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)

The novel and highly selective, conformationally restricted enkephalin analogue for delta-opioid receptors, [D-Pen2,D-Pen5]enkephalin (DPDPE; Pen = penicillamine), was studied in various in vivo tests for analgesia, tolerance and physical dependence. Intracerebroventricular (i.c.v.) administration of DPDPE caused a dose-dependent, naloxone-reversible antinociception, measured with the heat-irradiant (tail-flick) method. Acute tolerance developed to the antinociceptive effect of DPDPE. DPDPE also caused mild signs of physical dependence (withdrawal hypothermia and body weight loss) after repeated peptide treatment. Severe signs of morphine withdrawal (e.g. withdrawal jumping) on the other hand, could not be reversed by the administration of DPDPE. It is concluded that the activation of central delta-opioid receptors may play a role in controlling pain mechanisms, and that this activation is followed by the rapid development of a tolerance to this action.
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PMID:Analgesic and tolerance-inducing effects of the highly selective delta opioid agonist [D-Pen2,D-Pen5]enkephalin in mice. 284 84

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

Trauma is the leading cause of death for persons aged 1 to 38 years. Successful management is facilitated by prehospital endotracheal intubation, transport to regional trauma centers, rapid resuscitation by an on-site team of trained physicians, timely operative intervention, and provision of care by well-prepared anesthesiologists familiar with the potential complications typical of traumatized patients. No particular anesthetic agent or technique is ideal. Causes for intraoperative hypotension include hypovolemia, hemopneumothorax, pericardial tamponade, an intracranial mass, acidosis, and hypothermia. The anesthesiologist should play an active role in all phases of trauma management, including provision of postoperative intensive care and pain relief.
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PMID:Anesthesia for trauma. 307 28

In addition to short-acting analgesic actions by itself and modulation of analgesic responses induced by endogenous opioids and neurotensin, central administration of thyrotropin-releasing hormone (TRH) potentiates footshock analgesia. The present study evaluated the effects of TRH upon the neurohormonally-mediated though nonopioid analgesia induced by swims in rats. Intracerebroventricular TRH (10 and 50 micrograms) dose-dependently potentiated swim (21, 15, 2 degrees C baths) analgesia on the tail-flick test, an effect which was not due to the hypothermic or basal pain threshold changes. Intravenous (8 mg/kg) TRH potentiated swim (21 degrees C) analgesia; the 600:1 difference in potency between routes strongly suggests central sites of neuromodulatory action. Intracerebroventricular diketopiperazine (50 micrograms), a TRH metabolite, and RX77368 (50 micrograms), a TRH analogue, also potentiated swim (21 degrees C) analgesia, effects also independent of hypothermia and basal reactivity to pain. Finally, given the excitatory interaction between TRH and acetylcholine as well as the cholinergic involvement in swim analgesia, intracerebroventricular TRH potentiated pilocarpine (10 mg/kg, IP) analgesia.
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PMID:Neuromodulatory effects of TRH upon swim and cholinergic analgesia. 310 67

Intra-articular and skin surface temperatures of the temporomandibular joint (TMJ) were investigated in 34 patients with rheumatoid arthritis (RA). History was taken, and a clinical examination of the stomatognathic system was performed. The intra-articular temperature measurement was made with a thermocouple inserted through a needle, and the skin surface measurement was made with a thermocouple lateral to the condylar pole. The intra-articular temperature was lower for 37% and higher for 30% of the patients, whereas skin surface temperature was lower for 18% and higher for 6%, compared with normal individuals. Intra-articular and skin surface temperatures were positively correlated, and the average difference between skin surface and intra-articular temperatures was 1.6 degrees C. The intra-articular temperature was most strongly and positively correlated to the number of joint regions affected by RA and negatively correlated to the number of tender masticatory muscles, whereas skin surface temperature was most strongly and positively correlated to room temperature and negatively correlated to the number of tender masticatory muscles. These results indicate that pain and tenderness of masticatory muscles in RA are associated with hypothermia of the TMJ.
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PMID:Intra-articular and skin surface temperature of the temporomandibular joint in patients with rheumatoid arthritis. 316 62

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the central nervous system were studied in various experimental animals as compared with those of disopyramide, mexiletine and lidocaine, and the following results were obtained. 1. Acute toxicity of SUN 1165 in mice was similar to that of mexiletine, and twice as potent as compared with that of disopyramide and lidocaine. Main acute toxic symptoms of SUN 1165 were muscle relaxation, ataxia, clonic convulsions, tremor and a decrease in spontaneous activity in mice, rats and rabbits. In addition to these symptoms, vomiting in dogs was observed. These toxic symptoms were similar to those of lidocaine. In the case of disopyramide, ataxia, tremor and a decrease in spontaneous activity were observed in mice and rats. On the other hand, mexiletine caused central nervous excitatory symptoms, that is, tremor, Straub tail, clonic convulsions, jumping, running and opisthotonus in mice and rats, and vomiting in dogs. 2. SUN 1165 even at large doses (50-100 mg/kg p.o.) exerted no significant effects on the following changes: hexobarbital-induced induced hypnosis, oxotremorine-induced tremor, apomorphine-induced hypothermia, reserpine-induced ptosis and hypothermia, 5-hydroxytryptophan syndrome and fighting behavior in mice, and conditioned avoidance response in rats. 3. An ineffective dose of SUN 1165 (12.5 mg/kg p.o.) on spontaneous locomotor activity was lower than of disopyramide and lidocaine, however, higher than that of mexiletine. 4. SUN 1165 at large doses showed antagonistic action on toxic extensor seizures induced by maximal electroshock, picrotoxin, or strychnine in mice, but anticonvulsive effects of SUN 1165 were less potent than those of mexiletine and lidocaine. SUN 1165 had no effect on clonic convulsions induced by pentetrazol and pictrotoxin in mice, while both mexiletine and lidocaine prolonged the duration of clonic convulsions. 5. The muscle relaxant effect of SUN 1165 (50%-toxic dose, TD50 = 30 mg/kg p.o.) was more marked than that of lidocaine (TD50 = 92 mg/kg p.o.) on traction test in mice. However, effect of SUN 1165 (TD50 = 62 mg/kg p.o.) on motor incoordination was similar to that of disopyramide, mexiletine and lidocaine on the rotarod test in mice. 6. The analgesic effect of SUN 1165 was as weak as that of disopyramide, mexiletine and lidocaine on chemically and mechanically-induced pain response in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 1st communication: effect on the central nervous system. 319 80

