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PubMed1975

Mechanism of action of narcotics in the production of menstrual dysfunction in women.

The ability of morphine to block ovulation in animals prompted investigation of the frequency and mechanisms of menstrual abnormalities in women addicted to narcotic analgesics. Menstrual histories obtained from 76 former heroin addicts receiving daily methadone maintenance revealed that more than one-half of these women had experienced menstrual abnormalities while taking heroin or methadone. In order to determine the specific physiologic effects of narcotic analgesics on reproductive function, detailed endocrinologic studies were carried out in seven of these patients who complained of amenorrhea or irregular menses while receiving methadone. Four of the seven women manifested abnormalities of the control of gonadotropin secretion. Three of these four failed to exhibit cyclic gonadotropin release, as evidenced by an absence of increased levels of follicular phase follicle-stimulating hormone, midcycle gonadotropin peaks or luteal phase progesterone increments. In the fourth patient a prolonged follicular phase (30 days) of the menstrual cycle was detected. One of these four patients also had low basal gonadotropin levels and failed to exhibit luteinizing hormone increments greater than control levels in response to ethinyl estradiol (positive feedback). The remaining three women exhibited normal patterns of gonadotropin secretion during the observation period. In these women, menstrual bleeding occurred in response to withdrawal from luteal phase (10 to 20 ng/ml) progesterone levels and to exogenous ethinyl estradiol, suggesting normal uterine responsivity to progesterone and estrogen. Although not documented, it is likely that oligo-ovulation was the cause of the irregular menses in these three patients. Amenorrhea is commonly associated with methadone ingestion or heroin addiction and appears to be related to an alteration of the hypothalamic mechanisms controlling gonadotropin secretion. Tolerance to these effects of methadone may develop after chronic ingestion.

Adult↗

PubMedDate not supplied

Review of drug abuse and measures to reduce the illicit demand for drugs by region. Division of Narcotic Drugs of the United Nations Secretariat.

This article, which was prepared on the basis of two documents (E/CN.7/1987/9 and E/1987/17-E/CN.7/1987/18) of the Commission on Narcotic Drugs, summarizes information on drug abuse and measures to reduce the illicit demand for drugs at the global level and by region. The Commission on Narcotic Drugs noted at its February 1987 session that the drug abuse situation continued to deteriorate in most parts of the world. The most striking feature of the problem was the escalation of heroin and cocaine abuse, but the abuse of other substances also continued to spread. The injection of drugs had contributed significantly to the increasing spread of acquired immunodeficiency syndrome (AIDS) and hepatitis B. The age of first users was falling from adolescence to preadolescence and even earlier. Young users were experimenting with a variety of substances, most often with those that were easy to obtain. In most countries, drug abuse had spread to all social strata. The majority of abusers were males, but the proportion of female abusers was growing.

Adolescent↗

PubMed1989

[Epidural anesthesia with a combination of narcotic analgesics and local anesthetics in the surgical treatment of arterial occlusion of the leg].

Comparative characteristics of epidural anesthesia with local anesthetics and a combination of the latter with narcotics in the reconstruction of arterial segments of lower extremities in 123 patients were given. The use of narcotics decreases the frequency of introduction of the drugs into the epidural space, does not induce persistent arterial hypotension and practically excludes different complications associated with epidural anesthesia.

Analgesics, Opioid↗

PubMed1989

[The brain catecholamine system in narcotic-dependent rats under the action of oxytocin].

Intraventricular injection of oxytocin exerted a selective effect on catecholamine metabolism in microchondrial fractions of different brain formations of normal and narcotic drug-dependent animals. The drug-dependent group showed a higher level of the brain catecholamines as compared to the controls, oxytocin decreasing the catecholamine level in this group. The oxytocin modulatory role in the processes of narcotic drug-dependence, is discussed.

Animals↗

PubMedDate not supplied

Risk appraisal of narcotic sedation for children.

