Our previous results suggested that alveolar S is supplied by 2 tissue pools: one released via an increase in Vt and the other via β-adrenoceptors. In the present experiments we further investigated this concept. Rats were infused with 20μCi/kg3H-choline 5h prior to lung lavage. Putative agonist or antagonist was administered i.p. 240 or 90 min, respectively, after infusion. Propranolol (5,10mg/kg) atropine (3mg/kg) and indomethacin (15mg/kg) affected neither alveolar phospholipids (PLalv) nor radioactivity as a percentage of that in lung tissue (dpmPLalv/dpmPLtiss). Whereas salbutamol (280μg/kg) consistently increased both parameters, pilocarpine (1.5,3,10mg/kg) had no effect. We found that the dose of pilocarpine used by others (150mg/kg) markedly increased Vt and sighing; we suggest that the associated S increase reported is secondary. We used the rat isolated perfused lung to compare the effect of salbutamol and a large breath on PLalv. When we titrated the perfusate concentration of salbutamol to increase PLalv the same extent as a large breath, the dpmPLalv/dpmPLtiss was significantly greater in the former. We suggest that salbutamol releases a pool that is smaller but turning over more rapidly and hence is more highly labeled than that released by a large breath. In conclusion, we found no evidence of a role for the autonomic nervous system or prostaglandins in S-homeostasis in resting unanesthetised rats; possibly when these are inhibited a second control mechanism takes over.
|Pages (from-to)||No. 8638|
|Publication status||Published - 1 Jan 1985|