Abstract

Hypercapnia induces prolongation of expiratory time (T e) during early development. In the present study, we determined the response to steady state hypercapnia of three neural phases of the total respiratory cycle, inspiration (T i), stage 1 or passive expiration, T e-1 and stage 2 or active expiration, T e-2. Experiments were performed in decerebrate, vagotomized, spontaneously breathing piglets aged 5–10 days. Neural phases of the respiratory cycle were based on electrical activities of the thyroarytenoid (TA, laryngeal adductor) and triangularis sternii (TS, chest wall expiratory muscle) in relation to diaphragm (D) activity. We observed that hypercapnia induced prolongation of both expiratory phases. The greater prolongation of T e-1 was associated with an increase in TA activity and an increase in laryngeal resistance, which peaked early in T e-1, and then progressively decreased. These findings demonstrate that, in early postnatal life, a hypercapnia induced increase in respiratory drive is associated with centrally mediated prolongation of both phases of expiration, a greater prolongation of T e-1, and an increase in laryngeal resistance during post-inspiration. We speculate that the latter serves to optimize gas exchange by reducing large fluctuations in functional residual capacity.

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