Control of alveolar surfactant in XXXX at rest and during prolonged hyperpnoea: pharmacological evidence for two tissue pools of surfactant.

@entity1169 @entity6555 @entity3045 @entity294 @entity2134 @entity515 @entity2507 @entity3897 @entity35 @entity3352
1. @entity1169 , @entity3897 and @entity3352 (i.p.) affect neither the amount (PLalv), nor the specific activity (PLalvsp.act.) of alveolar surfactant-type phospholipids lavaged from the lungs of unanaesthetized @entity35 , either at rest or made hyperpnoeic for 24 h with 5% @entity515 /13%O2/82%N2. 2. Whereas @entity3045 (280 micrograms kg-1 body weight, i.p.) consistently increased PLalv and PLalvsp.act., @entity2134 (1.5, 3, 10 and 50 mg kg-1, i.p.) and @entity6555 (1 and 5 mg kg-1, i.p.) had no effect. The dose of @entity2134 reported by others to release surfactant (150 mg kg-1) induced marked salivation, @entity294 , chromodacryorrhoea and a three-fold increase in tidal volume. 3. In the isolated perfused lung of the @entity35 , @entity3045 (1.5 microM) consistently increased PLalvsp.act, whereas @entity2134 (0.1 and 1 microM) had no effect on these variables. 4. In the isolated perfused lung, the maximum amount of surfactant that could be released by @entity3045 (0.5 mM) was smaller than that which could be released in response to an increase in tidal volume (peak inflation pressure 28 cm @entity2507 ). 5. When the concentration of @entity3045 in the isolated perfused lung was adjusted to produce the same increase in PLalv as did a single simulated deep breath, the PLalvsp.act was significantly increased by @entity3045 , but not by the simulated deep breath. 6. We conclude, that neither the autonomic nervous system nor the prostaglandin system is essential for the release of surfactant at rest or during hyperpnoea. Furthermore, we suggest that two pools of surfactant, with different release mechanisms, exist in lung tissue.
