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PubMed1982

Hepatic glutathione and hepatotoxicity: changes induced by selected narcotics.

Propoxyphene and morphine lowered hepatic glutathione and increased serum glutamic-pyruvic transaminase (SGPT) activity when administered to male mice. Maximal changes were seen at 3 to 6 hr after administration, but the effects lasted for as long as 18 hr. Morphine-induced hepatic changes potentiated both acetaminophen and cocaine-induced hepatotoxicity. Naltrexone, a narcotic antagonist, abolished the glutathione depletion produced by both propoxyphene and morphine, but did not alter the propoxyphene-induced elevations of SGPT. Naltrexone also was tested against other narcotic agonists we have previously demonstrated to be hepatotoxic. Naltrexone pretreatment of antagonized L-alpha-acetylmethadol (LAAM)-induced depletion of glutathione and elevations of SGPT. Similarly, naltrexone antagonized norLAAM-induced depletion of glutathione and elevations of SGPT, but only lessened the magnitude of the changes induced by SKF525-A. The narcotic agonists morphine, LAAM, norLAAM and propoxyphene lower hepatic glutathione and induce hepatocellular damage, but these two effects appear to be unrelated.

Acetaminophen↗
PubMed1981

Intrauterine exposure to narcotics and cord blood prolactin concentrations.

Umbilical cord serum prolactin concentrations were determined in 17 full-term infants of mothers using narcotic agents during pregnancy and in 18 infants of similar birth weight and gestational age whose mothers did not use narcotics. The median value for the narcotic-exposed group was 266.6 ng/ml (range, 157.5 to 448.7 ng/ml); in the normal group the median was 193.7 ng/ml (range, 69.8 to 693.1 ng/ml). These differences were statistically significant (P less than .05). Although only full-term and borderline premature infants who were not appreciable risk for respiratory distress syndrome (RDS) were studied, it may be speculated that elevated prolactin blood levels in fetuses of addicted mothers may at least in part explain the reported decrease in the incidence of RDS in this group.

Birth Weight↗
PubMed1981

Narcotic effects on phenol red disposition in mice.

Morphine administration reduces phenol red clearance in mice. Increasing subcutaneous morphine doses from 10 to 40 mg/kg caused a progressive increase in plasma phenol red concentrations and reduced dye elimination in urine. Intravenous phenol red given at 50 to 200 mg/kg was cleared from plasma at 24 to 30 microliters/min/kg b. wt. At these dosages of dye plasma clearance of phenol red was reduced at least 33% by morphine pretreatment (20 mg/kg s.c.). Lowered dye clearance by morphine was reflected in smaller apparent volumes of phenol red distribution. The morphine effect on the elimination constant (kel) of phenol red was variable. The narcotic caused a rise in kel at the lowest phenol red dose and lowered this constant at the high phenol red dose. Like morphine, hydromorphone and methadone had an antidiuretic effect in mice and reduced renal elimination of phenol red. Naloxone had no effect on phenol red disposition but reversed completely the effect of morphine. This finding shows that the effect of the narcotic was not due to competition or displacement from transport sites. Morphine did not cause a change in urine pH. Since the urine did not become more acidic after morphine, back diffusion of undissociated due is not likely as the cause of its reduced renal elimination. Reduced renal elimination of phenol red by narcotics is probably due to reduced renal blood flow and glomerular filtration as shown by lowered p-aminohippurate and iothalamate clearance in mice.

Animals↗
PubMed1977

Effects of alpha-methyl-p-tyrosine, adrenolytic compounds, pimozide and other neuroleptics, on the narcotic cue.

Using a two-lever food-reinforced operant procedure, rats (n=11) were trained to discriminate the narcotic analgesic fentanyl (0.04 mg/kg, s.c.) from saline. In rats so trained, alpha methyl-p-tyrosine (150 mg/kg, i.p.) was found not to affect the discriminability of fentanyl. Pretreatment (s.c.) with either adrenolytic compounds (10 mg/kg aceperone, 40 mg/kg dibenamine, 10 mg/kg phenoxybenzamine, 20 mg/kg propranolol) or sedative neuroleptics (0.63 mg/kg azaperone, 1.25 mg/kg chlorpromazine, 10 mg/kg pipamperone) likewise failed to attenuate the narcotic cue. Pimozide (0.63 mg/kg) and, to some extent, spiperone (0.04 mg/kg) reduced the percentage of responding on the selected lever, and pimozide antagonized drug lever selection in some animals. The results suggest that specific neuroleptics (e.g. pimozide) may affect the subjective effects induced by narcotics in humans.

Animals↗
PubMed1993

Management of minor adverse effects encountered during narcotic administration.

