Autonomic responses to blast overpressure can be elicited by exclusively exposing the ear in rats

Abstract

Blast overpressure has become an increasing cause of brain injuries in both military and civilian populations. Though blast's direct effects on the cochlea and vestibular organs are active areas of study, little attention has been given to the ear's contribution to the overall spectrum of blast injury. Acute autonomic responses to blast exposure, including bradycardia and hypotension, can cause hypoxia and contribute to blast-induced neurotrauma. Existing literature suggests that these autonomic responses are elicited through blast impacting the thorax and lungs. We hypothesize that the unprotected ear also provides a vulnerable locus for blast to cause autonomic responses. We designed a blast generator that delivers controlled overpressure waves into the ear canal without impacting surrounding tissues in order to study the ear's specific contribution to blast injury. Anesthetized adult rats' left ears were exposed to a single blast wave ranging from 0 to 110 PSI (0-758 kPa). Blast exposed rats exhibited decreased heart rates and blood pressures with increased blast intensity, similar to results gathered using shock tubes and whole-body exposure in the literature. While rats exposed to blasts below 50 PSI (345 kPa) exhibited increased respiratory rate with increased blast intensity, some rats exposed to blasts higher than 50 PSI (345 kPa) stopped breathing immediately and ultimately died. These autonomic responses were significantly reduced in vagally denervated rats, again similar to whole-body exposure literature. These results support the hypothesis that the unprotected ear contributes to the autonomic responses to blast.

Keywords: Autonomic responses; Blast waves; Ear; Neurotrauma.

Fig. 1

The isolated blast generator. A. Schematic of the blast generator. B. Waveforms of blast waves at different intensities. Note the primary change due to varying pressures of calibration is the peak overpressure while rise time remains stable. Total positive phase increases with increasing blast pressure, but negative phase time remains stable. Insert: “Ideal” blast wave in an open space (Friedlander waveform), adapted from Goel et al. (2012) for comparison. C. Input-Output regressions for sensor port peak pressure (empty circles) and actual blast pressure measured at the speculum (filled circles) at varying input pressures.

Fig. 2

Respiratory rate responses to blast via the ear. A. Apnea after a 53.0 PSI (365 kPa) blast in one rat. B. Respiratory rate increase after a 59.6 PSI (411 kPa) blast in one rat. C. Linear regression of blast intensity and respiratory rate change (R² = 0.69, p < 0.0001). Crosses are four rats that immediately stopped breathing after the blast. Circles are rats that survived the blast exposure.

Fig. 3

Heart rate responses to blast via the ear. A. Heart rate decreased after exposure to a blast of 59.6 PSI (411 kPa). Spikes are due to occasional extra- and skipped-beats. B. Linear regression of blast intensity and heart rate change (R² = 0.70, p < 0.0001).

Fig. 4

Blood pressure responses to blast via the ear. A. Blood pressure changes after exposure to a blast of 60 PSI (414 kPa). B. Linear regression of blast intensity and mean arterial pressure (MAP) (R² = 0.81, p < 0.0001).

Fig. 5

ECG response to blast via the ear. ECG signals before and after exposure to a blast of 109 PSI (752 kPa). P-R interval were prolonged with progressive heart beats until one QRS complex was dropped completely, indicative of a type 2 heart block with Wenckebach phenomenon.

Fig. 6

Vagal mediation of autonomic response blast via the ear. Rats with bilateral vagus nerve denervation exhibited significantly less changes in respiratory rate and heart rate than the rats with intact vagus nerves (p = 0.015 and p = 0.001, respectively). Cardiorespiratory changes in rats with bilateral vagus nerve denervation were not significantly different from those in intact rats receiving 0 PSI (0 kPa) blasts (p = 0.461 and p = 0.281, respectively).