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 shoc
k from blast wave injury. This study was a prospectively randomized, contro
lled animal study.
Methods: By using a previously described model of blast wave injury, we ran
domized rats to one of four groups: control, blast-only, bilateral cervical
vagotomy plus atropine 200 mu g/kg IP only, and bilateral cervical vagotom
y plus atropine 200 mu g/kg IP before blast injury. Cardiopulmonary paramet
ers were recorded for 90 minutes after the blast or until death.
Results: Bradycardia, hypotension, and absence of compensatory peripheral v
asoconstriction, typically seen in animals subjected to a blast pressure in
jury, were prevented by bilateral cervical vagotomy and intraperitoneal inj
ection of atropine methyl-bromide. Hypoxia and lung injury were not statist
ically significant between the blasted groups, suggesting equivalent injury
.
Conclusion: Our data implicate a vagally mediated reflex such as the pulmon
ary defensive reflex as the cause of shock seen immediately after a blast p
ressure wave injury.