Since the use of narcotics was initially advocated 28 years ago, serious adverse reactions, including fatalities, have been reported. At least four factors appear to contribute to these reactions: multiple drug administration, excessive dosage, inadequate monitoring, and ineffectual emergency care. Because of the relatively high incidence of life-threatening reactions and the complexity of the required emergency care, the routine use of pediatric sedation techniques that require large doses of narcotics cannot be advocated for use in the private office.

Alphaprodine↗

PubMed1986

Reducing postoperative pain, narcotics, and length of hospitalization.

Bupivacaine wound infiltration together with efficient esophagogastric decompression and immediate elemental feeding in 43 consecutive, well-instructed patients who had undergone cholecystectomy reduced their postoperative analgesia requirements to an average of 17 (+/- 46, SD) mg of meperidine during the initial 24 hours. No analgesics were requested by 35/43 patients (81%) and 40/43 were discharged within 24 hours of surgery. All 86 conventionally treated control patients required narcotics, averaging 4.4 (+/- 0.3, SD) doses and amounting to 290 (+/- 25, SD) mg of meperidine or its equivalent during their first postoperative day and were discharged in 6.5 (+/- 0.7, SD) days. None were discharged in less than 3 days. Home interview by a visiting nurse was carried out for a block of 19 treated patients and their families. Six patients were interviewed prospectively within 33 to 64 hours of surgery, with a repeat visit 1 to 2 months later. Retrospectively studied patients were only seen 1 to 4 months after surgery. These interviews confirmed the patients' and their families' satisfaction with their bodily functions, their limited discomfort, and their independence from the hospital. Wound infiltration with a long-acting local anesthetic, efficient removal of swallowed air, and immediate, full enteral nutrition contribute to reduced postoperative pain and narcotic use in well-instructed patients, thus leading to safe and satisfactory early discharge.

Adolescent↗

PubMed1987

Alfentanil hydrochloride: a new short-acting narcotic analgesic for surgical procedures.

The chemistry, pharmacology, pharmacokinetics, clinical use, adverse effects, dosage, and administration of the short-acting synthetic narcotic analgesic alfentanil hydrochloride are reviewed. Alfentanil is a tertiary amine with an ionization constant of 6.5, resulting in approximately 10% ionization at physiologic pH. When compared with fentanyl, alfentanil has a faster onset and one third the duration of action, one fourth to one tenth the potency, less lipid solubility, greater protein binding, and a much greater unionized fraction at physiologic pH. Alfentanil is approximately 20-40 times less potent than sufentanil on a weight basis, but it has a faster onset and shorter duration of action. After i.v. injection, alfentanil is distributed in the body according to a two- or three-compartment model. When given to young and middle-aged patients for various surgical procedures, alfentanil has an elimination half-life of 70-99 minutes independent of the dose or route of administration. Clinical studies comparing alfentanil with fentanyl in short surgical procedures are reported; alfentanil produces earlier peak analgesic effect, faster recovery of consciousness, and a more pronounced narcotic effect without increased adverse effects. When alfentanil was given in high doses for anesthesia induction, chest-wall rigidity occurred frequently. Like fentanyl, alfentanil was found to produce a high incidence of nausea and vomiting. It was more effective when administered by infusion than by bolus. Alfentanil is useful for supplementation of analgesia for outpatient surgical procedures, as an infusion for maintenance of anesthesia during surgery, and perhaps as an induction agent.

Alfentanil↗

PubMed1987

Transcutaneous electrical nerve stimulation for reducing narcotic use after cesarean section.

This study evaluated the potential efficacy of transcutaneous electrical nerve stimulation in reducing narcotic requirements following cesarean section. The total required dose of postoperative analgesic (meperidine) was found to be 511 mg in the experimental group and 456 mg in the control group. There was no significant difference in narcotic use or hospital stay between the experimental and control groups.

Adult↗

PubMedDate not supplied

[Influence of piracetam on the effects of narcotic analgesics and opioid peptides].

