Pulmonary surfactant controls the surface tension at the air-liquid interface within the lung. This system had a single evolutionary origin that predates the evolution of the vertebrates and lungs. The lipid composition of surfactant has been subjected to evolutionary selection pressures, particularly temperature, throughout the evolution of the vertebrates.

Cold profoundly influences lung compliance in homeothermic mammals. Much of this effect has traditionally been attributed to the inactivation of the surfactant system. However, many mammals undergo large fluctuations in body temperature (heterothermic mammals). Here, the surfactant lipid composition and lung compliance of warm-active dunnarts (Sminthopsis crassicaudata) and the homeothermic mouse (Mus musculus) [body temperature (Tb) = 35-37 degrees C] were compared with those of dunnarts killed after 1,4 or 8 h of torpor (Tb < 20 degrees C). Lung compliance was measured before and after the removal of surfactant, and tissue compliance was determined by inflating the lung with saline. Relative to total phospholipid (PL), mouse surfactant contained proportionately less phosphatidylinositol but more cholesterol (Chol) and phosphatidylglycerol than that of the dunnart. Lung compliance was lower in dunnarts than in mice, consistent with an allometric effect. Surfactant levels, including total PL, Chol, and disaturated phospholipid (DSP) increased during torpor. The relative proportions of Chol and DSP increased after 4 and 8 h, respectively. In marked contrast to previous studies on the behavior of isolated lungs from homeothermic mammals, in our study the lung compliance of dunnarts remained unchanged throughout torpor. Tissue compliance decreased at 1 and 4 h of torpor, but this decrease was abolished by 8 h. It appears that the surfactant of the dunnarts counteracted the negative effect of tissue compliance at 1 and 4 h, an effect not present in homeothermic mammals. However, because lung compliance was maintained at 1 h of torpor in the absence of a compositional change in surfactant lipids, the changes in lipid composition observed at 4 and 8 h of torpor are thought to relate to functions of surfactant other than that of maintaining lung compliance.

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Pulmonary surfactant, a mixture consisting of lipids and proteins and secreted by type II cells, functions to reduce the surface tension of the fluid lining of the lung, and thereby decreases the work of breathing. In mammals, surfactant secretion appears to be influenced primarily by the sympathetic nervous system and changes in ventilatory pattern. The parasympathetic nervous system is not believed to affect surfactant secretion in mammals. Very little is known about the factors that control surfactant secretion in nonmammalian vertebrates. Here, a new methodology for the isolation and culture of type II pneumocytes from the lizard Pogona vitticeps is presented. We examined the effects of the major autonomic neurotransmitters, epinephrine (Epi) and ACh, on total phospholipid (PL), disaturated PL (DSP), and cholesterol (Chol) secretion. At 37 degrees C, only Epi stimulated secretion of total PL and DSP from primary cultures of lizard type II cells, and secretion was blocked by the beta-adrenoreceptor antagonist propranolol. Neither of the agonists affected Chol secretion. At 18 degrees C, Epi and ACh both stimulated DSP and PL secretion but not Chol secretion. The secretion of surfactant Chol does not appear to be under autonomic control. It appears that the secretion of surfactant PL is predominantly controlled by the autonomic nervous system in lizards. The sympathetic nervous system may control surfactant secretion at high temperatures, whereas the parasympathetic nervous system may predominate at lower body temperatures, stimulating surfactant secretion without elevating metabolic rate.