Presented are four clinical scenarios of patients receiving narcotics to control pain of various etiologies. In all cases minor adverse effects necessitated intervention so that continued use of these agents was possible. The four cases illustrate common adverse effects, including nausea, vomiting, pruritus, and dysphoria, that may occur during narcotic administration. Management strategies to deal with these and other common non-life-threatening effects of narcotic agents are presented.

Adult↗
PubMed1996

The role of specific eicosanoids in mediating the acute narcotic effects of ethanol.

The pharmacological effects of ethanol may be in part due to increased membrane fluidity, resulting in increased phospholipase A2 activity and the subsequent conversion of released arachidonic acid (AA) into pharmacologically relevant eicosanoids (prostaglandins/leukotrienes). A significant correlation between the in vivo and in vitro potency of prostaglandin synthetase (PES) inhibitors to antagonize PES activity and their ability to antagonize the acute narcotic and rate-depressant effects of ethanol support this hypothesis. However, inhibition of PES not only decreases the production of at least five prostaglandins and thromboxane but may shunt free AA into the lipoxygenase cascade with subsequent formation of leukotrienes. The purpose of the present study was to systematically investigate numerous points in the AA cascade to determine the eicosanoid products relevant to the acute narcotic effects of ethanol. Ethanol-induced loss of the righting reflex in mice was used as the behavioral endpoint. The relative importance of PES metabolites vs. lipoxygenase metabolites was determined via administration of specific enzyme inhibitors (phospholipase, lipoxygenase and dual PES/lipoxygenase inhibitors) and receptor agonists/antagonists (prostaglandin and leukotriene). Pretreatment with specific lipoxygenase inhibitors, dual PES/lipoxygenase inhibitors and leukotriene antagonists suggest a negligible role for lipoxygenase metabolites in acute ethanol-induced narcosis. Pretreatment with prostaglandin agonists and antagonists suggest a significant role for prostaglandin E (PGE) and a minor role for prostaglandin D in mediating the acute effects of ethanol. The PGE agonist 16,16-dimethyl PGE significantly enhanced the narcotic effects of ethanol (> 400%), whereas the prostaglandin receptor antagonist L-640,035 significantly decreased the effects of ethanol (-54%). These results further support the hypothesis that eicosanoid formation is important in the biochemical and behavioral effects of ethanol.

Animals↗
PubMed1997

Intrathecal narcotics for labor analgesia.

Intrathecal narcotics are a relatively recent addition to the list of analgesic options that are available for the management of labor pain. Pain during the first stage of labor is related to repetitive uterine contractions and resultant cervical dilatation, while pain during the second stage is due to stretching of the perineum. Traditionally, continuous epidural analgesia has been used as the reference standard for providing comfort during labor. Intrathecal narcotics represent a safe and effective alternative that provides significant, rapid relief of labor pain during the first stage of labor. The drugs most often used for intrathecal administration include sufentanil, fentanyl, meperidine and morphine. Use of intrathecal narcotics does not significantly affect the natural progression of labor, and no adverse fetal outcomes have been reported.

Analgesia, Obstetrical↗
PubMed1998

[Drug and narcotic use among Danish drivers].

An investigation was made of the presence of drugs and narcotics in samples from Danish drivers having violated the Danish Road Traffic act in 1993. Four hundred and twenty-five cases were received, but only 317 cases were analysed for drugs or narcotics. In 256 cases drugs or narcotics were found present with a total of 531 findings. In 112 of the cases only one compound was found present. Benzodiazepines, morphine, methadone, cannabinoids and amphetamine were the most frequently occurring compounds with 239, 52, 42, 32 and 28 findings, respectively. The study has shown that especially the benzodiazepines together with the illicit drugs seem to constitute a threat to traffic safety. For two countries very much alike, namely Denmark and Norway this study has shown a remarkable difference in the number of samples analysed and the results found.

Adult↗
PubMed1986

Narcotic withdrawal syndrome in young adults after the therapeutic use of opiates.

Five young adults with malignant neoplasms developed symptoms of narcotic withdrawal six to 48 hours after the abrupt discontinuation of narcotic therapy that had been administered for six to 21 days. The symptoms, which included agitation, irritability, muscular jerks, abdominal pain, diarrhea, burning sensations, "gooseflesh," and itching, rapidly resolved when narcotic therapy was reinstituted. Four patients were then successfully weaned from opiates without recurrence of their withdrawal symptoms; the fifth patient continues to receive methadone hydrochloride treatment for continuing pain.

Adolescent↗
PubMed1994

Gender and ethnic stereotyping and narcotic analgesic administration.

