AUTONOMIC CONTROL OF THE PULMONARY SURFACTANT SYSTEM AND LUNG COMPLIANCE IN THE LIZARD

An increase in body temperature in the bearded dragon, Pogona vitticep s, is accompanied by an increase in the amount of pulmonary surfactant , a mixture of proteins and lipids, with the latter consisting predomi nantly of phospholipid and cholesterol. This increase may result from a temperature-induced change in autonomic input to the lungs, as perfu sing the isolated lungs of P. vithiceps with either acetylcholine or a drenaline increases surfactant phospholipid release. However, whether acetylcholine acts via intrapulmonary sympathetic ganglia or directly on alveolar Type II cells is unknown. Moreover, the relative importanc e of circulating catecholamines and pulmonary sympathetic nerves on th e control of the surfactant system is also obscure. Here, we describe the mechanism of the modulation of the surfactant system and the effec t of this modulation on lung compliance. The role of acetylcholine was determined by perfusing isolated lungs with acetylcholine, acetylchol ine and the ganglionic antagonist hexamethonium, or acetylcholine, hex amethonium, and the muscarinic antagonist atropine. Perfusing with ace tylcholine significantly increased phospholipid release but did not af fect cholesterol release. While histological examination of the lung r evealed the presence of a large autonomic ganglion at the apex, blocki ng sympathetic ganglia with hexamethonium did not prevent the acetylch oline-mediated increase in phospholipid. However, the increase was inh ibited by blocking muscarinic receptors with atropine, which indicates that acetylcholine acts on muscarinic receptors to stimulate phosphol ipid release. By increasing pulmonary smooth muscle tone, acetylcholin e decreased opening pressure and increased static inflation pressures, Plasma levels of noradrenaline and adrenaline increased with increasi ng temperature and were accompanied by a greater surfactant content in the lungs. While surfactant content was also higher in animals that e xercised, plasma levels of adrenaline, noradrenaline, and dopamine wer e not elevated following exercise. Hence, surfactant release in the li zard lung may increase in response to an increase in plasma catecholam ine levels. Acetylcholine, and hence the parasympathetic nervous syste m, may act to stimulate surfactant release but does not act via pulmon ary sympathetic ganglia. We conclude that promoting surfactant secreti on via an increase in circulating catecholamines may be inappropriate for a cold lizard with a requirement to conserve energy. As body tempe rature decreases, release of surfactant via nonadrenergic mechanisms, including cholinergic stimulation, may become increasingly important.