Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphine blocking and anticonvulsant effects of propranolol were investigated in mice. Three different convulsant procedures (electroshock, pentylenetetrazol and thebaine) were used. In addition, LD50's of morphine after different doses of propranolol were done. Sotalol was used as a control drug to check which of the effects of propranolol could be regarded as due to beta blockade. Morphine LD50 in mice is not altered by pre-treatment with propranolol. The anticonvulsant characteristics of propranolol are different from those of sotalol, the former acting mainly on the tonic phase of the seizures. This study does not support the hypothesis that propranolol is a morphine antagonist but reinforces the idea that propranolol has definite central nervous system effects.
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PMID:Propranolol and morphine. 18 41

The effect of acute administration of morphine on cerebral excitability was investigated in rats with two convulsant drugs: flurothyl (hexafluorodiethyl ether) and pentylenetetrazol (PTZ). In the flurothyl study, adult male Sprague-Dawley (S-D) rats were injected subcutaneously with morphine sulfate in doses ranging from 0.5 to 256 mg/kg. At 15, 30, 60 and 120 minutes after morphine injection, flurothyl was administered by inhalation and the seizure thresholds were determined. In the PTZ study, 64 mg/kg of morphine sulfate were injected subcutaneously into both S-D and CFN (Wistar-derived) rats. Thresholds to PTZ seizures were measured after administering the convulsant either by the intraperitoneal or intravenous route. The data revealed an anticonvulsant action of morphine on both flurothyl and PTZ. Peak time for this effect on flurothyl seizures was 30 minutes after subcutaneous administration of the opiate, with the maximal anticonvulsant activity appearing at the 64-mg/kg dose. The increase in seizure threshold in S-D rats at this dose was 36% with flurothyl, 94% with intravenous PTZ and 352% with i.p. PTZ. Morphine had a less dramatic influence on raising the latter seizure threshold in the CFN than in the S-D strain. The graded dose-related anticonvulsant action is independent of the respiratory depression associated with morphine administration and appears to be a reflection of an altered central nervous system excitability produced by the narcotic in rats.
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PMID:Anticonvulsant action of acute morphine administration in rats. 97 66

The influence of 6-hydroxydopamine on morphine-induced convulsions were investigated in rats. Morphine, in doses up to 100 mg/kg did not produce any convulsive pattern in vehicle-pretreated rats. The pretreatment of rats by 6-hydroxydopamine strongly potentiated the seizure producing activity of morphine and the dose-response curve of seizure severity shifted to the right. These results suggest that brain catecholamines are involved in the mechanism of morphine-induced convulsions.
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PMID:Potentiation of morphine-induced seizure by 6-hydroxydopamine. 99 11

1 Morphine (1-200 mg/kg s.c.) reduced the incidence and prolonged the latency of priming-induced audiogenic siezures in a dose-dependent manner. 2 This effect was reversed by naloxone (1 and 2 mg/kg) although naloxone was itself inactive. 3 This priming-induces seizure model may be useful in the study of tolerance and physical dependence.
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PMID:Effect of morphine and naloxone on priming-induced audiogenic seizures in BALB/c mice. 100 Jan 29

Opioid agonists were used to investigate the modulation of seizures in the seizure-susceptible El mouse. Morphine and D-Ala2-D-Leu5-enkephalin (DADLE) were injected subcutaneously or intracisternally as prototypic agonists for mu and delta opioid receptors. Systemic or intracisternal injection of both morphine and DADLE decreased the incidence of seizures and the seizure score in El mice in a dose-dependent manner. The anticonvulsant effects of morphine and DADLE were reversed by naloxone (2 mg/kg, s.c.). This implies that opioid agonists have anticonvulsant properties which are mediated by mu and delta opioid receptors. In conclusion, a deficit in endogenous opioid peptides, which act as anticonvulsants may play a significant role in the etiology or pathophysiology of seizures in the El mouse.
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PMID:Effects of morphine and D-Ala2-D-Leu5-enkephalin in the seizure-susceptible El mouse. 132 4

In the present study, we examined the clonic seizure immediately preceding head-weaving behaviour elicited by 8-OH-DPAT (40 mg/kg, ip) administration in mice. 8-OH-DPAT, known to be a central 5-HT1A receptor agonist, can induce a clonic seizure. Propranolol (1, 5, 10 mg/kg, ip) and methysergide (10, 20 mg/kg, ip) reduced 8-OH-DPAT (40 mg/kg, ip)-induced head-weaving behaviour and clonic seizure, while ketanserin (125, 250, 500 micrograms/kg, ip) was without effect. Trimethadione (500 mg/kg, sc) and phenobarbital (70 mg/kg, sc) completely inhibited clonic seizure and partially inhibited the head-weaving behaviour. Morphine (50 mg/kg, sc) completely inhibited both 8-OH-DPAT-induced head-weaving behaviour and clonic seizure. These effects of morphine are naloxone (20 mg/kg, sc)-reversible. These results suggest that the clonic seizure immediately preceding head-weaving behaviour elicited by 8-OH-DPAT is mediated mainly by serotonergic receptor 1A and also by additional factors.
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PMID:[8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT)-induced clonic seizure in mice]. 183 45

Operative and postoperative analgesia has become in a few years a major concern for pediatric anesthesiologists. The fact that pain can have dramatic metabolic and hemodynamic consequences has been well documented. This study shows the activity in our department in the field of analgesia during 1989. 82% of the 2,675 children having undergone surgery have received analgesia during the operative period either by the way of an i.v. narcotic or an regional block. No morbidity or mortality resulted from these techniques during the operative period. When a regional block was prolonged by the mean of a catheter, there were no major complication (2 seizures). The use of oral, rectal and i.v. analgesics follows the classic recommendations. Morphine by all routes of administration is used increasingly in our department. Two moderate respiratory depressions occurred in 1989 due to error in dosage with no consequence for the child. The authors underline the importance of well established protocols which have been discussed and approved by all, the importance of emergency procedures and treatment, which only can guaranteed the necessary safety.
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PMID:[Intraoperative and postoperative analgesia in pediatric surgery. 1 years' experience]. 209 46

