Description:
<jats:p>Acute lung injury (ALI) is a severe clinical problem where the progression of lung damage contributes to altered ventilatory patterns. Changes in central control of breathing may influence the pathophysiology of ALI. We have previously shown ALI induced upregulation of inflammatory cytokine production in the <jats:italic>nucleus tractus solitarius</jats:italic> (nTS). The effects of this immune‐modulation on central neural circuits are unclear. We hypothesized that ALI alters synaptic inputs to the nTS neurons. To test this hypothesis, we cut transverse slices (300 micrometers) of brainstem from juvenile (P15–P18) male Sprague‐Dawley rats 7d after intratracheal instillation of bleomycin (0.2 units) or saline. Whole‐cell perforated patch‐clamp recordings were done to characterize the spontaneous excitatory synaptic events in nTS neurons from bleomycin (n=4) and saline (n=2) animals. At least 200 synaptic events were analyzed from each cell and a student's t‐test was used for comparison. In bleomycin animals, the amplitude of spontaneous excitatory post‐synaptic currents (EPSCs) was significantly reduced (18.1 vs. 19.7 pA, p = 0.02) and the decay time of EPSCs was significantly longer (6.8 vs 5.7 ms, p < 0.01). Our data suggest that bleomycin lung‐injured animals have altered central processing of vagal afferent input that may contribute to breathing dysregulation in ALI.</jats:p>