American Review of Respiratory Disease

In a previous study, we showed that increasing minute ventilation () in rabbit lung by adding a dead space augmented pulmonary surfactant in the airspaces by a cholinergically mediated mechanism. Using the same model in the present study of 148 rabbits, we found that increasing augmented airspace phospholipid, the main component of surfactant, from 2.50 ± 0.61 (mean ± SD) mg per g of lung during normal to 3.15 ± 1.22 (mean ± SD) mg per g of lung during increased (P = 0.02). Both blocking beta-adrenergic receptors with propranolol or sotalol and inhibiting prostaglandin synthetase with indomethacin or sodium meclofenamate prevented the expected increase in phospholipid during increased (P < 0.05). The beta-2 agonist, terbutaline, increased phospholipid by 43 per cent during normal (P < 0.01), and propranolol blocked this increase (P < 0.05). Isoproterenol, arachidonic acid, prostaglandins E1, E2, F, and a cyclic endoperoxide analog of prostaglandin H2 (U-46619) injected during normal failed to increase phospholipid. We concluded that acetylcholine (previous study), beta-adrenergic mediators, and prostaglandins are involved in controlling alveolar surfactant during increased .


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