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Pain continues to be undertreated, and numerous barriers to adequate pain management have been identified. Some clinicians believe that the words which health professionals use to describe analgesics may be a hidden barrier. Possible implications of using the term "narcotic" are described.
The protein fraction isolated from blood of seal, Phoca groenlandica, has been found to produce hyperalgesic effect on rats exposed to thermic or electrocutaneous nociceptive stimulation, but fail to affect writhes provoked by intraperitoneal injection of acetic acid solution on mice. When combined with morphine, the fraction lowered completely its narcotic analgetic action in the above mentioned tests. On the contrary, these same proteins combined with promedol or fentanil enhanced and prolonged analgetic effect of the latter. Tested in vitro the protein showed neither opioid nor anti-opioid activity. Therefore it is reasonable to suppose that neurophysiological activity of the isolated fraction is due to the peptides formed on enzymatic hydrolysis of proteins in vivo rather than these proteins as such.
Based on a historical outline, the survey describes the classifications of narcotic drugs according to present international conventions and Danish legislation. The classification of drugs according to the Danish act concerning euphoriant substances is compared to the classifications in Danish medical and pharmaceutical legislation.
The basal difference in action of the studied drugs was that nootropics (phenybut in a dose of 40 mg/kg and pyracetam in a dose of 200-400 mg/kg) did not change the initial action of pain reinforcement on synchronism in responses of the cortical neurones of alert nonimmobilized rabbits by inhibitory type (coincidence of the presence and absence of impulse activity) towards its decrease, while narcotics of various types (ethanol in a dose of 4-6 mg/kg, morphine-like opiate DAGO and opioid peptide DADLE in doses of 250 mkg/kg) eliminated the action of pain reinforcement on synchronism in responses of the cortical neurones both by inhibitory and activation (time of coincidence only of the presence of impulse activity) types. These and other drugs mainly weakened the initial action of both the inhibitory and reinforced light flashes of synchronism in neurones activity both by inhibitory and activation types. There was no constant parallelism between changes of synchronization and the frequency of the cortical impulses.
Oxilorphan is a fully synthetic morphinan derivative containing the 14-hydroxy group characteristics of naloxone and naltrexone. As a narcotic antagonist, oxilorphan was 4 times more potent than dl-cyclazocine, equipotent to naloxone and about one-fourth as potent as naltrexone parenterally. Duration studies in rodents were inconclusive, but in antagonism of morphine analgesia and miosis in the dog, oxilorphan was longer acting than naloxone and equivalent to dl-cyclazocine. Oxilorphan was inactive in the conventional animal thermal analgesic tests. However, oxilone did exhibit relatively weak analgesic activity in preventing phenylquinone-induced abdominal contraction at doses about 700 times higher than those required for antagonist activity. The analgesic potency of oxilorphan was only 120 and 1/300 the potency of morphine and dl-cyclazocine, respectively, but was significantly greater than naltrexone and naloxone. Mice chronically treated with increasing doses of oxilorphan failed to exhibit withdrawal jumping after naloxone challenge. General central nervous system activity studies showed oxilorphan to be relatively free from central side effects at doses at which dl-cyclazocine produced pronounced effects.
Fifty-six patients with chronic pain due to advanced cancer were treated with an sc infusion of morphone (34 patients) or hydromorphone (22 patients) using a portable disposable infusor. The infusion was maintained for 26 +/- 14 days. Twenty-five patients (45%) were discharged to the home for a mean period of 18 days (range, 2-138). The mean daily increase in dose was 2.6% +/- 1.4% of the initial dose. The sc site needed to be changed every 8 days (range, 2-31). Local toxicity consisted of infection in two patients (3%), chemical irritation in three (5%), and bleeding in one (2%). After 48 hours of treatment, 54 of 56 patients (96%) preferred the sc infusion to their previous parenteral treatment. We conclude that this is a safe and simple method for the administration of narcotics to inpatients and outpatients.
In this editorial, we review the narcotic bowel syndrome, its etiology, presentation, and treatment. We suggest this is an often overlooked diagnosis in many clinical settings.
Administration of intravenous narcotics in a patient's home is a relatively new therapeutic method of controlling excruciating cancer-related pain. As with any new therapy, there are many questions and concerns related to administration and management. This article presents information derived from a literature review designed to improve understanding and technique.
