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Journal Article

Citation

Irwin RJ, Lerner MR, Bealer JF, Mantor PC, Brackett DJ, Tuggle DW. J. Trauma 1999; 47(1): 105-110.

Affiliation

Department of Surgery, University of Oklahoma Health Sciences Center, and Department of Veterans Affairs Medical Center, Oklahoma City 73126, USA.

Copyright

(Copyright © 1999, Lippincott Williams and Wilkins)

DOI

unavailable

PMID

10421195

Abstract

OBJECTIVE: Bomb blast survivors occasionally suffer from profound shock and hypoxemia without signs of external injury. We hypothesize that a vagally mediated reflex such as the pulmonary defensive reflex is the cause of shock from blast wave injury. This study was a prospectively randomized, controlled animal study. METHODS: By using a previously described model of blast wave injury, we randomized rats to one of four groups: control, blast-only, bilateral cervical vagotomy plus atropine 200 microg/kg i.p. only, and bilateral cervical vagotomy plus atropine 200 microg/kg i.p. before blast injury. Cardiopulmonary parameters were recorded for 90 minutes after the blast or until death. RESULTS: Bradycardia, hypotension, and absence of compensatory peripheral vasoconstriction, typically seen in animals subjected to a blast pressure injury, were prevented by bilateral cervical vagotomy and intraperitoneal injection of atropine methyl-bromide. Hypoxia and lung injury were not statistically significant between the blasted groups, suggesting equivalent injury. CONCLUSION: Our data implicate a vagally mediated reflex such as the pulmonary defensive reflex as the cause of shock seen immediately after a blast pressure wave injury.

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