• R J Irwin, M R Lerner, J F Bealer, P C Mantor, D J Brackett, and D W Tuggle.
• Department of Surgery, University of Oklahoma Health Sciences Center, and Department of Veterans Affairs Medical Center, Oklahoma City 73126, USA.
• J Trauma. 1999 Jul 1;47(1):105-10.

ObjectiveBomb 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.MethodsBy 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.ResultsBradycardia, 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.ConclusionOur 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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