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.