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PubMedDate not supplied

The sensitivity of the respiratory center and some circulatory and subjective responses after nalorphine and naloxone injections.

In five volunteers the sensitivity of the respiratory centre to carbon dioxide after naloxone and nalorphine injections was studied using "double blind" method and increments of doses. Alterations in the respiratory centre sensitivity were reflected by changes in respiratory minute volume, which was measured before and after drug injections, as well as after carbon dioxide stimulation. Comparison of results and their statistical verification showed that nalorphine alone causes respiratory depression and carbon dioxide stimulation is, beside the weak initial action, almost ineffective. Naloxone causes very small, if at all, respiratory depression and the respiratory centre answers efficiently to carbon dioxide stimulation.

Carbon Dioxide↗
PubMedDate not supplied

[Effects of naloxone, nalorphine and dalargin on the course of shock due to the combination of mechanical trauma and acute blood loss].

Acute experiments on 75 adult rabbits were made to study action of intravenous injections of naloxone (0.1 mg/kg), nalorphine (0.5 and 2.0 mg/kg) and dalargin (0.1 mg/kg) in early and late periods of irreversible shock caused by combination of non-shockogenic mechanical trauma of the hip and safe blood loss from the femoral artery. In early shock antagonists of opiate receptors did not influence the outcomes while injection of dalargin prolonged survival of the animals noticeably. In late shock injection of the drugs had no significant influence on the course of the pathological process while reinfusion did not help the animals to survive. In the late shock injection of the above drugs after blood reinfusion increased the rabbits' survival.

Animals↗
PubMed1977

[The effect of nalorphine on analgesia induced by peripheral stimulation].

The blockade of effects induced by percutaneous peripheral stimulation were abolished by injection of an opiate antagonist as nalorphine. Our results lead to the hypothesis that central and peripheral stimulations act by the same mechanism in producing blockade of noxious impulses. One may suggest that peripheral stimulations induce release of endogenous morphine-like substances which in turn give descending inhibition.

Analgesia↗
PubMed1979

[Comparison of the effects of analgesia-producing peripheral and central stimulations in cats. Effect of nalorphine (author's transl)].

The effects of weak intensity percutaneous peripheral stimulations (SPPc) on the transmission of nociceptive messages induced by stimulation of the dental pulp have been studied on anaesthetized cats. 1. The jaw opening reflex (ROG) and the evoked potentials in the thalamic center median (CM), by stimulation of the dental pulp, disappear after a mean of 30 min after the start of SPPc. 2. These effects are analogous to those obtained by stimulation of the periaqueductal gray matter (St.GC) or by I.V. morphine injection. 3. The I.V. injection of the morphine antagonist (Nalorphine) blocks both the effects of the SPPc and those of the St.GC. 4. The authors put forth the hypothesis of a common mechanism of action of the SPPc and the St.GC which, through the liberation of endogenous morphinomimetic substances, would activate descending inhibitor impulses.

Animals↗
PubMed1977

Effects of morphine, methadone, nalorphine and naloxone on responding under schedules of electric shock titration.

Under two titration schedules, responses of squirrel monkeys adjusted the intensity of a continuous electric shock. In one schedule, responses produced food pellets but also increased a shock intensity which otherwise was decreased at a fixed rate (punishment titration). In another schedule, responses decreased a shock intensity which otherwise was increased at a fixed rate (escape titration). Responding maintained under the punishment titration schedule was only decreased by morphine, methadone, nalorphine and naloxone. This decrease in response rate was associated with a decrease in intensity of continous electric shock. Comparable rates of responding maintained under the escape titration schedule were either unaffected or increased over the same dose range of the same drugs. These effects on rate of responding were associated with either no effect or a slight decrease in intensity of continuous electric shock. When control rate of responding under the escape titration schedule was then increased by requiring five responses to decrease shock intensity, morphine, but not d-amphetamine, decreased responding at doses which had no effect or even increased responding when only one response was required to decrease shock intensity. These findings indicate that titration schedules are not always useful for studying the analgesic effects of drugs, but that specific effects of drugs are determined by specific details under which responding is maintained.

Analgesics↗
PubMed1981

Inhibition of ganglionic transmission by narcotic analgesics; an effect antagonized by naloxone, nalorphine and calcium.

Methadone, azidomorphine, oxycodone and fentanyl inhibit synaptic transmission in isolated sympathetic ganglia of the frog and rat, just as did morphine and pethidine in our previous investigations. This inhibitory effect can be antagonized not only by naloxone and nalorphine but also by increasing calcium concentration of the perfusion fluid of the ganglia. The inhibitory effect on transmission of narcotic analgesics takes place on specific opiate receptors of the peripheral ganglia.

Analgesics, Opioid↗
PubMed1984

[Changes in the arterial pressure and evoked potential in the sensorimotor cortex induced by nalorphine injected in the hypothalamus during painful electric shock in rabbits].

During the hypotensive phase of electronocuous shock in rabbits, injection of nalorphine to the hypothalamus provoked elevation in the blood pressure (BP), recovery of the evoked potential (EP) of the sensorimotor brain cortex in response to electrodermal stimulation (EDS) of the hind limb. Injection of the drug to the central gray of the midbrain resulted in an insignificant short-term elevation of the BP followed by its drop. It is concluded that the endogenous opioid system of the hypothalamus is of importance in the genesis of the hypotensive response and suppression of the EP of the rabbit sensorimotor brain cortex in response to EDS during electronocuous shock.

Animals↗
PubMed1978

The discriminative stimulus properties of cyclazocine: generalization studies involving nalorphine, morphine and LSD.

Rats learned to discriminate cyclazocine (2 mg/kg, i.p.) from saline using a two-lever operant (FR-4) procedure within 10 sessions under each drug condition. The cyclazocine discriminative stimulus (DS) was both dose- and time-related, being antagonized by naloxone at doses approximately 80 times that necessary to block the discriminative stimulus effect of morphine. Cyclazocine also generalized to nalorphine, but not to morphine, pentazocine or LSD. These data suggest that cyclazocine produced DS control of behavior by acting at CNS sites different from those affected by morphine or LSD.

Animals↗
PubMed1982

[Effect of nalorphine and naloxone on the course of electric pain shock in rabbits].

Electrical stimulation of the rabbit sciatic nerve resulted in the development of shock. Injection of physiological saline (1 ml, i. v.) did not change the progressive fall of the blood pressure or depression of palpitation and respiration. The animals died 135--191 min after discontinuance of the stimulation. Injection of nalorphine (0.4 mg/kg, i. v.) or naloxone (0.1 mg/kg i. v.) greatly improved the animals' condition. The blood pressure, palpitation and respiration returned to normal in 90--120 min after the injections. No lethal cases were recorded in this group of animals. It was shown in a supplementary group of animals that naloxone did not change the reserpine-produced hypotension.

Animals↗