Piracetam possesses some properties not related to the nootropic activity. The purpose of the work was to study piracetam influence on effects of narcotic analgesics and opioid peptides at intracerebroventricular administration. In experiments on cats it was found that piracetam in a dose-dependent way prevented the emetic effect of morphine and leu-enkephalin. In experiments on rats (tail-flick test) piracetam was shown to be able of blocking the analgesic effect of fentanyl. Experiments on the study of the anticataleptogenic effect of piracetam also showed antagonism between piracetam and agonists of opioid receptors. Thus, it was shown on a number of models that piracetam exhibits antagonistic properties with respect of opioid peptides and narcotic analgesics.

Analgesics, Opioid↗

PubMed1988

Mivacurium chloride (BW B1090U)-induced neuromuscular blockade during nitrous oxide-isoflurane and nitrous oxide-narcotic anesthesia in adult surgical patients.

The neuromuscular and cardiovascular effects of mivacurium were studied in 90 adult patients during nitrous oxide-oxygen-isoflurane (n = 45, ISO group) and nitrous oxide-oxygen-narcotic (n = 45, BAL group) anesthesia. Neuromuscular blockade was measured using electromyographic activity of the adductor pollicis muscle after supramaximal stimulation of the ulnar nerve at 2 Hz for 2 seconds at 10-second intervals. To estimate dose-response relations, three subgroups of nine patients in the ISO group received mivacurium doses of 0.025, 0.03, and 0.04 mg/kg, respectively. Similarly, three subgroups of nine patients in the BAL group received mivacurium doses of 0.03, 0.04, and 0.05 mg/kg, respectively. The ED50 and ED95 of mivacurium in each group were estimated from linear regression plots of log dose vs probit of maximum percentage depression of neuromuscular function. The estimated ED50 values for the ISO and BAL groups were 0.029 and 0.041 mg/kg, respectively. The estimated ED95 values for the ISO and BAL groups were 0.045 and 0.058 mg/kg, respectively. Recovery indexes were measured in 26 patients who received ED95 or greater doses of mivacurium in either the ISO or BAL groups. The recovery index was shorter in the BAL group (5.5 +/- 1.6 minutes [n = 10]), than in the ISO group (7.4 +/- 3.0 minutes [n = 16]). The addition of isoflurane (0.5-0.75% end-tidal concentration) to nitrous oxide-narcotic anesthesia augments the degree of neuromuscular blockade from a given dose of mivacurium and also prolongs the recovery index.

Adult↗

PubMed1978

The effects of several narcotic analgesics on brain levels of 3-methoxy-4-hydroxyphenylethylene glycol sulfate in the rat.

The acute administration of levorphanol, morphine, anileridine, methadone, cyclazocine and pentazocine was found to increase brain levels of 3-methoxy-4-hydroxyphenylethylene glycol sulfate (MOPEG-SO4) in rats. Drug-induced increases in brain levels of this norepinephrine metabolite were dose-dependent and peak drug effects generally occurred 1 hr after intraperitoneal injection. Six to 8 hr after opiate agonist or partial agonist administration, MOEG-SO4 levels returned to control values or below. The narcotic effect appeared to be stereospecific, since high doses of d-methadone and dextrorphan produced either no change or only minimal increases in brain MOPEG-SO4 levels when compared with saline-treated controls. The relative potency of the analgesics tested in producing increases in brain MOPEG-SO4 levels appeared to correlate reasonably well with the ability of these drugs to produce other characteristic pharmacological effects. The drug-induced increases in brain MOPEG-SO4 levels were antagonized by naloxone. The rate of disappearance of MOPEG-SO4 from the brains of animals treated with pargyline was not decreased by the opiate agonists or partial agonists tested indicating that these drugs did not inhibit the acid transport process. These results indicate that the production of an increase in brain norepinephrine turnover is a specific component of the pharmacological actions of narcotic analgesics.

