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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 and delta9-tetrahydrocannabinol(THC)on the tail-flick reflex, body temperature, and catecholamine synthesis were examined in the mouse in order to compare their effects in a single species and strain under uniform conditions. Naloxone antagonism of THC and cross-tolerance between morphine and THC were also studied. Both morphine and THC produced antinociception, hypothermia, and increased catecholamine synthesis at 30 min after s.c. injection. Morphine produced greater increases in dopamine synthesis and was a more potent antinociceptive agent, while THC produced greater increases in norepinephrine synthesis and was a more potent hypothermic agent. Naloxone pretreatment (1 mg/kg) partially antagonized the hypothermia and increase in catecholamine synthesis produced by THC. There was also cross-tolerance between morphine and THC, but it was asymmetric in that THC-tolerant animals were cross-tolerant to only the hypothermic action of morphine and morphine-tolerant animals cross-tolerant to only the antinociceptive action of THC.
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PMID:A comparison of some pharmacological actions of morphine and delta9-tetrahydrocannabinol in the mouse. 9 3

Previous studies have indicated that morphine alters nerve impulse activity differently in various brain areas of intact animals. Because morphine has profound effects on visceral organs and on the spinal cord, cervically transected preparations, in which hypothermia was prevented, were used for recording spontaneous impulse activity before and for 30 min after morphine simultaneously from six regions of the brain: caudate (Cau), midbrain reticular formation (MBRF), central grey (CG), cingulate cortex (CC), hippocampus (Hip), and substantia nigra (SN). Morphine (5 and 15 mg/kg, i.p.) caused a naloxone-preventable depression of impulse activity in most brain areas. The depression was, however, especially pronounced in the CG, more so with the lower than the higher dose; naloxone completely blocked the low-dose effect. The MBRF responded with increased impulse activity after 5 mg/kg, but with depression after 15 mg/kg; naloxone blocked both responses. Activity in both the Hip and CC was depressed by the low dose of morphine, but not by the high dose; naloxone blocked the depression. Both doses of morphine generally depressed the variance in impulse activity, with a clear preferential depression of CG variance; naloxone blocked the CG variance effect, but not that of other brain areas.
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PMID:Morphine-induced regional and dose-response differences on unit impulse activity in decerebrate rats. 41 34

Morphine caused an apparently dose-dependent hypothermia in mice. Co-administration of naloxone antagonised this effect. Pretreatment with a single dose of morphine induced detectable tolerance to the hypothermic effect of a second dose of morphine given 3 h later and naloxone was more effective in antagonising the hypothermic effect of morphine in morphine-pretreated mice than in saline-pretreated animals. The present study has shown that morphine pretreatment can augment the antagonistic effect of naloxone towards the hypothermic action of morphine.
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PMID:The effect of morphine pretreatment on hypothermia induced by morphine in mice. 42 32

1 The effect of morphine on body temperature was studied in conscious, unrestrained cats provided with implanted third or lateral cerebral ventricular cannulae, jugular venous catheters and retroperitoneal thermocouples.2 Intraventricular injections of 2.5-50 mug and intravenous injections of 1-10 mg/kg morphine sulphate produced dose-related hyperthermic responses. Similar mean increases in body temperature after administration of a given dose were elicited in cats which had not previously received morphine and, provided that tolerance was avoided by spacing injections at least 72 h apart, in cats which received a series of injections of morphine. Morphine was at least 850 times more potent when injected into the third ventricle than when given intravenously. Increasing the dose of morphine sulphate injected into the third ventricle to 1250 mug only prolonged the hyperthermia. Morphine did not produce hypothermia at any dose tested.3 Injection of 10 mug morphine sulphate into the third ventricle produced similar hyperthermias at ambient temperatures (tas) of 4-6, 21-23 and 33-36 degrees C. The increase in body temperature was associated with shivering at the lower tas. At the highest ta, shivering was not evoked, but respiratory rate decreased after morphine if it was initially elevated. These results suggest that morphine increased the level at which body temperature was regulated.4 Neither metiamide nor indomethacin antagonized morphine so histamine and prostaglandins were apparently not required for the hyperthermic effect.
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PMID:Hyperthermic responses to central and peripheral injections of morphine sulphate in the cat. 64 64

Morphine was more lethal to mice housed in groups (aggregated) than to mice housed individually (isolated). The aggregation effect on morphine lethality was increased when ambient temperature was increased to 29 degrees C and abolished when ambient temperature was lowered to 19 degrees C. At 29 degrees C morphine produced hypothermia in isolated mice and hyperthermia in aggregated mice. Both isolated and aggregated mice were hypothermic after morphine administration at 19 degrees C. At 29 degrees C the locomotor activity of morphine-treated aggregated mice was significantly greater than that of morphine-treated isolated mice, whereas at 19 degrees C no significant difference was found. The locomotor activity time course of morphine-treated aggregated mice at 29 degrees C closely resembled the rectal temperature time course, which suggests that the hyperthermia in those animals involves an increase in heat production via an increase in locomotor activity. However, the hyperthermia observed was not sufficient to explain the increased lethality in aggregated mice. Differences between the aggregation effect on morphine lethality and that previously reported for amphetamine were discussed.
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PMID:The effect of aggregation on the lethality of morphine in mice. 74 72

