Contribution of the spontaneous crossed-phrenic phenomenon to inspiratory tidal volume in spontaneously breathing rats.

Spinal cord hemisection at C2 (C2HS) severs bulbospinal inputs to ipsilateral phrenic motoneurons causing transient hemidiaphragm paralysis. The spontaneous crossed-phrenic phenomenon (sCPP) describes the spontaneous recovery of ipsilateral phrenic bursting following C2HS. We reasoned that the immediate (next breath) changes in tidal volume (V(T)) induced by ipsilateral phrenicotomy during spontaneous breathing would provide a quantitative measure of the contribution of the sCPP to postinjury V(T). Using this approach, we tested the hypothesis that the sCPP makes more substantial contributions to V(T) when respiratory drive is increased. Pneumotachography was used to measure V(T) in anesthetized, spontaneously breathing adult male rats at intervals following C2HS. A progressive increase in V(T) (ml/breath) occurred over an 8 wk period following C2HS during both poikilocapnic baseline breathing and hypercapnic respiratory challenge (7% inspired CO(2)). The sCPP did not impact baseline breathing at 1-3 days postinjury since V(T) was unchanged after ipsilateral phrenicotomy. However, by 2 wk post-C2HS, baseline phrenicotomy caused a 16 ± 2% decline in V(T); a comparable 16 ± 4% decline occurred at 8 wk. Contrary to our hypothesis, the phrenicotomy-induced declines in V(T) (%) during hypercapnic respiratory stimulation did not differ from the baseline response at any postinjury time point (all P > 0.11). We conclude that by 2 wk post-C2HS the sCPP makes a meaningful contribution to V(T) that is similar across different levels of respiratory drive.