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PubMed1982

Doxapram and the fractured femur.

In a double-blind trial the effects of a single dose of doxapram (1--1.5 mg/kg) on the postoperative arterial oxygen tension of patients who had undergone surgical fixation of a fractured neck of femur was measured. In contrast to other reports of the effect of a single dose of doxapram, there was no improvement in arterial oxygen tension with respect to the control group. It is reasoned that doxapram may exert its effect by increasing the functional residual capacity in the immediate postoperative period. The central analeptic properties of doxapram may be grossly underestimated. The widely held assumption that patients with a fractured neck of femur are significantly hypoxic pre-operatively is questioned.

Aged↗
PubMed1977

Antagonism of fentanyl with naloxone during N2O+O2+ halothane anaesthesia.

To investigate the antagonistic effect of naloxone on fentanyl-induced respiratory depression, 55 patients (randomly divided into various study and control groups were studied during nitrous-oxide-oxygen-halothane anaesthesia. Respiratory depression after 0.1 mg of fentanyl was totally reversed by 10 microgram/kg of naloxone, measured as 100% restoration of spontaneous respiration, normal minute volume and end-tidal CO2, while 15 microgram/kg of naloxone was needed to antagonize 0.2 mg of fentanyl. The respective control groups remained apnoeic. If no fentanyl had previously been administered, there was no difference in the respiratory behaviour of naloxone-treated and control patients, which indicates that no unspecific analeptic effect of naloxone could be demonstrated. The circulatory changes after fentanyl were nearly reversed by naloxone, as has been found earlier with other narcotics. Recovery from anaesthesia was scored from 0 to 10 (using a modification of Apgar scores for newborns), and somewhat higher mean scores were obtained with the naloxone-treated patients than with their controls. However, higher postoperative pain scores were recorded in these patients as well as a higher incidence of nausea and vomiting. The study demonstrates the dose-relationships of fetanyl and naloxone for estimation of total antagonism; however, the use of naloxone for partial antagonism at the termination of anaesthesia cannot be based on these findings.

Adult↗
PubMed1986

Pharmacokinetics of physostigmine after intravenous, intramuscular and subcutaneous administration in surgical patients.

The pharmacokinetics of physostigmine after intravenous, intramuscular or subcutaneous administration as well as its arousal effect after anaesthesia have been studied in surgical patients in the early postoperative period. After intravenous administration physostigmine had a very rapid plasma elimination with a plasma clearance ranging from 47 to 163 l/h with a mean +/- s.d. of 92.5 +/- 37.7 l/h. The volume of distribution was 46.5 +/- 19.2 l, while distribution and plasma elimination half-lives were 2.3 and 22 min, respectively. A fraction of the dose was probably hydrolyzed in blood since its blood elimination half-life in vitro was approximately 190 min. After both intramuscular and subcutaneous administration the systemic availability was almost complete, the plasma terminal half-lives only being somewhat longer than after intravenous administration. Plasma clearance, volume of distribution and elimination half-life of physostigmine were not correlated to age or body weight of the patients. The rapid plasma clearance of physostigmine resulted in a short duration of antisedative effect. After administration of 1 mg physostigmine salicylate i.v., drug-induced sedation was rapidly reversed with a duration of 30-60 min. The duration of action was similar after intramuscular injection but onset was delayed by 20-30 min. It was concluded that a plasma concentration of 3-5 ng/ml of physostigmine should be exceeded if an adequate analeptic effect is to be achieved, meaning that 2 mg of physostigmine had to be administered subcutaneously in order to achieve a satisfactory reversal of sedation. The short duration of action may hamper the use of physostigmine as an agent for reversal of drug-induced sedation and anticholinergic effects after surgery.

Adult↗
PubMed1996

The influence of alfentanil pre-treatment on ventilatory effects of doxapram following induction of anaesthesia with propofol.

BACKGROUND: Hypoventilation may occur following induction of anaesthesia with propofol and is potentiated by concurrent use of opioid drugs. This effect is undesirable in patients who will continue to maintain spontaneous respiration during anaesthesia and surgery. The analeptic drug doxapram is known to have selective respiratory stimulatory effects but its action during induction of anaesthesia has been inconsistent. METHOD: In a double-blind, placebo-controlled study, the influence of alfentanil pre-treatment on the ventilatory effects of doxapram given during induction of anaesthesia with propofol was studied in 40 patients. Four groups of ten patients (two groups pre-treated with 7 micrograms.kg-1 of alfentanil and two groups with saline) were randomly allocated to receive either 0.5 mg.kg-1 doxapram or saline following infusion of propofol to loss of verbal contact. RESULTS: In the groups that received doxapram, minute volumes were significantly increased and end-tidal carbon dioxide concentrations were significantly reduced compared to control groups, although the duration and extent of these effects were less in the group that received alfentanil. Doxapram also reversed an alfentanil-induced reduction in respiratory rate. No adverse cardiovascular or neurological stimulatory effects of doxapram were evident at any time. CONCLUSION: We conclude that doxapram 0.5 mg.kg-1 is effective in augmenting ventilation that has been obtunded following induction of anaesthesia with propofol in patients pre-treated with alfentanil.