Three different syndromes produced by congeners of morphine have been identified in the nondependent chronic spinal dog. These syndromes have been attributed to interaction of agonists with three distinguishable receptors (mu, kappa and sigma). Morphine is the prototype agonist for the mu receptor, ketocyclazocine for the kappa receptor and SKF-10,047 for the sigma receptor. The morphine syndrome (mu) in the dog is characterized by miosis, bradycardia, hypothermia, a general depression of the nociceptive responses and indifference to environmental stimuli. Ketocyclazocine (kappa) constricts pupils, depresses the flexor reflex and produces sedation but does not markedly alter pulse rate or the skin twitch reflex. SKF-10,047 (sigma), in contrast to morphine and ketocyclazocine, causes mydriasis, tachypnea, tachycardia and mania. The effects of these three drugs can be antagonized by the pure antagonist naltrexone, indicating that they are agonists. Further, chronic administration of morphine, ketocyclazocine and SKF-10,047 induces tolerance to their agonistic effects. Morphine suppresses abstinence in morphine-dependent dogs while ketocyclazocine does not. Ketocyclazocine at best precipitated only a liminal abstinence syndrome in the morphine-dependent dog, indicating that it had little affinity for the morphine receptor. Ketocyclazocine thus appears to be a selective agonist at the kappa receptor. Further, it has been shown that buprenorphine is a partial agonist of the mu type which both suppressed and precipitated abstinence in the morphine-dependent dog while morphine and propoxyphene are stronger agonists. Apomorphine and SKF-10,047 produce similar pharmacologic effects suggesting that sigma activity may involve a dopaminergic mechanism.
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PMID:The effects of morphine- and nalorphine- like drugs in the nondependent and morphine-dependent chronic spinal dog. 94 47

The modifications produced by 6-hydroxydopamine (6-OHDA) on the analgesic and toxic effects of morphine have been studied in mice and cats. After intracerebral injections of 6-OHDA, mice had a lower threshold for morphine-induced convulsions. Morphine analgesia assayed by the phenylquinone test was apparently antagonized in the 6-OHDA pretreated mice, but the 6-OHDA mice showed more reactivity to the phenylquinone. Intraventricular injection of 6-OHDA in cats produced an acute syndrome with mydriasis, bradycardia, bradypnea, hypothermia and EEG slowing, which subsided after several days, 6-OHDA was successful in blocking the morphine mania, but the animals died within 24 h.
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PMID:Antinociceptive and stimulant effects of morphine after chemical sympathectomy. 95 25

Three postoperative analgesic protocols were assigned randomly to 24 healthy dogs after thoracotomy at the left fourth intercostal space. Morphine was administered parenterally to eight dogs after tracheal extubation; selective intercostal nerve blocks with bupivacaine hydrochloride and epinephrine were administered to eight dogs before closure of the thorax; and bupivacaine hydrochloride and epinephrine were administered through an interpleural catheter to eight dogs after tracheal extubation. Heart rate, respiratory rate, rectal temperature, hematocrit, plasma protein, blood gas, and pain score evaluations were recorded before surgery and 30 minutes, 1 hour, 2 hours, and 3 hours after extubation. Morphine caused significant decreases in blood pH and blood oxygen tensions, and significant increases in carbon dioxide tensions. Dogs treated with intercostal nerve blocks had no significant changes in these parameters, and dogs treated with interpleural bupivacaine had significant decreases in blood oxygen tension. All dogs had significant decreases in rectal temperature, and hypothermia was prolonged after morphine. Analgesia was initially adequate in most dogs, but some dogs in each treatment group had recurrence of pain and were treated with interpleural bupivacaine. One dog developed pneumothorax. Interpleural administration of bupivacaine produced analgesia equal to that produced by systemic administration of morphine or selective intercostal nerve block with bupivacaine. Bupivacaine was easily readministered through an interpleural catheter. Respiratory compromise was less in dogs treated with bupivacaine than in dogs treated with morphine. After intercostal thoracotomy, interpleural bupivacaine provided prolonged analgesia with fewer blood gas alterations than morphine.
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PMID:Analgesia in dogs after intercostal thoracotomy. A comparison of morphine, selective intercostal nerve block, and interpleural regional analgesia with bupivacaine. 190 Nov 83

Morphine produced a hypothermic effect in restrained rats which was antagonized by naloxone. This effect was completely inhibited by gamma-acetylenic-GABA, an inhibitor of GABA transaminase and by baclofen, a specific GABAB agonist. Pretreatment with diazepam, an agonist of the benzodiazepine receptor, partially inhibited morphine-induced hypothermia. Flumazenil, a benzodiazepine receptor blocker, potentiated the action of morphine on body temperature. A role of brain GABA in the thermoregulatory effects of morphine is proposed on the basis of these results.
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PMID:GABAergic mechanisms in morphine-induced hypothermia. 207 23

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)
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PMID:Hepatobiliary effects of morphine are mediated in the brain. 217 93


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