Analgesics, Opioid↗

PubMed1988

The use of electronarcosis as anaesthetic in the cichlid, Oreochromis mossambicus (Peters). II. The effects of changing physical and electrical parameters on the narcotizing ability of alternating current.

The effects of wave form, voltage, frequency and current as well as application time on the narcotizing ability of alternating current were investigated. A 60 Vrms, 50 Hz sine wave current applied for 30 s produced narcosis of sufficient duration to enable handling and blood sampling. A triangle wave form was inferior in narcotizing ability to both sine wave and square wave forms. Duration of narcosis increased with increasing water conductivity but was reduced by increasing water temperatures.

Animals↗

PubMed1986

Renal toxicity of non-narcotic analgesics. At-risk patients and prescribing applications.

Acute and chronic renal damage may occur with many analgesics. Acute effects on the kidney occur mainly with aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). One of the most obvious effects in healthy individuals is fluid retention which is thought to be mediated through inhibition of the renal effects of prostaglandins. Aspirin and NSAIDs also cause a decrease in glomerular filtration rate and renal blood flow and although these changes may occur in healthy individuals they are more pronounced in high renin states and in patients with pre-existing renal disease. Clinical syndromes associated with the renal effects of NSAIDs include oedema, acute renal failure and the nephrotic syndrome. Advanced age, dehydration, concurrent diuretic use and pre-existing renal disease are risk factors for these syndromes. Chronic effects of non-narcotic analgesics on the kidney were suspected before their acute effects became apparent. The key chronic renal lesion in the kidney attributed to prolonged ingestion of non-narcotic analgesics is renal papillary necrosis. The incidence of analgesic-associated renal papillary necrosis in different countries has generally paralleled the national regular use of analgesics. Although phenacetin was widely implicated as the cause of renal papillary necrosis, there is now increasing evidence that aspirin and other NSAIDs may cause renal papillary necrosis in patients who have not taken phenacetin. There is some evidence that this problem is reduced by legislative control of over-the-counter sales. Uroepithelial tumours have also been attributed to chronic abuse of analgesic mixtures. Such tumours are characterised by a reversal of the usual sex ratio, being more common in females.

Acute Kidney Injury↗

PubMed1986

Liver damage with non-narcotic analgesics.

Non-narcotic analgesics can produce a variety of hepatic lesions but clinically significant liver damage is uncommon with normal therapeutic use. The pattern of hepatotoxicity caused by the salicylates, non-steroidal anti-inflammatory drugs (NSAIDs), paracetamol (acetaminophen) and the pyrazolones differs but many of these drugs can cause generalised reactions which involve the liver. Depending on the drugs in question, the risks of liver injury may be conditioned by factors such as age, sex, dose and duration of treatment. Hepatotoxicity associated with the use of salicylates and most NSAIDs has been reported most often in females with collagen diseases but this may simply reflect the greater use of these drugs in such patients. Paracetamol-induced liver damage occurs almost exclusively as a result of overdosage. Except for the microvesicular fatty changes in hepatocytes in patients with Reye's syndrome attributed to salicylate, the acute centrilobular necrosis caused by paracetamol in overdosage and the marked cholestasis produced by benoxaprofen, the pathological changes in hepatic reactions to non-narcotic analgesics are rather variable and nonspecific. About 50% of patients given salicylate in full anti-inflammatory dosage develop minor abnormalities of liver function. There is usually a mild to moderate increase in plasma aminotransferase activity with patchy necrosis and degeneration of hepatocytes. These changes are related to plasma salicylate concentration and are usually rapidly reversible. In a small minority of patients, particularly the young, liver damage is more severe and may be associated with liver failure, acidosis, hypoglycaemia and encephalopathy. This picture closely resembles Reye's syndrome. In overdosage, paracetamol can cause acute hepatic necrosis. Without specific treatment, some 8% of adults suffer severe liver damage with plasma aminotransferase activity greater than 1000 U/L and about 1% die with hepatic failure and encephalopathy. The administration of sulfhydryl compounds such as N-acetylcysteine within 8 to 10 hours effectively prevents liver damage and death. Liver damage has been attributed to the therapeutic use of paracetamol. However, in most reports the dose was excessive and many patients were chronic alcoholics (who seem to be at increased risk). In these cases the features were typical of acute overdosage. A consistent and characteristic pattern of hepatotoxicity is evident with relatively few non-steroidal anti-inflammatory and pyrazolone analgesics. A rank order of relative risk cannot be established and the incidence in relation to use is not known.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetaminophen↗

PubMed1979

[Use of narcotic analgesics for the postoperative anesthetization of oncological patients].

