Hydrolysis of triglycerides in the isolated perfused rat lung

Abstract

The purpose of this study was to investigate the hydrolysis of saturated and unsaturated triglycerides by lung lipoprotein lipase and to measure the incorporation of triglyceride fatty acids into lung tissue lipids. Lipolytic activity was studied in the isolated ventilated rat lung, perfused for 100 rain in a recycling system with Krebs Ringer bicarbonate containing bovine serum albumin, 5.6 mM glucose, and 1.5 or 10 mM triglyceride. Saturated triglycerides were hydrolyzed at significantly (p<0.05) lower rates than unsaturated triglycerides; tricaprylin, trimyristin and tripahnitin were hydrolyzed at 8.1 + 1.8, 5.4 + 1.5 and 9.5 + 1.8/~mol free fatty acids/g dry wt/100 min, respectively, whereas triolein and trilinolein were hydrolyzed at 20.2 + 1.8 and 20.6 + 0.3 ~mol free fatty acids/g dry wt/100 min, respectively. The polyunsaturated triglycerides, tdlinolein and triarachidonin were hydrolyzed at even higher rates (44.3 + 3.0 and 50.9 + 5.4 #mol free fatty acids/g dry wt/100 min, respectively). Intralipid infused at a conoentration of 10 mM triglyceride was hydrolyzed at a significantly higher rate than at 1.5 mM triglyceride (58 + 6.3 #mol free fatty adds/g dry wt/100 min vs 16.6 + 1.7/~mol free fatty aeids/g dry wt/100 min, respectively). Labeled unsaturated triglycerides were broken down at significantly higher rates than labeled saturated triglycerides. Incorporation of triglyceride-fatty acid into lung lipid was greater into neutral lipids than into phospholipids. The data su~ggest that (a) the factors that appear to affect lung lipoprotein iipase activity are composition and concentration of circulating triglyceride, (b) uptake of fatty acids into the tissue was proportional to the rate of hydrolysis of the emulsion, and (c) triglyceride-fatty acids could therefore be used by the lung for metabolic needs.

Fat Embolism: What We Have Learned from Animal Models

“…Although oleic acid is a well-known pulmonary toxicant, as mentioned above, it is not a suitable model for fat embolism syndrome. The conversion of triolein to oleic acid by pulmonary tissue [31] provides support for the proposed sequence of events postulated by Szabo [32].…”

Very low density lipoproteins stimulate surfactant lipid synthesis in vitro.

“…Other investigations using the isolated perfused rat lung system have demonstrated that the lung is actively involved in the catabolism of triglycerides in VLDL (19)(20)(21)(22). Further, in vivo and in vitro studies indicate that rat lung expresses high levels of LPL activity (18,21,22). This activity is detected primarily in lipid interstitial cells and alveolar macrophages (23)(24)(25).…”

“…For example, prior studies reveal that the pulmonary vascular bed is exposed to high levels of circulating plasma triglycerides (17, 18). Other investigations using the isolated perfused rat lung system have demonstrated that the lung is actively involved in the catabolism of triglycerides in VLDL (19)(20)(21)(22). Further, in vivo and in vitro studies indicate that rat lung expresses high levels of LPL activity (18,21,22).…”