Blast injuries represent a problem for civilian and military populations. Primary thoracic
blast injury causes a triad of
bradycardia,
hypotension and apnoea. The objective of this study was to investigate the reflex nature of this response and its modulation by
vagotomy or administration of
atropine. The study was conducted on terminally anaesthetised (
alphadolone/
alphaxalone, 18-24 mg x kg x h(-1), I.V.) male Wistar rats randomly allocated to the groups indicated below.
Blast injuries were produced with
compressed air while
sham blast involved the sound of a blast only. Primary
blast injury to the thorax resulted in a
bradycardia (measured as an increase in the interval between beats, or heart period (HP) to 489 +/- 37 ms from 133 +/- 3 ms with a latency of onset of 4.3 +/- 0.3 s, mean +/- S.E.M.),
hypotension (fall in mean arterial blood pressure (MBP) from 128.1 +/- 3.7 mmHg to 34.8 +/- 4.1 mmHg, latency of onset 2.0 +/- 0.1 s) and apnoea lasting 28.3 +/- 2.3 s.
Sham blast had no effect. The
bradycardia and apnoea following thoracic blast were abolished by cervical
vagotomy while the
hypotension was attenuated.
Atropine (0.3 mg x kg(-1), I.V.) caused a significant reduction in the
bradycardia (HP increasing from 124 +/- 3 ms to 142 +/- 4 ms) but did not modulate either the
hypotension or apnoea. It is concluded that a reflex involving the vagus nerve mediates the
bradycardia, apnoea and a component of the
hypotension associated with thoracic blast. The pattern of this response is similar to effects that follow stimulation of the pulmonary afferent C-fibres.