Increased chylomicron triglyceride hydrolysis by connective tissue flow inperfused rat hindlimb: implications for lipid storage

Skeletal muscle has two circulatory routes, nutritive (in contact with musc le) and non-nutritive (part of which is located in the connective tissue), and the balance of flow between the two is controlled by neural input and c irculating vasomodulators, The purpose of this study was to assess muscle t riglyceride hydrolysis given that the two circuits may have a differing vas cular distribution of hydrolytic activity. The isolated rat hindlimb was pe rfused with 6% Ficoll(R) and a radiolabeled chylomicron-lipid emulsion cont aining apolipoprotein C-II, Serotonin (0.5-1 mu M), a model vasoconstrictor previously shown to preferentially increase connective tissue flow inhibit ed hindlimb oxygen uptake (from 16.7 +/- 0.6 to 10.2 +/- 1.0, mean +/- SE, n = 7 (P < 0.001)) and stimulated [C-14]-labeled fatty acid uptake into mus cles (from 184 +/- 28 to 602 +/- 132, mean +/- SE, n = 7 (P = 0.009)). Thes e effects were reversed by the vasodilator carbamyl choline. Vasopressin re sulted in increased oxygen consumption but no change in triglyceride hydrol ysis. Cholesteryl oleate uptake (an indicator of endocytosis of the chylomi cron or remnant particle) was unaltered by serotonin. It is concluded that chylomicron triglyceride hydrolysis is enhanced by vasoconstrictors that in crease connective tissue flow in the perfused rat hind-limb, Increased hydr olysis appears to be primarily due to an increased access of triglyceride t o hydrolytic enzymes, presumably lipoprotein lipase associated with the fat cells commonly observed interlaced amongst bundles of muscle fibers.