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At least 1,621 records · Page 90Linked to original sources
PubMed1983

Narcotics and spasm of the sphincter of Oddi. A retrospective study of operative cholangiograms.

The operative cholangiograms of 112 patients undergoing elective cholecystectomy were reviewed independently and retrospectively by two radiologists who were not aware of the anaesthetic technique used. Fifty four patients who received opioid drugs either pre- and/or intra-operatively comprised one study group whilst 58 patients who received no opioids comprised the other. Spasm of the sphincter of Oddi was observed in two patients in the opioid group and in one patient in the non-opioid group. The use of opioid drugs as part of the anaesthetic management for cholecystectomy did not appear to interfere with the radiological interpretation of operative cholangiography nor to increase the low incidence of spasm of the sphincter of Oddi.

Adolescent↗
PubMed1979

Pharmacological and clinical importance of narcotic antagonists and mixed antagonists--use in cardiology.

1 The treatment of pain of cardiac origin requires a knowledge of the haemodynamic action of the analgesic agents used. 2 The haemodynamic effects of morphine, diamorphine, pavaveretum, pethidine and pentazocine are reviewed. 3 Clinical experience with the new antagonist analgesic buprenorphine is reported. 4 These studies indicate that buprenorphine may be the agent of choice for the relief of severe pain in patients with unstable circulation.

Buprenorphine↗
PubMed1990

The respiratory effects of reversing midazolam sedation with flumazenil in the presence or absence of narcotics.

The purpose of this study was to determine the effects of reversal of sedation with flumazenil (F), in the presence or absence of opiates, on arterial oxygen saturation (SaO2) and end-tidal CO2 (ETCO2). Twenty-four patients undergoing surgery and epidural anaesthesia were studied. Twelve patients (Group A) were orally premedicated with diazepam and 0.1 mg.kg-1 morphine i.m. Intraoperative sedation consisted of midazolam 0.1 mg.kg-1 and pethidine 0.7 mg.kg-1 i.v. Twelve patients (Group B) were premedicated with diazepam and sedated intraoperatively with 0.1 mg.kg-1 midazolam. In the recovery room, six patients in each group were randomly allocated to receive 1 mg of flumazenil while the others were allowed to awaken spontaneously (control). Sedation (eyes open vs closed), SaO2, ETCO2, respiratory rate, blood pressure and pulse were non-invasively monitored for 90 min. Administration of flumazenil resulted in a statistically significant increase in the number of patients with eyes open in both groups at 5 min, lasting 15 min in Group A and 30 min in Group B patients. An increase in SaO2 from 15-45 min after injection of flumazenil was observed only in Group B. No significant difference between groups in any other parameter was found. We concluded that reversal of benzodiazepine (BZ) sedation with flumazenil improved SaO2 in patients sedated with only BZ; in the presence of BZ and opiates, flumazenil did not affect respiratory parameters.

Anesthesia, Epidural↗
PubMed1976

The effects of narcotics on fetal acid base status.

This paper reports two randomized control trials on the effects of nalorphine, pethidine, morphine and heroin on fetal and maternal acid base status. The drugs decreased pH and increased pCO2 in the mother, and decreased pH and base excess in the fetus. The changes in the fetus were independent of the changes in the mother. In equivalent dosages, nalorphine increased maternal pCO2 more than pethidine and morphine. The effects of heroin were found to be greater than that of other drugs, and we suggest that heroin should be avoided where the fetus is already at risk.

Acid-Base Equilibrium↗
PubMed1975

Effect of morphine on adrenergic transmission in the mouse vas deferens. Assessment of agonist and antogonist potencies of narcotic analgesics.

1. Morphine inhibits the electrically evoked (0.1-0.15 Hz, 1 ms) contractions of the longitudinal muscle of the mouse vas deferens but not of the rabbit, guinea-pig, rat, cat, hamster or gerbil. This effect is stereospecific and is antagonized by naloxone or naltrexone. 2. Normorphine is equiactive with morphine but its effects are more rapid in onset and decline. 3. In the mouse vas deferens, the resting outflow of tritium-labelled catecholamines is unaffected by morphine. The electrically evoked outflow is depressed by morphine or normorphine in a dose-dependent manner. The ID50 for inhibition of contraction and for depression of outflow is 0.5 muM. 4. The relative agonist potencies of compounds without antagonist component (codeine, pethidine, morphine, normorphine, heroin, levorphanol, Ba-20227, etorphine) show good correlation with the relative agonist potencies determined in the guinea-pig ileum and for analgesia in man. 5. For compounds with dual agonist and antagonist properties, the dose-response curves for agonist activity are shallow. When the lowest concentrations giving a depression of the contraction of the mouse vas deferens are used, a good correlation is obtained with the guinea-pig ileum. 6. The relative antagonist potencies of naloxone, nalorphine, levallorphan, and cyclazocine agree well with those obtained in the guinea-pig ileum; these, in turn, correlate well with the values obtained in the morphine-dependent monkey. 7. The fact that the agonist effects of drugs with dual agonist and antagonist action show little or no dependence on concentration, makes the mouse vas deferens particularly suitable for the assay of assay of antagonist activity. 8. As an assay preparation, the mouse vas deferens is less robust and consistent in its responses than the guinea-pig ileum.

Analgesics, Opioid↗
PubMed1983

Stereospecific enhancement of evoked release of brain acetylcholine by narcotic antagonists.

1--Electrical stimulation of nerves in the forepaw of anaesthetized rats caused an increase in the release of acetylcholine (ACh) from the cerebral cortex in vivo. Actions of naloxone (Nal) enantiomers and naltrexone (Ntx) were tested on this release in normal animals and those lacking pituitary gland for 3 weeks. 2--In normal animals systemic administration of (-)-Nal or Ntx, but not (+)-Nal caused a significant increase in the evoked release of ACh. Spinally administered (-)-Nal did not produce this effect. Cortical application of (-)-Nal produced a smaller increase in the evoked release of ACh. 3--In hypophysectomized rats the stimulatory action of (-)-Nal or Ntx on ACh release was significantly reduced. The ability of (-)-Nal to reverse inhibitory action of morphine or the enkephalin (FK 33,824) was not affected by hypophysectomy. 4--It is suggested that (-)-Nal and Ntx increase the stimulated release of cortical ACh by blocking the inhibitory action of an endogenous opioid at a subcortical site. An intact pituitary appears essential for a full expression of the Nal effect on evoked ACh release.

Acetylcholine↗