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reserpine/turse

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ArtiklidKliinilistes uuringutesPatendid
Leht 1 alates 29 tulemused
Reserpine treatment in doses of 1.0 and 5.0 mg/kg body weight, given 6 h before antigen challenge significantly suppresses the contact sensitivity reaction to picryl chloride in sensitized mice. The suppression involves both the edema formation, measured as ear swelling, and the accumulation of
N-Methylthiobenzamide (NMTB) is a pneumotoxin which causes pulmonary edema and hydrothorax in rodents. Reserpine has been shown to attenuate the pneumotoxicity induced by NMTB. Some of that evidence suggests that the protection afforded by reserpine occurs independently of its capacity to reduce

Reserpine in experimental cerebral edema.

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Reserpine in experimental cerebral edema: further observations.

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Effects of reserpine and chlorpromazine in prevention of cerebral edema and reversible cell damage.

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[Method of assessment of facial edema and attempt to influence post-extraction edema by reserpine].

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[IS THE PULMONARY EDEMA INDUCED BY OZONE INHALATION MODIFIED BY THE PREVIOUS ADMINISTRATION OF RESERPINE?].

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[A case of acute cerebral edema during reserpine therapy].

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[Influence of reserpine on egg white edema in rat paw].

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Penile paralysis and paraphimosis associated with reserpine administration in a stallion.

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Reserpine was administered to an 8-yr-old Thoroughbred stallion at a dosage of 5 mg subcutaneously (s.c.) every 2 wk for a 2-mo period to control unmanageable behavior. Reserpine produced a satisfactory calming effect that lasted for about 2 wk. After the last injection, the stallion developed
The lethal protein of the hornet (Vespa basalis) venom is a phospholipase A1 toxin (mol. wt approximately 32,000) with a potent hemolytic activity. Subplantar injection of the toxin caused a dose-dependent swelling in the rat hind paw. Its potency was higher than those of phospholipases A2 and

A role for serotonin in alpha-naphthylthiourea-induced pulmonary edema.

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alpha-Naphthylthiourea (ANTU) damages the pulmonary capillary endothelium producing a marked pulmonary edema. Since the pulmonary microvasculature regulates the circulating levels of serotonin (5-HT), the role of 5-HT in the pathophysiology of ANTU-induced pulmonary edema was examined. Mice treated
Asebotoxin III (ATX-III), a diterpenoid isolated from the leaves of Asebi, Pieris japonica, was found to produce hemorrhage into the lungs when the toxin in a dose of 2-8 micrograms was injected into the lateral ventricle of guinea pigs under urethane anesthesia (0.8 g/kg, i.p.). The occurrence of
In order to find some treatments for respiratory failure caused by pulmonary edema, we investigated the mechanism of neurogenic pulmonary edema. Previously, stimulation of sympathetic nerves caused an increase in pulmonary vascular permeability, possibly due to neuropeptide Y. Neuropeptide Y
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