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At least 37 records · Page 2Linked to original sources
PubMed1989

Fentanyl produces cholinergically-mediated analeptic and EEG arousal effects in rats.

Fentanyl (20 micrograms/kg i.p.), administered to naltrexone-pretreated, pentobarbital-anesthetized rats, produced a shortening of the duration of narcosis. This analeptic effect was blocked by atropine, but not by methylatropine, indicating that a central cholinergic mechanism was involved. Fentanyl also increased sodium-dependent high affinity uptake of choline activity in the hippocampus and cortex that had been depressed by the barbiturate. Injection of 0.8 ng of fentanyl into the pontis oralis in the pontine reticular formation also produced analepsis in naltrexone-pretreated, pentobarbitalized rats. Hippocampal EEG recordings also showed the appearance of cholinergically-mediated theta activity, which was indicative of arousal activity in the hippocampus. These results suggest that fentanyl, in addition to possessing potent opiate activity, also activates a nonopioid-mediated central cholinergic arousal system.

Anesthesia↗
PubMed1991

Interactions between adrenergic systems, anaesthetic and TRH analogue induced analeptic effects on VBT transmission.

Previous behavioural and electrophysiological studies have indicated an antinarcotic action of thyrotropin-releasing hormone (TRH) and its analogues in antagonizing the action of CNS depressant drugs, including baclofen and a variety of anesthetics. While beta-adrenergic receptors are implicated in the level of anaesthesia/arousal, whether the analeptic action of TRH involves adrenergic systems for its expression is uncertain. The object of the present experiments, therefore, was to examine interactions between adrenergic systems and the anti-anaesthetic effects of TRH analogue CG3703. It was found that pretreatment with the beta-block (+/-)propranolol did not abolish or reduce the ability of CG3703 to antagonize urethane-induced depression of VBT transmission. These results suggest therefore, that beta-adrenergic systems are unlikely to be involved in the anti-anaesthetic effect of the tripeptide.

Animals↗
PubMed1975

Interaction between local anesthetics and analeptic drugs.

Although clinicall undesirable, the fortuitous pharmacologic interactions between local anesthetic agents and analeptic drugs may be protective when large doses of both agents are used. Mice pretreated with procaine, lidocaine, and tetracaine had a lower incidence of seizures when convulsive doses of either nikethamide or doxapram hydrochloride were given intraperitoneally. Mortality was also decreased in the groups given nikethamide and was zero in the animals treated with doxapram. All animals treated with pentylenetetrazol convulsed and only lidocaine (also used as an anticonvulsant) was able to reduce mortality in this group. Of the local anesthetic agents, tetracaine afforded the least protection from death, whereas lidocaine seemed to be most effective.

Anesthetics, Local↗
PubMed1989

Dexamethasone does not suppress the respiratory analeptic effect of corticotropin-releasing hormone.

Human CRH (hCRH), which acts as a major neuroregulator within the hypothalamic-pituitary-adrenal axis, is also a respiratory stimulant. The broad distribution of CRH receptors in brain areas involved in respiratory regulation is consistent with this finding. This study was designed to investigate whether ACTH or cortisol mediates the respiratory stimulation effect of CRH. Bolus injection of 100 micrograms hCRH induced significant respiratory stimulation in all 10 normal subjects studied. hCRH given after the administration of 2 mg dexamethasone, which greatly reduced plasma cortisol levels, had the same respiratory effect on respiration. Thus, increase in plasma ACTH and cortisol concentrations are probably not involved in the respiratory analeptic effect of CRH.

Adult↗
PubMed1996

[EEG studies on the analeptic effect of montirelin hydrate (NS-3), a TRH analog, in posterior hypothalamic area-lesioned rats].

Effects of a novel TRH analog, montirelin hydrate (NS-3), on the EEG were compared with those of TRH in intact and posterior hypothalamic area (PHA)-lesioned rats. In the intact rats, NS-3 at 0.01 mg/kg and TRH at 1 mg/kg produced no changes in the sleep-waking cycle. NS-3 at 0.1 mg/kg caused an increase in the time spent in the arousal stage and delayed the onset of the slow wave sleep (SS). On the other hand, TRH at 10 mg/kg increased the time spent in the SS stage and decreased the time in the A1 stage during 2 to 4 hr after injection without increasing the arousal stage, although it delayed the onset of SS. No abnormal EEG was observed after NS-3 or TRH administration in the intact rats. Electrolytic ablation of the PHA elicited continuous behavioral resting and caused increases in the slow-wave components in the cortical EEG and loss of generation of the hippocampal rhythmic slow activity. NS-3 at 0.01 mg/kg and TRH at 1 mg/kg caused the reappearance of the hippocampal rhythmic slow activity. In addition, NS-3 at 0.1 mg/kg and TRH at 10 mg/kg decreased the slow-wave components and increased the fast-wave components in the cortical EEG. In conclusion, NS-3 showed a distinct analeptic effect with a 100-fold higher potency than that of TRH in both the intact and PHA-lesioned rats.