Adolescent↗
PubMedDate not supplied

Naloxone does not reverse ethanol analgesia in man.

The effects of intravenously administered ethanol and morphine on pain threshold, reaction time, motor skills and short-term memory were investigated, and the ability of naloxone to reverse any changes was studied. Morphine (loading dose 0.2 mg/kg with an infusion of 0.004 mg/kg per min) and ethanol (loading dose 0.75 ml/kg with an infusion of 0.0025 ml/kg per min) produced a similar increase in pain threshold of 6.3 (s.e.m. = 1.5, n = 8) pain units and 7.7 (s.e.m. = 1.9, n = 8) pain units, respectively. Naloxone 0.015 mg/kg produced a significant reduction in pain threshold in the morphine group, but not in the ethanol group, and there was a significant difference between the groups following naloxone (P less than 0.05, t-test, 7 d.f.). Ethanol produced a significantly greater deterioration in motor skills than did morphine (P less than 0.05, t-test, 7 d.f.) and performance in both groups was improved following naloxone (P less than 0.05, t-test, 7 d.f.). There was no significant change in the other modalities studied. It is concluded that the reversal of ethanol effects by naloxone is probably due to a non-specific analeptic action rather than blockade of opioid receptors.

Analgesics↗
PubMed1990

Randomized double-blind trial of injectable heptaminol for controlling spontaneous or bromocriptine-induced orthostatic hypotension in parkinsonians.

Heptaminol is a molecule with experimental cardiovascular analeptic properties. In this double-blind vs placebo trial, the potency, so far unproven, of the injectable form of a 626 mg dose of heptaminol chlorhydrate on spontaneous or induced orthostatic hypotension (OH), was assessed. Nineteen patients were included in the study: 7 displayed spontaneous OH, and in the other 12 OH was induced by bromocriptine, as monitored 103 min/after an oral intake of 6.6 mg on average. Neither spontaneous nor induced OH were recorded in 32% of the Parkinsonian population registered, with no obvious distinctive characteristics. Potency tilt-trials, performed 15, 30 and 45 min after parenteral administration of heptaminol, revealed a significant and expressive potency of the molecule on the systolic blood pressure after 15 min (P less than 0.05). Clinical and biological tolerance was excellent. Low plasma renin activity and the absence of response to orthostatism indicated, in this population of Parkinsonian extrapyramidal syndromes, a loss in positive tonus likely to be of sympathetic origin. The anti-hypotensive action of heptaminol does not seem to be related to any renal or even sympathetic interaction.

Blood Pressure↗
PubMed1958

A comparison of some pharmacological properties of dioscorine and dioscine.

The alkaloids, dioscorine and dioscine, both obtained from yams, have been compared in respect of their convulsant activity, toxicity, analeptic action, local anaesthetic activity, adrenaline potentiating action, antidiuretic effect, and anti-acetylcholine activity. The alkaloids have similar properties, but in most respects dioscorine was the more potent. Aqueous solutions of dioscine are unstable.

Acetylcholine↗
PubMed1959

Drug antagonism and audiogenic seizures in mice.

The occurrence of audiogenic seizures in mice has been used as the basis of a method for measuring the antagonism between sodium thiopentone and bemegride or leptazol. Thiopentone in doses of 8 and 16 mg./kg. protected all the mice against the occurrence of audiogenic seizures. Bemegride and leptazol were administered in doses having molecular concentrations which bore a simple relationship to the doses of thiopentone. Bemegride was four times as powerful as leptazol in antagonizing the protective effect of thiopentone, and comparison of their regression lines showed that both analeptics acted in the same way. The antagonistic effect of bemegride occurred with doses less than its normal convulsant dose, but the doses of leptazol needed to antagonize thiopentone were within the convulsant range, and it increased the severity of any audiogenic seizures.

Animals↗
PubMed1977

Effect of carbamazepine on the in vitro uptake and release of norepinephrine in adrenergic nerves of rabbit aorta and in whole brain synaptosomes.

