The structural integrity of the capillary wall is such that capillary lumin
al distensibility is largely determined by support provided by the tissue i
n which it is located. Given that O-2 flux density is greatest across the s
keletal muscle capillary endothelium, any changes in capillary diameter (d(
c)) would be expected to affect O-2 diffusing capacity as well as hemodynam
ic resistance. We used intravital microscopy techniques to study the maxima
lly vasodilated rat (n = 5) spinotrapezius muscle microcirculation in vivo
within the physiological sarcomere length range, at high and low mean arter
ial pressures (MAP) systematically altered by blood withdrawal and infusion
. We tested the hypothesis that in vivo capillary diameter alterations in r
esponse to changes of MAP would be reduced at extended sarcomere lengths. A
t 2.4-mu m sarcomere length, mean d(c) ((d) over bar(c)) within the spinotr
apezius increased from 5.6 +/- 0.1 to 5.9 +/- 0.1 mu m (P < 0.01) as MAP in
creased from 33 to 94 mm Hg. However, there was absolutely no change (i.e.,
5.2 +/- 0.1 vs 5.2 +/- 0.1 mu m) in (d) over bar(c) in response to changes
in MAP at 3.2-mu m sarcomere length. Furthermore, at sarcomere lengths <2.
8 mu m there was a significant increase (P < 0.01) in (d) over bar(c) (n =
40) as MAP increased, whereas (d) over bar(c) (n = 49) remained unchanged w
ith alterations of MAP when sarcomere length was greater than or equal to 2
.8 mu m (P > 0.05). These data suggest that pressure-induced alterations in
capillary luminal diameter and thus "in vivo capillary distensibility" are
dependent upon the presiding sarcomere length. Furthermore, we conclude th
at the MAP-induced increases in capillary luminal diameter at the shorter s
arcomere lengths are modest (similar to 5%) and unlikely to affect O-2 diff
using capacity and vascular resistance appreciably. (C) 1999 Academic Press
.