Animals↗
PubMedDate not supplied

The interaction of barbiturates and analeptics.

The interaction of pentobarbitone sodium with three analeptics viz. micoren, pentylenetetrazol and methedrine was studied in mice. Micoren prolonged pentobarbitone sleeping time. pentylenetetrazol shortened the sleeping time. Methedrine also shortened the sleeping time, but clonic convulsions of mild to severe intensity were noticed 45-60 minutes after the drug injection.

Aminobutyrates↗
PubMed1978

[Study of a new respiratory analeptic: injectable almatrine. Apropos of 22 cases of acute hypoventilation: respiratory activity and electroencephalographic control].

2620 is a respiratory analeptic which acts by stimulation of peripheral chemoreceptors. It was administered intravenously in 22 patients in acute respiratory insufficiency. Doses during the first hour varied between 0.7 and 3 mg/kg. A careful study of the effects on respiration showed a significant increase in minute ventilation without any proportional increase in frequency for doses of between 1.7 and 3 mg/kg. Continuous recording of the electroencephalogram over a period of one hour revealed no convulsant effect even in particularly vulnerable patients. In seven patients, tracings showed a change in the sense of increased consciousness which corresponded with the clinical course of the diseases responsible for the state of hypoventilation.

Acute Disease↗
PubMed1979

The efficacy of four respiratory analeptics on healthy young men in a CO2 rebreathing experiment.

Four respiratory analeptics were examined in a CO2 rebreathing experiment with increase from 0--6% in the inspiratory CO2 concentration during 30 min on 24 healthy young men. The respiratory response curves (VE/pCO2) showed a parabolic shape. They were examined on parallel shift and change of slope. The "excitability ratio" is the first derivative of the response parabola and as such becomes a linear function of the actual arterial CO2 partial pressure. The following effects have been shown: 1. 150 mg amiphenazole (2.07 mg/kg) cause a small rise in the ventilation by accelerating the frequency at increased CO2 partial pressures above 45 mmHg. 2. 240 mg theophylline ethylenediamine (3.32 mg/kg) produce a nearly parallel upward-shift of the respiratory response curve, i.e., the respiratory minute volume increases independently by a deepening of the respiration. 3. 450 mg prethcamide (6.22 mg/kg) cause a slight increase of the "excitability ratio" at CO2 partial pressures above 45 mmHg. The CO2-dependent respiratory minute volume is not changed significantly but the pattern of breathing changes by accelerating the frequency and decreasing the tidal volume. 4. 40 mg fominobene (0.55 mg/kg) raise the "excitability ratio" convincingly at CO2 partial pressures above 40 mmHg. However, the total volume ventilated during the experiment does not increase because of a diminished ventilation at rest.

Adult↗
PubMed1979

Effects of the analeptic drug, 4-aminopyridine, upon post-operative respiratory depression in patients. A preliminary study.

The analeptic agent, 4-aminopyridine, was given to patients who had undergone elective ear, nose and throat surgery and showed severe central respiratory depression due to intra-operative fentanyl administration. The respiratory depression due to fentanyl was found to be partially antagonised by 4-aminopyridine. In view of these preliminary findings it is suggested that the drug might find a use in combatting postoperative fentanyl-induced respiratory depression.

Aminopyridines↗
PubMed1980

[Analysis and criticism of hemodynamic investigations during respiratory analeptic dispensing (author's transl)].

Almitrine is a respiratory analeptic acting on peripherical chemoreceptors. The hemodynamic effects have been studied with chronic respiratory diseases. The works have shown that almitrine produces an increase of pulmonary arterial pressure due to the raising of pulmonary vascular resistances by stimulation of peripherical chemoreceptors. Studying again the hemodynamic investigations with chronical respiratory failure it has been interesting to consider the effects of the produce with patients whose gazometric parameters have been normalized by artificial ventilation at FiO2 = 1, so as to produce a saturation of peripherical chemoreceptors. The results show that infused almitrine keeps hypertensive properties on pulmonary arterial with raising of pulmonary arterial resistances; the pulmonary vasoconstrictor effect is kept in spite of a normalization of blood gases. So it is necessary to look after pulmonary arterial pressure of patients receiving almitrine, that whatever the pre-existing pulmonary arterial pressure may be.

Aged↗