D-Tyr-Ser-Gly-Phe-Leu-Thr (DSLET), beta-endorphin, morphiceptin and morphine were microinjected at 48-h intervals into the amygdala or hippocampus of awake rats in an attempt to identify the opiate receptor types involved in opioid kindling. DSLET, beta-endorphin, morphiceptin and morphine were injected into the lateral ventricle to assess the possibility of kindling seizures by this route. The delta-receptor agonist DSLET effectively kindled convulsions when microinjected into amygdala or ventral hippocampus. The convulsions were suppressed or strongly attenuated by ICI 174,864, a specific antagonist of the delta-receptor, microinjected into the same brain site, but were not affected by ICI 174,864 administered peripherally. When microinjected into amygdala or hippocampus, beta-endorphin and morphiceptin also kindled convulsions, which were antagonized by naloxone but not by ICI 174,864. Morphine evoked EEG epileptiform activity but did not kindle convulsions from limbic brain sites. DSLET occasionally evoked epileptiform spiking and submaximal convulsions when injected into ventricle, and morphiceptin evoked epileptiform spiking only, but tolerance to these effects occurred after repetition of the injections. Thus, convulsions can be kindled by activation of either mu-, delta- or epsilon-receptors when opioids are injected directly into limbic tissue. However, the ability of these compounds to kindle seizures is markedly reduced when they are administered into ventricle. The striking differences between the present results and previous results obtained by peripheral or intraventricular administration of opioid peptides suggest that the route of administration, among other variables, is a crucial factor in assessing the epileptogenic properties of opioid peptides.
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PMID:Involvement of multiple opiate receptors in opioid kindling. 216 33

The specificity of the hypoglycemic response to the intrathecal (i.t.) administration of the naturally occurring (-)-enantiomer of morphine previously reported from our laboratory was studied in mice. (+)-Morphine HBr (50 micrograms) caused a behavioral syndrome (scratching, biting, seizures) comparable to that produced by (-)-morphine sulfate (50 micrograms), but did not cause hypoglycemia. Many opioids, at a dose of 50 micrograms i.t. in nonfasted mice, showed either a saline-like hyperglycemic response or no significant effect on blood glucose. (+)-Morphine, ketocyclazocine, U-50,488, (-)- and (+)-N-allyl-normetazocine, beta-endorphin, (-)- and (+)-naloxone and naltrexone caused hyperglycemia. Significant changes from basal blood glucose were not produced by [D-Pen2, L-Pen5]-enkephalin, [D-Ser2]-Leu-enkephalin-Thr or sufentanil in 50-micrograms doses, or by codeine (300 micrograms), levorphanol (400 micrograms) or methadone (200-400 micrograms). Agonists which produced both hypoglycemic and behavioral effects were, in order of decreasing potency, hydromorphone greater than normorphine greater than morphine greater than 6-acetylmorphine greater than oxymorphone much greater than heroin. Morphine-induced hypoglycemia was partially antagonized by the i.t. coadministration of naloxone methobromide (10 micrograms). Fasting for 24 hr increased the sensitivity to hypoglycemic and lethal effects of morphine. D-Ala2-N-Me-Phe4-Gly5-ol]-enkephalin (5-50 micrograms i.t.) tended to decrease blood glucose in both nonfasted and fasted mice, but these effects were moderate and appeared to be unrelated to dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoglycemia induced by intrathecal opioids in mice: stereospecificity, drug specificity and effect of fasting. 235 29

To characterize further the hypoglycemic effect of intrathecally (i.t.) administered morphine, species and drug specificity, effects of morphine-induced tolerance and pentobarbital-induced anesthesia and effects on liver glycogen were studied in nonfasted animals. In rats, morphine (125 micrograms i.t.) produced the same behavioral toxicity (scratching, biting, seizures) and hypoglycemia as previously reported in mice. In mice, the glycine antagonist strychnine (5 micrograms i.t.) and the morphine metabolite morphine-3-glucuronide (2 micrograms i.t.) mimicked the behavioral, but not the hypoglycemic, effects of high-dose i.t. morphine. Kainic acid (0.1 micrograms i.t.), which caused high-frequency hindlimb movements, also did not cause hypoglycemia. Naltrexone (1 mg/kg/ s.c.) or the s.c. implantation of morphine pellets for 3 days attenuated the hypoglycemic effect, but not the behavioral effects, of morphine (40 micrograms i.t.). The hyperglycemic effect of s.c. morphine(20 mg/kg) was blocked by i.t. morphine. Anesthesia with pentobarbital (75 mg/kg i.p.) attenuated the hypoglycemic effect of morphine (40 micrograms i.t.). Morphine i.t. also caused a time- and dose-dependent decrease in liver glycogen levels and was more potent in causing glycogenolysis (30 min ED50 = 19 micrograms) than in causing hypoglycemia (30 min ED50 = 30 micrograms). It is concluded that the hypoglycemic effect of i.t. morphine appears to be independent of its behavioral effects, displays tolerance and is accompanied by hepatic glycogen depletion.
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PMID:Studies on the mechanism of hypoglycemia induced by intrathecal morphine: dissociation from behavioral effects, effects of tolerance and depletion of liver glycogen. 273 44


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