We have tested the hypothesis that breathing releases pulmonary surfactant via distortion of the alveolar type II cell. Gas exchange was maintained in the anaesthetized rat by applying high frequency (10 Hz) oscillations (HFO) to the chest wall; this resulted in apnoea within two to three breaths. After instrumentation under anaesthesis for 30 min, rats were infused with [3H]choline and [14C]choline, and we compared the tubular myelin-rich (PLalv-1) and -poor (PLalv-2) alveolar phospholipids and the microsomal and lamellar body phospholipids (PLlb) together with their specific activities after three forms of ventilation for 90 min: HFO (group 1), conventional mechanical ventilation (group 2) and spontaneous breathing (group 3). Group 4 was killed after surgical instrumentation and in group 5 the lungs were removed immediately after induction of anaesthesia. Groups 1-3 did not differ in any measured variable. Groups 1-4, which were anaesthetized for 30-120 min, had a lower PLalv-2 than did group 5. In contrast, PLlb was greater in groups 1-3, which were anaesthetized for 120 min, than in groups 4 and 5. In conclusion, we have successfully maintained normal gas exchange during complete apnoea by applying external HFO in rats for periods up to 90 min. Compared to mechanically ventilated or spontaneously breathing anaesthetized rats, surfactant turnover was unaltered by HFO, despite a markedly tidal volume. However, the barbiturate anaesthetic itself appeared to inhibit surfactant turnover. We suggest that distortion of the type II cell may be the stimulus for surfactant release at tidal volumes above resting values.
- Anesthesia, surfactant release
- High frequency oscillation, surfactant release
- Mammal, rat
- Surfactant, release