The effects of carbamazepine, in vitro, on adrenergic neuronal and whole brain synaptosomal uptake and release of tritiated norepinephrine (3H-NE) were assessed. At 10(-4) M, carbamazepine inhibited 3H-NE uptake by 22% in rabbit thoracic aorta and in brain synaptosomes. At the same concentration, carbamazepine inhibited stimulation-induced release of 3H-NE by 42.6% and inhibited isometric contraction in rabbit ear artery helical strips by 31.6%. At 10(-5) M, carbamazepine exhibited a 17.6% inhibition of 3H-NE uptake in brain synaptosomes in the absence of effects on transmitter release. Cocaine, 10(-4) M, and imipramine, 10(-4) M, inhibited uptake by 88% and 85%, respectively, in aorta, and cocaine, 10(-4) M, inhibited synaptosomal uptake by 67.7%. Since antiepileptic blood levels of carbamazepine range between 1.3 and 3.0 X 10(-5) M, it was concluded that the observed effects of carbamazepine are insufficient to account for the anticonvulsant action of the drug. However, the blockade of 3H-NE uptake by brain synaptosomes at 10(-5) M serves to explain the recently described analeptic activity of this agent.

Adrenergic Fibers↗
PubMed2005

Novel neuroprotective tripeptides and dipeptides.

It has long been recognized that thyrotropin-releasing hormone (TRH) and certain TRH analogues are neuroprotective in a variety of animal models of CNS trauma. In addition to these neuroprotective actions, TRH and most TRH analogues have other physiological actions that may not be desirable for treatment of acute injury, such as analeptic, autonomic, and endocrine effects. We have developed a series of dual-substituted TRH analogues that have strong neuroprotective actions, but are largely devoid of these other physiological actions. In addition, we have developed a family of cyclized dipeptides (diketopiperazines), structurally somewhat related to a metabolic product of TRH, that appear even more effective as neuroprotective agents in vitro and in vivo, and may have nootropic properties. Here, we review these novel tripeptide and dipeptide compounds.

Animals↗
PubMed1976

The use of Dopram as a respiratory stimulant following Immobilon in the pony.

The effects of the analeptic agent, Dopram (doxapram hydrochloride) were investigated in 2 ponies during Immobilon - induced neuroleptanalgesia. Although Dopram was demonstrated to exert a degree of respiratory stimulation, this was concluded to provide no overall advantage. The etorphine-induced hypoxic hypoxia was only partially reversed, and there was additional cardiovascular stimulation, in contrast to the previously reported tendency for arterial blood pressure to return towards conscious control values during the course of action of Immobilon.

Acepromazine↗
PubMed1982

Effect of naloxone on ethanol- and pentobarbital-induced narcosis.

Single or repeated subcutaneous administrations of naloxone in doses of up to 4 mg X kg-1 did not alter the time for onset or the duration of ethanol- or pentobarbital-induced narcosis in rats. An increase in the naloxone dosage to 50 mg X kg-1 s.c. resulted in a small reduction of ethanol-induced sleep duration. Repeated i.p. or i.v. administrations of much higher doses of naloxone (300-400 mg X kg-1 and 120-180 mg X kg-1, respectively) did produce significant reductions in ethanol-induced narcosis. However, similar naloxone doses, when administered alone, i.v., had marked convulsant effect. It appears that naloxone, in low doses, is not an effective antidote for narcosis caused by ethanol or pentobarbital at the ethanol and pentobarbital doses tested, whereas the antagonism of ethanol-induced sleep by high doses of naloxone may be due to the analeptic action of this drug.

Animals↗
PubMed1985

Effects of chronic right-to-left cardiac shunt on hypoxic sensitivity of mongrel dogs.

Resting ventilation (VI), blood gases, hypoxic sensitivity, and the ventilatory responses to intravenous sodium cyanide (NaCN, 100 micrograms/kg), doxapram (DOX, 500 micrograms/kg), and dopamine (DOPA, 20 micrograms/kg) were analyzed in four normal mongrel dogs (group I-N) and seven mongrel dogs with chronic (5-11 yr) right-to-left cardiac shunt (group II). The group I-N animals were also studied during steady-state isocapnic hypoxia (group I-H). The shunt procedure used for these studies produced a model for ventilatory studies during chronic shunt hypoxemia. The increases in VI per percent decrease in O2 saturation, which occurred during a four-breath N2 test, were 30, 43, and 13 ml X kg-1 X min-1 in groups I-N, I-H, and II, respectively. The decrease in hypoxic sensitivity of the group II animals, compared with groups I-N and I-H, occurred in the presence of an increase in PaCO2 from 21.9 to 26.0 Torr during the four-breath N2 test. A decrease in PaCO2 from 34.7 to 30.0 and from 33.6 to 30.4 Torr was observed in groups I-N and I-H. The response to DOX, a general analeptic agent, was greatest in group II and least in group I-N. However, the ventilatory responses to NaCN and DOPA were not sufficiently different among the three groups to suggest a difference in carotid body function as assessed by these drugs.

