anticholinergic/edema

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[Effect of several neuroleptic, adreno-, sympatho- and cholinolytic substances on the development of experimental cerebral edema induced by nicotine].

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The influence of some neuroleptic, adreno, sympatho- and cholinolytic substances on the development of experimental brain edema induced with nicotine was studied in tests conducted on rats. It was ascertained that marked antiedemic properties display drugs blocking the alpha-adrenoreceptors

[Study on anticholinergics for the treatment of high altitude pulmonary edema].

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OBJECTIVE To evaluate the clinical effects and mechanism of anticholinergics in treating high altitude pulmonary edema (HAPE). METHODS 582 patients with HAPE (in 4700-5260 m) were divided into 2 groups: one group (393 patients) was treated with anticholinergic (Group A), and the other 189 cases were

[Effect of neuroleptic, adreno- and cholinolytic agents on cerebral cortical function in edema].

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Experiments on rats with experimental brain edema under water intoxication were made to study the effects of the neuroleptics aminazine and propazine, the central M-cholinoblocker amizyl and the alpha-adrenoblocker phentolamine on the time-course of the recovery of cortical electric activity after

[Experimental acute edema; cerebral swelling and its prevention with central cholinolytics].

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[Effect of cholinolytics on the development of toxic pulmonary edema and pleurisy].

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[Treatment with an acetylcholine antagonist of 34 cases of pulmonary edema at high altitude].

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Effect of centrally administered monoaminergic & cholinergic receptor antagonists on carrageenin-induced pedal edema in rats.

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Respiratory failure without pulmonary edema following injection of a glutamate agonist into the ventral medullary raphe of the rat.

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Injection of ibotenic acid (IA), a glutamate agonist, into the ventral medullary raphe (VMR; especially the nucleus raphe magnus) of the rat produced respiratory failure and death following a predictable course of events. The response to the IA injection was characterized initially by increased

[Effect of pharmacological agents on the development of experimental brain edema].

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The effect of some neuroleptics, adreno-, sympatho- and cholinolytic substances on the development of "traumatic" and "mono-iodoacetate" brain edemas was studied in tests with rats. It was established that the neuroleptic chlorpromazine, the alpha-adreno-blocking agents phentolamine and dopegit and

Resolution of hydrops fetalis caused by atrioventricular block: good postnatal evolution with terbutaline treatment.

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BACKGROUND Complete atrioventricular block (CAVB) is rarely seen, as it occurs in only 1:11 000 to 1:20 000 newborns. There is a serious risk of mortality in CAVB, mainly in those cases associated with hydrops, fetal cardiac frequency ≤ 55 beats/minute, and premature delivery. METHODS Case of

Effects of an anticholinergic and a corticosteroid on acute pancreatitis in experimental dogs.

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In a model developed to study acute pancreatitis in the dog, the disease process was comparable with the spontaneously occurring disease. Infusion of oleic acid into the accessory pancreatic duct induced, grossly and microscopically, acute hemorrhagic pancreatitis with pancreatic atrophy, fibrosis,

Effects of 39 Compounds on Calmodulin-Regulated Adenylyl Cyclases AC1 and Bacillus anthracis Edema Factor.

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Adenylyl cyclases (ACs) catalyze the conversion of ATP into the second messenger cAMP. Membranous AC1 (AC1) is involved in processes of memory and learning and in muscle pain. The AC toxin edema factor (EF) of Bacillus anthracis is involved in the development of anthrax. Both ACs are stimulated by

Combined inhaled anticholinergics and short-acting beta2-agonists for initial treatment of acute asthma in children.

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BACKGROUND There are several treatment options for managing acute asthma exacerbations (sustained worsening of symptoms that do not subside with regular treatment and require a change in management). Guidelines advocate the use of inhaled short acting beta2-agonists (SABAs) in children experiencing

Therapeutic potential of a non-steroidal bifunctional anti-inflammatory and anti-cholinergic agent against skin injury induced by sulfur mustard.

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Sulfur mustard (bis(2-chloroethyl) sulfide, SM) is a highly reactive bifunctional alkylating agent inducing edema, inflammation, and the formation of fluid-filled blisters in the skin. Medical countermeasures against SM-induced cutaneous injury have yet to be established. In the present studies, we

[Edemas and myocloni concerning a patient with Parkinson's disease treated by amantadine (author's transl)].

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The administration of diuretics to a 64 year old patient with Parkinsonian disease treated by amantadine, orphenadrine and Modopart and presenting an oedemia of the legs, induced the apparition of myoclonic jerks similar to those observed in a bismuth intoxication. The myoclonic jerks remained after

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