Abstract

We have used tow previously characterized models of hyperpnea in vivo and different modes of ventilation in the isolated perfused rat lung to investigate changes in the phospholipid content of tubular myelin-rich (PLalv-1) and -poor (PLalv-2) fractions isolated from lavaged material and of two lamellar body subfractions. A vesicular lamellar body subfraction (lbB) was preferentially released during 30-min swimming. However, during the subsequent 3-h recovery period there was a preferential supplementation of the classic-appearing lamellar body fraction (lbA). Hyperpnea induced by exposure to 5% CO2/13% O2/82% N2 led to an increase in lbA after 12 h and in lbB after 48 h. Whereas PLalv-2 was elevated above control values after 8 h, PLalv-1 remained unchanged until 24 h. In the perfused lung isolated from rats infused with [methyl-3H]choline chloride 3 h previously, salbutamol, a deep breath, and increased tidal volume (VT) all increased total alveolar phospholipids; however, the pattern of change was very different. Salbutamol markedly elevated PLalv-1 and increased the specific activity of both alveolar fractions. In contrast, a single deep breath increased PLalv-2 while slightly increasing the specific activity of PLalv-1. Finally, an increased VT decreased PLalv-1 while inducing a large increase in PLalv-2; it increased specific activity in both alveolar fractions. Both salbutamol and an increased VT decreased phospholipids in lbA. We conclude that lbA and lbB vary in their response to different stimuli. In vivo, PLalv-1, the tubular myelin-rich fraction, remains very constant, a fact consistent with its being the controlled variable in surfactant homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

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