Surfactant homeostasis in the rat lung during swimming exercise

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Abstract
Swimming rats for up to 2 h in water at 34 .+-. 1.degree. C increased the rate of breathing by 60% and tidal volume by 200-300%. In each case 20 .mu.Ci .cntdot. kg-1 [methyl-3H]choline chloride was infused via a caudal vein 3 h prior to the end of swimming. Maximum specific activity of tissue phospholipid (PL) and alveolar PL (PLalv) occurred in 1 and 12 h, respectively. Total PLalv, specific activity of PLalv and the percentage of total PL released (% A/T) increased within 10 min of start of swimming and were sustained for at least 2 h of swimming (PLalv in mg .cntdot. g dry lung-1: 5 s swim, 7.3 .+-. 0.96 [mean .+-. SD; n = 15 rats]; 1 h swim, 10.1 .+-. 1.1 (n = 23 rats]). After a 1 h swim, PLalv returned to control within 4 h. Pretreatment with propranolol hydrochloride (10 mg .cntdot. kg-1) (P), atropine methyl nitrate (3 mg .cntdot. kg-1) (A), indomethacin (15 mg .cntdot. kg-1) and cyproheptadine (1 mg .cntdot. kg-1) did not alter the increase in PLalv with swimming; both P and A reduced the increase in specific activity of PLalv and % A/T. Exercise releases surfactant from 2 pools: a readily released pool that responds to direct distortion of the alveolar type II cell and a pool that is under sympathetic nervous control.

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