The purpose of this study was to investigate whether nurses provide different amounts of narcotic analgesics to male and female patients, and different amounts to white and ethnic minority patients. A retrospective survey was conducted with the medical records of 101 male and 79 female uncomplicated adult appendectomy patients, 40 of whom were ethnic minority members. Narcotic analgesic doses for the entire postoperative period were converted to equianalgesic doses comparable to intramuscular morphine. Male patients received significantly larger initial doses than female patients. There was no gender difference in the total dose received postoperatively. White patients received significantly more total postoperative narcotic analgesics than ethnic minority patients. The gender difference provides modest external validation for prior experimental results. The ethnic difference suggests that irrelevant cues may be used in nurses' medication decisions.

Adolescent↗
PubMed1987

Postoperative paraplegia associated with epidural narcotic administration.

Epidural injections of buprenorphine were given for postoperative pain relief to a patient with pulmonary carcinoma who underwent a right upper lobectomy. Paraplegia occurred postoperatively and the patient's neurological status deteriorated after each injection of epidural narcotic. Laminectomies on the third postoperative day revealed an expanded oxidized cellulose (Oxycel) pledget in the epidural space. Neurologic dysfunction after epidural narcotic administration was caused by the oxidized cellulose which had migrated into the epidural space following use for surgical haemostasis and subsequently expanded with the narcotic solution and blood.

Aged↗
PubMed1998

Quantitative structure-activity relationships and volume fraction analysis for nonpolar narcotic chemicals to the australian cladoceran ceriodaphnia cf. dubia

The toxicity of eleven nonpolar narcotic chemicals to the cladoceran Ceriodaphnia cf. dubia was determined. C. cf. dubia was found to be approximately four times more sensitive to these narcotic chemicals than Daphnia magna tested under virtually identical conditions. The toxicity data were also used to develop and validate quantitative structure-activity relationships (QSARs) using a range of physicochemical properties of the chemicals. The three best QSARs, based on octanol-water partition coefficients and two lipid-water partition coefficients, were able to explain 98% of the variation in toxicity. The mean absolute percentage errors between the predicted and experimental EC50 values for these three QSARs were 17.3%, 20.6%, 24.6%. Neither the critical concentration (CC) nor the critical volume (CV) hypotheses validly modeled the toxicity data when octanol-water and triolein-water partition coefficients were used although the CV hypothesis was the better of the two. When a phospholipid-water partition coefficient was used the CV hypothesis was valid. The mean toxic membrane volume fraction of 0.48 x 10(-2) m3/m3 derived in this study agreed with published values for nonpolar narcotics and supports the use of this property to determine the mode of action of chemicals.

Journal Article↗
PubMed1986

Brain stem mucormycosis in a narcotic addict with eventual recovery.

In addition to the well-known infectious complications of intravenous narcotic abuse, a much rarer and more recently recognized association between intravenous narcotic addiction and mucormycotic abscesses of the central nervous system has been described. Only four cases have been cited in the literature, with a mortality rate of 100 percent in this group. This report describes a narcotic abuser who presented with obstructive hydrocephalus and a mucormycotic abscess of the brain stem, and recovered. Central nervous system mucormycosis should be included in the differential diagnosis of drug abusers who present with a rapid deterioration in neurologic status.

Adult↗
PubMed1978

Behavioral and physiological studies of non-narcotic analgesia in the rat elicited by certain environmental stimuli.

These experiments characterized the analgesia resulting from exposure to certain noxious and/or stressful manipulations. Rats exposed either to electric grid shock (0.35-2.0 mA for 10-30 sec) or to 5 min of presumably non-painful centrifugal rotation (about 7.0 transverse g's) were analgesic as measured by tail-flick, hot plate and responses to applications of a calibrated paw pinch or alligator clip. Analgesia produced by shock (SA) or centrifugal rotation (RA) persisted after termination of these manipulations. Neither SA nor RA were attended by generalized sensory, attentional or motoric deficits. Intraperitoneal injection of hypertonic saline also increased tail-flick latencies. Exposure to brief ether anesthesia or horizontal oscillation, both of which have been reported to increase ACTH secretion (a commonly used indicator of stress), did not produce analgesia as measured by the tail-flick test. The use of classical conditioning procedures to pair shock with environmental stimuli resulted in increased tail-flick latencies. The narcotic antagonist naloxone (1 mg/kg, i.p.) did not reduce the tail-flick inhibition produced by shock, rotation, hypertonic saline or classical conditioning. Chlordiazepoxide (5 mg/kg, i.p.) also failed to antagonize the increased tail-flick latencies produced by shock or conditioning. Tail-flick inhibition produced by shock or rotation was markedly reduced by complete spinal cord transection at thoracic levels. These results suggest that: (1) the selective modulation of nociceptive input at the level of the spinal cord can be mediated by a supraspinal system or systems physiologically distinct from those involved in analgesia produced by the administration of opiates; (2) non-narcotic modulation of nociceptive input occurring within the spinal cord can be learned by exposure to classical conditioning procedures; and (3) noxious stimuli are sufficient but not necessary to produce a non-narcotic analgesia; stress alone, however, is not always sufficient to produce this analgesia.