One hundred cases of intracorporeal concealment of narcotic drugs were observed over a 6-month period at the medico-judicial emergency centre of the Hotel-Dieu hospital, Paris. Twelve cases concerned dealers who had ingested packs at the time they were arrested. The other subjects had been carrying the drug in their digestive tract, rectum or vagina for transportation. The illicit drugs thus transported were cocaine in 20 cases (ingestion), heroin in 65 cases (ingestion 7, rectal or vaginal cavity 58) and cannabis in 3 cases. Packs for sale being fragile, the dealers were particularly exposed to overdosage. Their management prior to intoxication was the same as that of acute ordinary drug poisoning, i.e. washing out of the stomach. In carriers, the risk of severe poisoning was associated with ingestion. The lack of antidote makes cocaine poisoning particularly dangerous. Surgical extraction is now reserved to cases with intestinal mechanical complications and to those increasingly rarer cases of fragile transportation packs.
Inflight passenger problems associated with withdrawal or overdose from narcotics or other drugs have been assessed. The specific categories of common drugs of abuse covered are: opiates, amphetamines and cocaine, central nervous system depressants, marijuana, phencyclidine, LSD and mescaline, and peyote. One or more of these drugs may be abused by persons in all walks of life. Relatively recent newspaper accounts of inflight disturbances related to abuse substances have highlighted the problem. Some case histories are given by the authors along with recommendations for methods of dealing with these problems.
Extraordinary significant discoveries have been made in the pharmacology of opioid drugs in the last fifteen years. One has to go back to the beginning of the eighteenth century to find a comparably significant period. The advances in our understandings and uses of opioids have taken place in four different areas: postulating the existence of several types of receptors and the discovery of receptors sites, the isolation of endogenous opioids, the development of new opioid substances, and the use of new routes and modes of administration of narcotics.
We determined the heart rate (HR) response to enflurane, halothane, and isoflurane and the effects of narcotics on this response in 81 healthy patients scheduled for elective surgery. Patients were randomly assigned to one of six treatment groups: one of the three anesthetics (approximately 0.9 MAC) in 60% nitrous oxide, and either 0.15 mg/kg of intramuscular morphine 30-60 min before induction or 1 microgram/kg of IV fentanyl 10 min after skin incision. All patients received diazepam, 10 mg orally, 60-90 min before anesthesia, a rapid sequence intravenous induction, and mechanically controlled ventilation. During inhalational anesthesia and the first 10 min of surgery, no significant change in HR occurred in any group (compared to the preinduction HR), although patients given morphine premedication tended to have a decreased HR and those not given morphine premedication tended to have an increased HR. These trends partially account for significant differences that emerged between groups after induction of anesthesia. Patients given morphine premedication and halothane had lower HR (64 +/- 3 SEM) than patients given isoflurane (80 +/- 3) or enflurane (84 +/- 3) and no morphine premedication. Patients anesthetized with enflurane and morphine premedication had lower HR (71 +/- 3) than patients given enflurane without morphine premedication. Administration of fentanyl 10 min after incision (these patients had received no morphine) significantly decreased HR in the presence of any of the vapors. We conclude that inhalational anesthetics used in the clinical setting we employed do not significantly increase heart rate, and that prior administration of morphine or concurrent administration of fentanyl may significantly decrease HR.
The effects of three anesthetic techniques on liver function were compared in patients with mild alcoholic hepatitis who required surgery, both peripheral and superficial. Thirty patients were randomly assigned to receive one of three anesthetics: thiopental, nitrous oxide and oxygen, enflurane, plus muscle relaxant; thiopental, nitrous oxide and oxygen, narcotic, plus muscle relaxant; or spinal anesthesia with tetracaine. Measurements of hepatic function were made preoperatively (on the day of operation) and on the first and third postoperative days. Levels of serum bilirubin, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, and lactate dehydrogenase liver isoenzyme were similar in the three groups on both postoperative days. They were not significantly different from those obtained preoperatively, although mean values decreased by the first postoperative day and again on the third. The data suggest that the choice among the three anesthetic methods studied could be based on factors other than the presence of mild alcoholic hepatitis and that, when peripheral surgery is required, one may not anticipate a worsening of any biochemical disorder in the first three postoperative days.
