NEUROCHEMICAL CONTROL OF TISSUE RESISTANCE IN PIGLETS

Lung resistance may be influenced by chemoreceptor activity and modula ted by inspiratory neural output; however, it is unknown whether the c ontractile elements of lung tissue participate in these changes during early development. In anesthetized paralyzed open-chest piglets, we m easured phrenic electroneurogram, lung resistance (RL), and tissue res istance utilizing alveolar capsules to partition the hypercapnic and h ypoxic responses of RL into tissue (Rti) and airway resistance (Raw) c omponents. Inhalation of 7% CO2 significantly increased RL (7.4 +/- 0. 5 to 11.3 +/- 0.6 cmH(2)O . l(-1) . s), Rti (5.2 +/- 0.5 to 6.9 +/- 0. 5 cmH(2)O . l(-1) . s), and Raw (2.2 +/- 0.2 to 4.4 + 0.4 cmH(2)O . l( -1) . s). Inhalation of 12% O-2 caused more modest increases in RL, Rt i, and Raw. Oscillations in tracheal and alveolar pressures appeared i n synchrony with phrenic activity in response to both chemoreceptor st imuli. Cholimergic blockade eliminated these oscillations and signific antly reduced the hypercapnic and hypoxic responses of RL, Rti, and Ra w. These data demonstrate for the first time that hypercapnia and hypo xia elicit a cholinergically mediated increase in Rti which, just like the airway component of RL, is modulated by inspiratory neural output and is present during early development. Such coordination in neural function throughout the respiratory system may serve to optimize gas e xchange during early postnatal life.