Both gender-specific and gonadectomy-specific effects have been observed for the analgesic responses following continuous and intermittent cold-water swims (CCWS and ICWS respectively): female rats display significantly less analgesia than males, and gonadectomized rats display significantly less analgesia than sham-operated controls. The present study evaluated the effects of steroid replacement therapy with testosterone propionate (TP: 2 mg/kg, SC) upon CCWS and ICWS analgesia on the tail-flick and jump tests and hypothermia in sham-operated or gonadectomized male and female rats. Thirty days following surgery, rats received either no treatment, a sesame oil vehicle or TP for 14 days prior to, and then during testing. Relative to the no treatment condition, repeated vehicle injections in sham-operated rats eliminated the gender-specific, but did not affect the gonadectomy-specific effects upon CCWS and ICWS analgesia. TP reversed the deficits in CCWS and ICWS analgesia observed in both castrated and ovariectomized rats on both pain tests. TP only potentiated CCWS analgesia in sham-operated males on the tail-flick test. TP potentiated CCWS and ICWS hypothermia in gonadectomized rats and in male sham-operated rats. These data indicate that gonadal steroids play a major modulatory role in the etiology of swim analgesia, and that the observed gender effects are sensitive to possible adaptational variables.
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PMID:Gender-specific and gonadectomy-specific effects upon swim analgesia: role of steroid replacement therapy. 323 32

The etiology and clinical course of acute nontraumatic rhabdomyolysis and ensuing renal failure was surveyed in a series of 40 consecutive patients. In 28 cases the muscle damage occurred after excessive consumption of ethyl alcohol and/or other intoxications. Prolonged lying immobilized was the reason or contributing factor for rhabdomyolysis in 22 cases. The other evident etiologies were convulsions, vigorous physical exercise, arterial occlusion and hypothermia. Typical local signs of rhabdomyolysis--pain, swelling and weakness of the affected muscles--were absent in one fourth of the patients. In these cases the diagnosis was based on transient elevation of serum creatine kinase enzyme activity. Dialyses were required to manage acute renal failure in 24 subjects. All 36 survivors recovered normal renal function. Neurological defects in the extremities still persisted in 16 patients at three months' follow-up.
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PMID:Acute renal failure following nontraumatic rhabdomyolysis. 323 37

Continuous cold-water swims (CCWS) and intermittent cold-water swims (ICWS) elicit respective nonopioid and opioid analgesic responses in adult male rats. The present experiment evaluated whether gender differences were observed in naloxone's (14 mg/kg, SC) ability to alter differentially CCWS and ICWS analgesia on the tail-flick and jump tests in age-matched and weight-matched intact rats and in gonadectomized rats. CCWS analgesia was unaffected by naloxone on either test in age-matched males and females. Naloxone significantly reduced ICWS analgesia on the tail-flick (45%) and jump (37%) tests in intact males, but not age-matched females. Naloxone significantly reversed ICWS analgesia in weight-matched males on the tail-flick (1-14 mg/kg, 30-32%) and jump (14 mg/kg, 31%) tests. Naloxone also significantly reduced ICWS analgesia on the tail-flick (32%) and jump (41%) tests in castrated males, but not ovariectomized females. Changes in swim hypothermia could not account for the above effects. These data indicate gender differences in naloxone's differential modulation of swim analgesia, and reflect further differences in pain-inhibitory responses as a function of gender.
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PMID:Gender determinants of opioid mediation of swim analgesia in rats. 341 98

The effects of analgesic, thermoregulatory and endocrine functions of administering morphine sulphate (0.3 mg) into the lateral cerebral ventricle via an Ommaya catheter were assessed in eight patients with cancer pain. Satisfactory control of intractable pain was obtained in these patients, without any change in other sensory modalities. The delay in the onset of pain relief and the duration of analgesia ranged, respectively, from 20 to 40 min and from 12 to 16 h after drug injection. In addition, intraventricular administration of morphine caused a reduction in rectal temperature in these patients at an ambient temperature of 24 degrees C. The hypothermia in response to the injection of morphine was due to cutaneous vasodilation and sweating. There was no change in metabolism or in respiratory evaporative heat loss after morphine injection. Further, 10 to 20 min after intraventricular administration of morphine, the blood levels of prolactin, growth hormone and glucose were elevated in these patients. The changes in temperature and endocrine levels lasted for 1-3 h. In addition to the pain relief, these side-effects of morphine treatment were short-lasting and disappeared as the morphine treatment continued. The results indicate that activation of opiate receptors in the brain produced pain relief, hypothermia (due to cutaneous vasodilation and sweating), and increased blood levels of prolactin, growth hormone and glucose in patients with cancer pain.
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PMID:Intraventricular morphine produces pain relief, hypothermia, hyperglycaemia and increased prolactin and growth hormone levels in patients with cancer pain. 343 Jan 86


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