Recent studies document that substance abuse is a significant problem among anesthesia personnel. We have developed a system to better control the accountability of narcotics and other potentially addictive drugs. The system consists of a three-phase approach: (1) an individual anesthesia cart/narcotics box; (2) computer analysis of drug usage; and (3) an anesthesia drug audit. A standard stock issue of drugs is maintained by each resident. Drugs are issued daily to those residents administering anesthesia. Each drug transaction is recorded by the resident according to the patient's name, hospital number, type and length of the surgical procedure, type and amount of drug used, and the amount of each drug discarded. A weekly computer-generated report shows individual usage trends for each drug and a summary of "high" users for that period. The computer does not "flag" an individual as a drug abuser, but monitors trends in controlled substance usage. Those residents having a significant alteration in their drug usage pattern that is not explained legitimately are comprehensively audited.
Thiol-group reactive agents [alloxan, N-ethyimaleimide (NEM), ethacrynic acid, p-chlormercuribenzoate (PCMB)] were shown to induce a writhing syndrome in mice and rats when injected i.p. in appropriate dosage. Non-steroidal anti-inflammatory agents, narcotic analgesics and also psychotropic drugs inhibit the syndrome elicited in rats by ethacrynic acid. Rats pretreated with cysteine i.p. show a greatly reduced nociceptive response to ethacrynic acid or alloxan.
Butorphanol, a new, totally synthetic morphinan, which is chemically related to naloxone, has been demonstrated to have both analgesic and narcotic antagonist properties. In rodent antiwrithing analgesic tests, butorphanol was 4 to 30 times more potent than morphine and dl-pentazocine, respectively. As an antagonist, butorphanol was about equivalent to nalorphine and 30 times more potent than dl-pentazocine. On the basis of the naloxone-induced mouse jumping test and the lack of substitution in withdrawn morphine-dependent mice, it is estimated that the potential for physical dependence of butorphanol will be less than that of dl-pentazocine but greater than that of nalorphine and dl-cyclazocine. Animal data also show that agonistic actions of butorphanol, such as respiratory depression and miosis, reach ceiling effects which are lower than those seen with morphine with an increase in dosage. Thus, butorphanol differed from morphine which exhibited agonist effects in a dose-related manner. Butorphanol showed weak to moderate central depressant properties at doses which were considerably higher (greater than 100 X) than those producing analgesia. Minimal cardiovascular and respiratory effects were seen with butorphanol in conscious dogs.
Possible neuroanatomical substrates mediating some of the effects seen with thyrotropin-releasing hormone (TRH) in the pentobarbital (PB) narcotized rat were examined. This was accomplished by microinjecting picomole concentrations of TRH into 20 different brain sites. The behavioural effects examined were the capacity of TRH to antagonize PB-induced narcosis and hypothermia as well as TRH-induced shaking behavior. Microinjection of TRH into the septum was found to be significantly more effective in the reversal of PB narcosis than any other site examined. In contrast, the temperature and shaking response were evoked with approximately equal efficacy by TRH microinjection into a number of brain sites; including the preoptic/anterior hypothalamus, medial thalamus, thalamic, periventricular gray, interpeduncular nucleus and locus ceruleus. These results demonstrate the septal region to be the site of action for TRH reversal of PB narcosis and suggest the involvement of the septohippocampal system. In addition, they indicate that the neurogenesis of the shaking response is similar to that of the temperature response and that this differs from the neurogenesis of the analeptic response.
The effects of morphine, butorphanol, cyclazocine, ketocyclazocine, ethylketocyclazocine, and SKF-10,047 were tested, alone and in conjunction with naloxone or naltrexone, in rats responding under a fixed-interval, 5-min schedule of food presentation. Except for naloxone and naltrexone, all of the drugs decreased the average rate of responding in a dose-dependent manner. The rate-decreasing effects of morphine were markedly antagonized by naltrexone, while the effects of SKF-10,047 or high doses of cyclazocine were not antagonized by naltrexone or naloxone. Naltrexone and naloxone were able to antagonize the effects of butorphanol, ketocyclazocine, ethylketocyclazocine and low doses of cyclazocine, but these drugs were considerably more difficult to antagonize than was morphine. Thus, the interactions between these drugs and the narcotic antagonists allow the classification of the drugs into three groups, based on a marked shift, a moderate shift or no shift in the dose-response curve. This classification is consistent with the hypothesis of Martin et al., (Journal of Pharmacology and Experimental Therapeutics, 197: 517-532, 1976) regarding distinct receptors for morphine and related drugs (mu agonists), ketocyclazocine and ethylketocyclazocine (kappa agonists) and SKF-10,047 (sigma agonist).