M. Rucker et al., Vasomotion in critically perfused muscle protects adjacent tissues from capillary perfusion failure, AM J P-HEAR, 279(2), 2000, pp. H550-H558
Citations number
30
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
We analyzed the incidence and interaction of arteriolar vasomotion and capi
llary flow motion during critical perfusion conditions in neighboring perip
heral tissues using intravital fluorescence microscopy. The gracilis and se
mitendinosus muscles and adjacent periosteum, subcutis, and skin of the lef
t hindlimb of Sprague-Dawley rats were isolated at the femoral vessels. Cri
tical perfusion conditions, achieved by stepwise reduction of femoral arter
y blood flow, induced capillary flow motion in muscle, but not in the perio
steum, subcutis, and skin. Strikingly, blood flow within individual capilla
ries was decreased (P < 0.05) in muscle but was not affected in the periost
eum, subcutis, and skin. However, despite the flow motion-induced reduction
of muscle capillary blood flow during the critical perfusion conditions, f
unctional capillary density remained preserved in all tissues analyzed, inc
luding the skeletal muscle. Abrogation of vasomotion in the muscle arteriol
es by the calcium channel blocker felodipine resulted in a redistribution o
f blood flow within individual capillaries from cutaneous, subcutaneous, an
d periosteal tissues toward skeletal muscle. As a consequence, shutdown of
perfusion of individual capillaries was observed that resulted in a signifi
cant reduction (P < 0.05) of capillary density not only in the neighboring
tissues but also in the muscle itself. We conclude that during critical per
fusion conditions, vasomotion and flow motion in skeletal muscle preserve n
utritive perfusion (functional capillary density) not only in the muscle it
self but also in the neighboring tissues, which are not capable of developi
ng this protective regulatory mechanism by themselves.