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Responses of dogs to hyperoxic-, pentylenetetrazol-, and electroshock-induced convulsions

Responses of dogs to hyperoxic-, pentylenetetrazol-, and electroshock-induced convulsions METHODS HE EARLY OBSERVATIONS by Bert (5) that animals pressures rapbreathing oxygen at i ncreased atmospheric idly developed signs of central nervous system (0%) hyperexcitability, which led to grand ma1 convulsions, hav .e been repeatedly confirmed (2, 4, g, I g). The etiolOSY of oxygen convulsions is as yet unkn own. More recent work indicates that they may reflect cellular enzyme deficits resulting from exposure to oxygen at high pressure (OHP) (8, 2 I). Despite the volume of literature relating to the possible causes of oxygen convulsions, little has been reported regarding the physiologic changes that occur during these seizures. Recently, we have observed that unanesthetized dogs subjected to 4 and 5 atm abs of oxygen tension developed severe cardiovascular reactions in association Received for publication I 2 September I 966. 1 Recipient of National Institutes of Neurological Blindness Postdoctoral Research Fellowship Grant Present address : Alaska Native Medical Center, Alaska. Diseases and F:! 23,984-or. Anchorage, A group of I 7 mongrel dogs weighing between g and 15 kg was rendered quiescent by an initial intravenous dose of succinylcholine 4 mg/kg to inhibit musculoskeleta1 activity. Immediately following the first dose of succinylcholine, the trachea was intubated with a http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Responses of dogs to hyperoxic-, pentylenetetrazol-, and electroshock-induced convulsions

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Publisher
The American Physiological Society
Copyright
Copyright © 1967 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
Publisher site
See Article on Publisher Site

Abstract

METHODS HE EARLY OBSERVATIONS by Bert (5) that animals pressures rapbreathing oxygen at i ncreased atmospheric idly developed signs of central nervous system (0%) hyperexcitability, which led to grand ma1 convulsions, hav .e been repeatedly confirmed (2, 4, g, I g). The etiolOSY of oxygen convulsions is as yet unkn own. More recent work indicates that they may reflect cellular enzyme deficits resulting from exposure to oxygen at high pressure (OHP) (8, 2 I). Despite the volume of literature relating to the possible causes of oxygen convulsions, little has been reported regarding the physiologic changes that occur during these seizures. Recently, we have observed that unanesthetized dogs subjected to 4 and 5 atm abs of oxygen tension developed severe cardiovascular reactions in association Received for publication I 2 September I 966. 1 Recipient of National Institutes of Neurological Blindness Postdoctoral Research Fellowship Grant Present address : Alaska Native Medical Center, Alaska. Diseases and F:! 23,984-or. Anchorage, A group of I 7 mongrel dogs weighing between g and 15 kg was rendered quiescent by an initial intravenous dose of succinylcholine 4 mg/kg to inhibit musculoskeleta1 activity. Immediately following the first dose of succinylcholine, the trachea was intubated with a

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Feb 1, 1967

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