physostigmine/hypoxia

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Physostigmine reverses cognitive dysfunction caused by moderate hypoxia in adult mice.

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BACKGROUND Cognitive changes associated with moderate hypoxia in rodents may result from the diminished functioning of central cholinergic neurotransmission. We designed this study to examine whether treatment with physostigmine (PHY), an acetylcholinesterase inhibitor, could improve the impairment

Comparison of DuP 996, with physostigmine, THA and 3,4-DAP on hypoxia-induced amnesia in rats.

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DuP 996, 3,3-bis(4-pyrindinylmethyl)-1-phenylindolin-2-one, physostigmine (PH), tetrahydroaminoacridine (THA) and 3,4-diaminopyridine (3,4-DAP) were compared for their ability to protect against hypoxia-induced performance deficits in a passive avoidance (PA) task. The ability to retain PA response

Physostigmine-induced cerebral protection against hypoxia.

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Physostigmine, at 0.1, 0.2 and 0.3 mg/kg, was tested for effect on the survival of mice exposed to 5% O2-95% N2. Some treated animals survived for one hour under the hypoxic atmosphere (2 out of 14 at 0.1 mg/kg and 8 out of 28 at 0.2 and 0.3 mg/kg), an event never observed in untreated controls. The

Protective effect of hachimi-jio-gan, an oriental herbal medicinal mixture, against cerebral anoxia.

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The protective effect of Hachimi-jio-gan (HJ) against cerebral anoxia was investigated with various experimental models in mice. Minimal effective dose of HJ which significantly prolonged the survival time was 0.5 g/kg, p.o. for normobaric hypoxia and 0.5 g/kg, p.o. for KCN- (4 mg/kg, i.v.) induced

Survival under hypoxia. Age dependence and effect of cholinergic drugs.

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Survival under hypoxia (5% O2; 95% N2) was tested in mice 1 day to 50-weeks-old. Survival Rate (ratio of number of animals that survived 30 min under 5% O2 to total number of animals exposed) and the time from onset of exposure until the last gasp (Survival Time) were maximum in newborn animals and

Physostigmine has a life-saving effect in rats subjected to prolonged respiratory arrest.

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We have previously reported that centrally-acting cholinomimetic drugs have a prompt and sustained resuscitating effect in pre-terminal conditions of hemorrhagic shock in rats. Here we have studied the effect of physostigmine in another experimental condition of hypoxia in anesthetized rats, which

Protection against hypoxia-induced lethality in mice: a comparison of the effects of hypothermia and drugs.

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The role of hypothermia in the antihypoxic effects of drugs was examined in the present experiments. The effects of environmentally induced hypothermia and drugs were tested by exposing mice to 100% nitrogen gas for 80 sec and counting the number of survivors. In a series of 68 vehicle control

Cholinergic and anticholinergic drug effects on survival during hypoxia: significant gender differences.

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We examined central and peripheral components of cholinergic drug protection against hypoxia in male and female mice. Survival times were measured in groups of control and treated (i.p. injection) animals exposed to hypoxia (5% O2/95% N2). Body temperatures were also measured in separate groups of

Physostigmine antagonizes benzodiazepine-induced myoclonus in the baboon, Papio papio.

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The antagonism of some benzodiazepine (Bz) actions by physostigmine was investigated in 4 Papio papio baboons. As a model of these actions, the myoclonus induced in this species by clonazepam i.m. administration was used. The baboon develops, 20-30 min after Bz i.m. injection, a non-epileptic

[Protective effect of eptazocine, a novel analgesic, against cerebral hypoxia-anoxia in mice].

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Cerebral protective effect of eptazocine, a mu-antagonist-kappa-agonist, was investigated using mice subjected to hypoxia-anoxia. Eptazocine (1 to 10 mg/kg) prolonged the survival time of mice subjected to KCN (3 mg/kg, i.v.) injection in a dose-dependent manner, and this effect was completely

A re-examination of physostigmine-induced cerebral protection in the hypoxic mouse. A critical assessment of the model.

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Using the hypoxic (FiO2 = 0.05) mouse model as originally described, the survival time following pretreatment with physostigmine was examined. The maximum increase in survival time was 87% following a physostigmine dose of 0.4 mg/kg. This increase was considerably less than that previously reported

Memory training combined with the use of oral physostigmine.

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Impaired memory function is one of the most frequent and disabling symptoms observed after brain injury. A number of studies have examined the efficacy of using cholinergic agonists, such as physostigmine, in treating memory impairment resulting from various neurologic conditions. Few studies,

Possible role of cholinesterase inhibitors on memory consolidation following hypobaric hypoxia of rats.

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High altitude (HA) generates a deleterious effect known as hypobaric hypoxia (HBH). This causes severe physiological and psychological changes such as acute mountain sickness (AMS) and cognitive functions in terms of learning and memory. The present study has evaluated the effect of cholinesterase

[Effects of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane) on the synthesis of acetylcholine in anemic hypoxia].

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Pretreatment of mice with 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane) protected against effects of anemic hypoxia. Befemelane delayed the loss of the righting reflex (from 17.8 +/- 1.3 to 21.9 +/- 1.2 min, p less than 0.05) and death (from 19.6 +/- 1.3 to 23.3 +/- 1.1, p less

alpha-Tocopherol as agonist in hypoxia.

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In hypoxia, but not normoxia, alpha-tocopherol (vitamin E) acts as an agonist in guinea-pig isolated colon, producing dose-dependent increases in contractile activity. This effect is mimicked by agents, vitamin K1 and phytol, which contain a structural similarity to the phytol side chain of

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