The authors have studied the efficacy of narcotic analgesics in the postoperative period by a complex method, including a psychosomatic questionnaire, spirography, volumetry, analgesiometry, as well as a examination of the cardiovascular system and acid-base balance. Under examination were 183 patients subjected to surgery for tumors of the female genitalia and rectum (a lower laparatomy). The analgesic activity of promedol, omnopone, morphine and polyvinly-morpholidone in routine doses was estimated. It was noted that, if not contraindicated, narcotic analgesics may be successfully employed for analgesia in the early postoperative period.

Adult↗

PubMedDate not supplied

Rapid test for screening of narcotic analgesics in mice.

50 microliter of a solution of 0.35 N NH4OH containing 2.325% EDTA and 0.837% NaCl injected intradermally in mice elicited reproducible short term behavior typical for nociceptive stimulus. This behavior was inhibited specifically by narcotic analgesics. This procedure may be used as a specific test for screening and for dose--effect studies of narcotic analgetic drugs in mice.

Analgesics, Opioid↗

PubMed1980

[Action of opiate peptides and narcotic analgesics on the cerebral cortex].

The chronic experiments on freely moving cats have shown that the opiate peptides, FK33--824 (Tyr--D--Ala--Gly--MePhe--Met(o)--ol) and tetrapeptide (Tyr--D--Ala--Gly--Phe--NH2), as well as the narcotic analgesics, morphine, phentanyl and pentazocine in doses close to analgesic ones, suppress the recovery cycles of primary responses (PR) in the second somatosensory and associative zones of the brain cortex, recorded at paired stimulation of the fibres of thalamo-cortical radiation (TCR). In larger doses these agents slightly increase PR recorded at single stimulation of TCR, provoke the convulsive discharges on EEG and motor excitation of the animals. Naloxon eliminates all the mentioned effects of the tested opiate peptides and narcotic analgesics.

Analgesics, Opioid↗

PubMed1982

Epidural morphine for postoperative pain relief: a comparative study with intramuscular narcotic and intercostal nerve block.

The relatively new technique of epidural morphine analgesia was compared with two well established method of pain relief in 90 patients undergoing gallbladder surgery and divided randomly into three groups of 30 patients each. The first group received intramuscular narcotic analgesic ketobemidone, the second group was given 0.5% bupivacaine-epinephrine intercostal nerve block, and the third group received a single dose of 4 mg of epidural morphine for postoperative pain relief. The mean duration of analgesia after ketobemidone was 5.5 hours, and after intercostal block 11 hours. Of the patients given epidural morphine, 40% did not require further analgesia after the initial injection; the remaining patients in this group were pain free for a mean duration of 19 hours. The mean reduction in postoperative peak expiratory flow was most marked following ketobemidone and least after epidural morphine. Postoperative changes in PaO2 and PaCO2 reflected the changes in peak expiratory flow. Plasma levels of morphine after epidural injection were so low that a regional spinal analgesic action of epidural morphine appeared more likely than a systemic effect. Delayed respiratory depression was not encountered after epidural morphine. It is concluded that a single dose of 4 mg of epidural morphine provides excellent regional analgesia of long duration without drowsiness or circulatory of respiratory depression thus facilitating early ambulation. The technique is superior to more common methods of pain relief after gallbladder surgery, e.g., intercostal nerve block and intramuscular narcotics.

Adult↗