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Title: Physiology and pathophysiology of respiratory arrest by cyanide poisoning

Respiratory arrest, preceded by hyperventilation, is the primary cause of death in acute cyanide poisoning. Hyperventilation followed by apnea is also observed without intoxication. Hyperventilation and apnea in untoxicated subjects and animals are analyzed for the underlying physiological and biochemical changes and compared with those found during cyanide poisoning. The study reveals that the respiratory autoregulation appears to be the same under both conditions. Respiratory arrest is controlled by cerebral PCO2 and can occur without hypoxia or inhibition of cytochrome oxidase. It is postulated that respiratory arrest is a 'desperate act' thrust on the respiratory neurons by a critical exhaustion of their energy store (ATP) due to the rapid firing in the period of hyperventilation. The point of no return may be reached when anoxia and/or partial inhibition of cytochrome oxidase prevent the neurons from replenishing the ATP store. The formation of Fe3+ cyanide complexes. exemplified by the metHb producer DMAP, appears to give the best results with regard to the restoration of spontaneous respiration. The study of respiratory autoregulation may also be helpful in developing and understanding other therapeutic approaches.
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Resource Type:
Technical Report
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Other Information: This article is from 'Proceedings of the Medical Defense Bioscience Review (1993) Held in Baltimore, Maryland on 10-13 May 1993. Volume 2', AD-A275 668, p831-839
Research Org:
Army Medical Research Inst. of Chemical Defense, Aberdeen Proving Ground, MD (United States)
Country of Publication:
United States
45 MILITARY TECHNOLOGY, WEAPONRY, AND NATIONAL DEFENSE; 63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; CYANIDES; BIOLOGICAL EFFECTS 450600* -- Military Technology, Weaponry, & National Defense-- Chemical & Biological-- (1990); 560300 -- Chemicals Metabolism & Toxicology