Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After elective hospitalization, eleven healthy young women developed symptomatic hyponatremia that was rapidly followed by polyuria, hypernatremia, hyperglycemia, and death. The patients were 30 +/- 2 years old (+/- SE) with initial serum sodium of 140 +/- 1 mmol/L. They all awoke from analgesia but, 32 hours after completion of the procedure, they went from alertness to respiratory arrest in less than 1 hour. At this time, serum sodium was 116 +/- 2 mmol/L and blood glucose was 6.7 +/- 0.7 mmol/L. Without treatment for the hyponatremia, urine output spontaneously increased from 38 to 689 mL/h and urine osmolality fell from 546 to 83 mmol/kg body weight. Over the next 51 hours, blood glucose rose to a high of 24.1 +/- 2.5 mmol/L while serum sodium rose to a high of 167 +/- 2 mmol/L. None of the patients regained consciousness. At autopsy, all patients had cerebral edema with herniation along with hypoxic brain damage. The pituitary showed infarction of both anterior and posterior lobes in 7 of 7 patients examined, while 8 of 11 had necrosis of the medulla and 8 of 8 patients examined had hypothalamic necrosis. All had normal pancreas and kidneys at autopsy. Soon after respiratory arrest, all of the patients developed fixed, dilated pupils that often led to the diagnosis of brain death. Autopsy showed compression of the third cranial nerve (oculomotor) because of cerebral herniation. Thus, all of the patients were diagnosed as being brain dead when some may have been saved. These data suggest that in otherwise healthy young women, untreated symptomatic hyponatremia may lead to brain edema, cerebral herniation, and infarction of pituitary and hypothalamus, resulting in central diabetes insipidus and mellitus.
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PMID:Fatal central diabetes mellitus and insipidus resulting from untreated hyponatremia: a new syndrome. 848 18

The sedative effect of medetomidine was evaluated in 6 male Awassi sheep. Medetomidine at 40 micrograms/kg, i.m. induced sedation and recumbency in the sheep within 9 +/- 1 and 17 +/- 4 minutes, respectively. The duration of recumbency was 58 +/- 1 minutes. Medetomidine produced good analgesia and marked muscle relaxation in the recumbent animals for 30 to 45 minutes. The side effects of medetomidine were bradycardia, respiratory depression, stasis of the rumen with tympany, salivation and polyuria. The animals recovered from the sedative and side effects of medetomidine 1.5 to 2 hours after gaining the righting reflex without any apparent adverse effect. The results suggested that medetomidine could be a useful sedative analgesic in sheep.
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PMID:Medetomidine sedation in sheep. 821 47

Inbred mice, STR/N, are known to exhibit extreme polydipsia and polyuria but no abnormality in the response to exogenous vasopressin (AVP) and renal functions. Our previous studies have revealed that the brain opioid system is involved in the polydipsia of these mice. We here report that the STR/N mice show a decrease in the nociceptive threshold and a low, anti-nociceptive sensitivity to opioid receptors agonists. The paw-withdrawal latency (PWL) on a hot-plate in the STR/N mice was significantly shorter than that in their controls (BALB/c and C3H mice). This hyperalgesia was not affected by water restriction. Subcutaneous (s.c.) injections of morphine (5 mg/kg) and a kappa-opioid receptor agonist, U50,488H (16 mg/kg) had no effect on the PWL in the STR/N mice, whereas the control mice prolonged PWL after administration of the opioids. However, the STR/N mice gained the ability to show morphine analgesia after up-regulation of the opioid system by repeated administration of naltrexone (s.c., 5 mg/kg) for 3 consecutive days. The results suggest that the anti-nociceptive function of the opioid system is down-regulated in STR/N mice as is observed in chronic morphine-treated animals.
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PMID:Hyperalgesic response to noxious stimulation in genetically polydipsic mice. 1055 33