may partially support the hypothesis about participation of opioid system in ethanol action. However, ethanol effects were affected only by high doses of opiate antagonists, exceeding by far the doses antagonizing the morphine effects. Therefore the participation of additional, unspecific mechanisms, in addition to an opiate-mediated one, cannot be excluded.
 ...
PMID:Ethanol-opioid interaction in mice. 609 96

Activation of the immune system in response to either infection or lipopolysaccharide (LPS) produces neurophysiological, neuroendocrine and behavioral changes. Some of the physiological consequences of LPS are mediated by endogenous opioid peptides. The following studies were designed to characterize the effects of LPS in several behavioral paradigms, and to determine the role of opioids in mediating these effects. The effects of LPS on locomotor and self-care activity were assessed in the open field test. Rats were injected with either saline or a dose of LPS (25, 50, 100, or 1000 micrograms/kg). 4 h later, the animals were placed in an open field and the numbers of line crossings, rearings and grooming episodes were counted. LPS significantly suppressed the three open field behaviors in a dose-related manner. The effect of LPS on sensitivity to pain was determined using the hot-plate and tail-flick tests. Administration of LPS (200 micrograms/kg) increased pain sensitivity in the hot plate test 30 min after drug administration, but produced a significant analgesic response 4 h after drug administration in both tests. Further characterization of LPS-induced analgesia demonstrated that it began about 2 h after and disappeared 30 h after the administration of LPS. Administration of naltrexone completely blocked the analgesic effects of LPS 4 h after its administration, but had no effect on LPS-induced suppression of activity in the open field. The effect of LPS on body temperature was biphasic, producing hypothermia at 2 h and hyperthermia at 8-30 h after its administration. Naltrexone had no effect on the body temperature changes induced by LPS.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Behavioral effects of lipopolysaccharide in rats: involvement of endogenous opioids. 792 30

1. The effect of naltrexone pellets containing either 10 or 30 mg of naltrexone base on the development of tolerance and physical dependence on morphine was assessed in male Sprague-Dawley rats. Tolerance-dependence on morphine was induced by s.c. implantation of six morphine pellets, each containing 75 mg morphine base for 7 days. 2. Naltrexone pellet implantation blocked the development of tolerance to the analgesic and hyperthermic effects of morphine. Similarly, naltrexone pellet implantation reversed morphine withdrawal-induced body weight loss. The effect of pellets containing 10 and 30 mg naltrexone did not differ. 3. The effect of naltrexone (10 mg) pellet implantation on various signs of naltrexone-precipitated withdrawal such as body weight loss, hypothermia and increases in urinary and fecal output was investigated. Naltrexone pellet implantation did not alter the naltrexone-precipitated withdrawal-induced body weight loss. Concurrent naltrexone pellet implantation blocked the naltrexone-precipitated withdrawal-induced hypothermia, increased fecal and urinary output in morphine-dependent rats. 4. These results indicate that a single pellet of 10 mg of naltrexone can effectively block morphine tolerance and physical dependence in the rat. Such a procedure may be useful in studying biochemical, endocrinological and immunological mechanisms involved in opioid addiction processes.
 ...
PMID:Effects of naltrexone pellet implantation on morphine tolerance and physical dependence in the rat. 802

In order to evaluate the stressing role of swim hypothermia in producing swim stress-induced analgesia (SSIA), we examined whether a mere decrease in the animals' core temperature without swimming would be sufficient to elicit analgesia. The subjects were Swiss-Webster mice selectively bred for 37 and 40 generations for divergent magnitudes of SSIA. High (HA) and low analgesia (LA) mice were exposed for 15 min to temperatures in the range between -5 and +20 degrees C in 79% He/21% O2 (Heliox) atmosphere. The Heliox exposure produced ambient temperature-dependent hypothermia and analgesia, as assessed with a hot-plate test (56 degrees C). The post-Heliox analgesia was of much higher magnitude in HA than in LA mice. The steeper slope of regression of the magnitude of analgesia upon hypothermia in HA mice indicates that these mice are far more sensitive to the analgesic effect of hypothermia than LA mice. Naltrexone HCl (10 mg/kg i.p.) attenuated analgesia in ambient temperature-dependent manner in HA, but not in LA mice. In view of the apparent similarity of Heliox-induced analgesia and SSIA we suggest that hypothermia is a powerful component of swim stress to induce SSIA in the mouse.
 ...
PMID:Analgesia in selectively bred mice exposed to cold in helium/oxygen atmosphere. 1022 87


1 2 Next >>