Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspecific cellular reactivity was assessed in patients who underwent open heart surgery. The authors conclude that depressed PMN activity measured as O2- production is not linked to anaesthesiological procedures, hemodilution and hypothermia. No conclusive reports are possible on the role of pulmonary reinfusion or plasmatic and cellular mechanism of depression.
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PMID:[Effects of extracorporeal circulation and hypothermia on cellular immune activity in patients undergoing heart surgery]. 262 40

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

The cardiovascular effects of morphine were determined in anesthetized dogs at 37 and 30 degrees C. Intravenous (i.v., 1 mg/kg) but not intracisternal (i.c., 0.1 mg/kg) morphine produced a significant cardiovascular depression only at 30 degrees C. These effects were antagonized by i.v. naloxone (1 mg/kg) suggesting a peripherally mediated opiate mechanism. Moreover, hypothermia significantly increased plasma and cerebrospinal fluid morphine levels and enhanced the morphine-induced histamine release. The results suggest that opiates could have detrimental effects in patients with poor cardiovascular reserve in which high doses of opiates and hypothermia may be used concomitantly.
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PMID:Cardiovascular effects of morphine during hypothermia. 273 Feb 32

Hibernation was induced in hamsters by placing them in a cold room for an extended period of time, after which the hibernating state was confirmed by marked reductions in heart rate, body temperature, and the respiratory rate. The animals were either frozen intact in liquid nitrogen, or aroused and then frozen when body temperature reached 8, 12, 16, 20, 24 or 32 degrees C. A metabolite profile, including glucose-related metabolites, high-energy phosphates, gamma-aminobutyric acid (GABA) and cyclic nucleotides, was determined for both the cerebral cortex and cerebellum. In general, the metabolite changes in the two regions elicited by hypothermia were alike, although some differences were evident. The brains of hibernators were biochemically characterized by (1) a high concentration of energy reserves including glycogen, glucose, adenosine triphosphate, and P-creatine, (2) significantly elevated levels of lactate and GABA, and (3) near depletion of cyclic guanosine monophosphate with only a moderate depression of cyclic adenosine monophosphate. During arousal, the metabolites were restored to near normal values and there was little or no indication that the brain energy metabolism was compromised by the arousal process. The study provides certain insights into the metabolic adaptation of the brain to prolonged periods of profound hypothermia in a hibernating species.
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PMID:Metabolism in the hamster brain during hibernation and arousal. 274 44

This study was designed to assess the effects of acute nickel chloride administration on behavioral and autonomic thermoregulation in the rat. In one experiment, male rats of the Fischer 344 strain were injected with nickel chloride (IP) at dosages of 0 to 24.0 mg/kg and placed in an environmental chamber maintained at an ambient temperature (Ta) of 10 or 20 degrees C. Colonic temperature was measured 60 min postinjection. Nickel chloride caused a dose-related decrease in colonic temperature, and the hypothermia was accentuated at the cooler Ta. In a second study, rats injected with 0, 6.0, 12.0, or 24.0 mg/kg nickel chloride were placed in a temperature gradient which allowed the rats to select their preferred thermal environment. Nickel chloride at dosages of 12.0 and 24.0 mg/kg caused a significant reduction in the selected Ta. At these dosages the rats were also significantly hypothermic at 60 min postinjection. In a third experiment, whole-body oxygen consumption (i.e., metabolic rate) was measured at Ta's of 10, 20, and 30 degrees C following a 12.0 mg/kg injection of nickel chloride. Nickel chloride caused an initial depression in metabolic rate and hypothermia at Ta's of 10 and 20 degrees C but not at 30 degrees C. In conclusion, (a) nickel chloride affects both behavioral and autonomic control of thermoregulation in the rat and appears to induce a regulated decrease in body temperature and (b) the behavioral thermoregulatory response of the rat is less sensitive to nickel chloride when compared to the mouse.
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PMID:Effect of nickel chloride on body temperature and behavioral thermoregulation in the rat. 275 27

A series of studies were conducted in order to further characterize the previously reported effect of morphine to diminish hepatocellular concentrations of glutathione (GSH) in mice. Naive ICR mice administered morphine (i.p.) in doses up to 1000 mg/kg had diminished hepatic GSH concentrations, with a maximum depletion of approximately 50% occurring at doses of 250 mg/kg or greater. No such effect from an acute challenge with morphine was observed in morphine-tolerant mice. The intracerebro-ventricular administration of the opioid receptor antagonist naltrexone (250 micrograms) completely blocked the hepatic GSH depression resulting from the systemic (i.p.) administration of morphine (100 mg/kg). When morphine (100 micrograms) was administered by the i.c.v. route, GSH concentrations in liver and plasma were significantly altered while heart and kidney were unchanged. Variable responses to i.c.v. morphine were obtained in spleen, stomach and lung. The depression of hepatic GSH was found not to be a consequence of morphine-induced hypoxia or hypothermia, and could not be attributed to intracellular oxidation of GSH.
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PMID:Perturbation of glutathione by a central action of morphine. 275 29