Analgesia↗
PubMed1979

Inhibition of spinal cord interneurons by narcotic microinjection and focal electrical stimulation in the periaqueductal central gray matter.

Single cell evoked activity was recorded from spinal cord interneurons in rats prepared with microinjection cannulae or stimulating electrodes in the periaqueductal central gray matter (PAG). Morphine microinjections (4-16 microgram) inhibited the response evoked by a noxious stimulus in 55% of the wide dynamic range neurons tested. Microinjections of etorphine (0.25-0.5 microgram) inhibited 82% of the nociceptive neurons tested. Neither drug inhibited neurons which responded only to innocuous mechanical stimulation. The inhibition of wide dynamic range neurons produced by narcotic microinjection was antagonized by naloxone (1 mg/kg, i.p.) in 7 of 11 cases. Control experiments indicated that the effects obtained with microinjections could not be attributed to the drugs' diffusion to the spinal cord. Focal electrical stimulation of the PAG inhibited the responses to noxious stimuli of 60% of wide dynamic range neurons but was without effect on the responses of neurons that were activated only by innocuous stimuli. These experiments directly demonstrate that narcotic analgesics restricted to an intracerebral site of action activate a neural system which preferentially inhibits the responses of spinal cord wide dynamic range neurons to noxious stimuli. The system has a specificity for nociceptive input since non-nociceptive neurons were unaffected. Directly comparable results were produced by electrical stimulation of the PAG, supporting the concept that stimulation and narcotics modulate the transmission of nociceptive information by similar mechanisms.

Animals↗
PubMed1978

The role of the corpus striatum in neuroleptic- and narcotic-induced catalepsy.

Lesion experiments (in the rat) were designed to elucidate the function of the corpus striatum in neuroleptic- and narcotic-induced catalepsy, respectively. Bilateral lesions of the corpus striatum were observed to attenuate neuroleptic (CPZ)-induced catalepsy. However, analogous lesions of the corpus striatum potentiated narcotic (morphine)-induced catalepsy. These results suggests that (a) the corpus striatum may be a primary site of action of neuroleptic drugs (such as CPZ) in the production of catalepsy, and (b) narcotic (morphine)-induced catalepsy may not be exclusively mediated by the corpus striatum.

Animals↗
PubMed1994

Constitutive mu opioid receptor activation as a regulatory mechanism underlying narcotic tolerance and dependence.

Chronic administration of narcotic mu opioid agonists results in tolerance and dependence. We propose that agonist stimulation causes a gradual conversion of mu receptors to a constitutively active state (mu*) as a key step in tolerance and physical dependence. We provide evidence in support of the existence of mu* in human neuroblastoma cells, SH-SY5Y, and mu* upregulation during morphine treatment. Naloxone blocked mu* activity, acting as an antagonist with negative intrinsic activity which accounts for its high potency in eliciting withdrawal. In contrast, the mu selective antagonist CTAP did not affect mu* activity but inhibited naloxone's effect. The protein kinase inhibitor H7 was found to suppress mu* formation, suggesting that mu* is phosphorylated. In a model of acute morphine tolerance/dependence in mice, H7 prevented naloxone induced withdrawal jumping and reversed morphine (antinociceptive) tolerance. CTAP caused only mild withdrawal and attenuated naloxone induced withdrawal, as predicted for an antagonist without negative activity. These results support a role for constitutive mu receptor activation in narcotic tolerance and dependence, affording potential separation of acute and chronic narcotic effects.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Narcotic-induced suppression of natural killer cell activity in ventilated and nonventilated rats.

Surgical stress and general anesthesia can suppress immune function and thus may increase postsurgical infections and tumor metastasis. We previously reported that two narcotics commonly used in high-dose opiate anesthesia (fentanyl and sufentanil) suppress natural killer (NK) cell activity in rats. Such doses of narcotics also cause respiratory depression accompanied by hypoxia, hypercarbia, and acidosis, which might account for the observed narcotic-induced NK suppression. In the present study, we compared the effects of fentanyl on NK activity in ventilated and non-ventilated rats. Fentanyl significantly suppressed NK cell activity to the same magnitude in the two groups, although the groups significantly differed in CO2 and O2 levels. The fact that high-dose fentanyl-induced NK suppression can be demonstrated in ventilated rats accentuates the relevance of these findings to clinical studies showing NK suppression in the immediate postoperative period. Such immunosuppression could be a risk factor for patients undergoing surgery, especially in cancer-related operations.

Animals↗