Animals↗
PubMed1998

Effects of thyrotropin-releasing hormone on the sleep EEG and nocturnal hormone secretion in male volunteers.

Various peptides including corticotropin-releasing hormone (CRH) exert selective effects on sleep structure and noctural secretions of cortisol and growth hormone (GH). In animal studies analeptic effects and sleep disturbances after thyrotropin-releasing hormone (TRH) administration have been observed; studies of endocrine function in depressed patients suggest a pathological activity of CRH and TRH as compared with that in healthy volunteers. As the role of TRH in the regulation of the sleep endocrine pattern in humans has not yet been clarified, we performed a study to examine the effects of pulsatile administration of TRH on the sleep EEG pattern and the nocturnal secretions of cortisol and GH in 7 healthy male subjects. The sleep EEG was recorded from 23.00 to 07.00 h, and blood samples were collected every 20 min from 20.00 to 07.00 h for the analysis of GH and cortisol concentrations during intravenous administration of placebo or 4 x 50 microgram TRH at 22.00, 23.00, 24. 00, and 01.00 h. In contrast to the well-known effects of CRH on the sleep endocrine pattern, TRH exerts only a weak effect on the sleep EEG which is reflected in a slight decrease in sleep efficiency associated with a trend to wakefulness during the night. Furthermore, after TRH administration, the cortisol rise appeared earlier, and a nonsignificant tendency to an increased secretion of cortisol during the first half of the night was found. The GH secretion did not differ significantly after application of TRH or placebo. The activating, albeit weak, effect of TRH on the sleep EEG and nocturnal cortisol secretion in healthy volunteers confirms and adds to the results previously observed in animals. On the basis of these findings, we surmise that TRH may contribute to the disturbed sleep continuity seen in depressed patients, probably acting as a cofactor of CRH in a synergistic manner.

Adult↗
PubMed1977

Cardiovascular effects of synthetic substance P.

The cardiovascular action of substance P (SP) has been studied in anaesthetized dogs. An analeptic respiratory and hypotensive action has been noted. The chronology of both effects would suggest that SP could be rapidly metabolized. The action of SP on respiration and general metabolism could be attributed either to one of its metabolites or to a secondary effect. It has not yet been stated to which mechanism--enzymatic or hormonal--it might be due.

Animals↗
PubMed1983

Antagonism of pentobarbitone-induced respiratory depression by naloxone in rats.

The effects of naloxone, pentobarbitone, or their combination, on arterial blood gases were studied in urethane-anaesthetised rats. Naloxone itself did not significantly alter the blood gases. Pentobarbitone significantly decreased PO2 and elevated PCO2, and these effects were prevented by pretreatment with naloxone. Arterial blood pH was unaffected by any of the drugs. The findings suggest that naloxone lacks a specific analeptic effect, but can antagonise respiratory depression induced by pentobarbitone.

Animals↗
PubMed1987

Dose-dependent pharmacokinetics of a xanthine-related nootropic drug, ethimizol, in rats.

Pharmacokinetics of the respiratory analeptic ethimizol, 4,5-bis(methylcarbamoyl)-1-ethylimidazole, with recently recognized nootropic properties, its metabolite 4-carbamoyl-5-methylcarbamoyl-1-ethylimidazole and of two metabolites of unknown structure was studied in plasma of rats after intravenous administration of the [2-14C]-labelled compound in 5 doses: 1.1, 3.3, 10, 20, and 30 mg/kg. The apparently monoexponential time course of dose normalized ethimizol plasma concentrations were not superimposable and the derived pharmacokinetic parameters were dose-dependent. The elimination rate constant and the initial volume of distribution decreased with increasing dose. The AUC versus dose relationship displayed disproportionate increases with increasing dose. Plasma ethimizol failed to obey the Michaelis-Menten kinetics and in an attempt to rationalize the observed nonlinearity a complete competitive product inhibition was suggested. Similar to the parent drug, the three metabolites exhibited a distinctly dose-dependent behavior as could be deduced from their dose-normalized concentration-time curves.

Animals↗
PubMed1994

Effects of low-dose TRH on cognitive deficits in the ECT postictal state.

A low dose (0.5 mg) of thyrotropin-releasing hormone (TRH), a short-acting tripeptide with known analeptic properties, was administered to eight depressed patients 5 minutes after ECT session 3 or 4 in a double-blind, placebo-controlled crossover design. After TRH infusion the patients displayed selectively better performance on a battery of neuropsychological tests than they did after placebo infusion. Further exploration with pharmacological probes to mitigate ECT postictal cognitive deficits is warranted.

Adult↗