Atresia coli was identified in 26 calves. In calves with abdominal distension, progressive depression, and the absence of feces since birth, atresia coli should be suspected. Surgery was performed on 24 calves, involving decompression of the distended large intestine followed by colonic anastomosis. Nine calves were subsequently discharged; 3 of those calves reached breeding age. As an adult, 1 of the calves produced 5 offspring unaffected by atresia coli. Early postoperative mortality was associated with hypothermia, peritonitis, and ischemic necrosis of the large intestine. Calves with visible signs of peritonitis at surgery had a poor prognosis. Four calves had motility disturbances of the colon after surgery. These were characteristic of a functional obstruction and were unresponsive to treatment. Surgery was most successful in calves that were bright, alert, and ambulatory.
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PMID:Atresia coli in calves: 26 cases (1977-1987). 275 84

Scimitar horned oryx (Oryx dammah), kept under confined and unconfined conditions were immobilised with etorphine in combination with acepromazine or xylazine or both, and with xylazine alone. Both groups of animals were successfully sedated with etorphine and xylzine, with or without acepromazine, although hypothermia and mild hypoxaemia and a fall in packed cell volume were frequently noted. Xylazine alone produced a dose dependent degree of sedation in semitame subadult animals kept in confinement, but only slight depression in their wild, unconfined counterparts. If xylazine was not included in the immobilising mixture induction was traumatic and full sedation not achieved. Heart rates and arterial pressures (systemic and pulmonary) were also monitored but no remarkable changes were noted. The only abnormalities in blood biochemistry were raised aspartate transminase and creatine kinase. Ruminal regurgitation could be a major problem if endotracheal intubation was not achieved early in the procedure.
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PMID:Physiological effects of etorphine, acepromazine and xylazine in the scimitar horned oryx (Oryx dammah). 277 9

Pentazocine and tripelennamine, which have been abused in combination by humans, were evaluated for pharmacologic interactions on autonomic, behavioral, and antinociceptive measures in chronic spinal dogs. Pentazocine (0.31-5 mg/kg, IV) produced miosis, hypothermia and antinociception which was mediated by spinal and supraspinal reflexes; these effects were antagonized by naltrexone. Tripelennamine (0.63-2.5 mg/kg, IV) elicited mydriasis, hyperthermia and antinociception; these effects were not blocked by naltrexone. Tripelennamine produced antinociception only on the supraspinally-mediated skin twitch reflex. Interactions between pentazocine and tripelennamine varied depending on the response measured. Effects of both drugs on pupils were additive. Temperature effects were infra-additive, with the hyperthermic effects of tripelennamine predominating over the pentazocine hypothermia, resulting in a complete physiologic antagonism of pentazocine hypothermia. Antinociception, measured by flexor reflex depression, represented only the effect of pentazocine, whereas skin twitch reflex antinociception reflected either infra-additive or additive properties. The coadministration of nonconvulsive doses of pentazocine and tripelennamine produced seizures indicating a potentiated adverse interaction. In summary, the patterns of the pentazocine-triplennamine interactions were complex and the effects of tripelennamine could not be attributed to opioid activity.
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PMID:Interactions between pentazocine and tripelennamine on autonomic and nociceptive measures in the dog. 278 Jul 81

Effects of lisuride, a central dopamine and serotonin agonist of the ergot type, in animal models of depression were investigated in comparison with those of desipramine, mianserin and rolipram. Lisuride, like desipramine and mianserin, inhibited reserpine-induced hypothermia in mice (0.5-5.0 mg/kg, i.p.) and suppressed muricide in olfactory bulbectomized rats (ED50 = 0.16 mg/kg, i.p.) in a dose-dependent manner. The anti-muricidal effect was slightly enhanced by the repeated administration of 0.25 mg/kg lisuride. Lisuride (0.05-0.25 mg/kg, i.p.), like desipramine, dose-dependently reduced the duration of immobility in rats forced to swim, and this effect was antagonized by haloperidol. The reduction of immobility time was enhanced by the repeated administration of lisuride; at the same time, the ambulation in rats increased. Furthermore, the immobility-reducing effects of desipramine and rolipram were markedly enhanced by the co-administration of a low dose of lisuride (0.025 mg/kg, i.p.), which by itself had no effect on the immobility time. These results indicate that lisuride may be useful for the treatment of depression and indicate that a low dose of lisuride may enhance the clinical effectiveness of antidepressants such as desipramine.
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PMID:[Effects in animal models of depression of lisuride alone and upon coadministration with antidepressants]. 279 64


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