Abstract
The structural integrity of the capillary wall is such that capillary luminal distensibility is largely determined by support provided by the tissue in which it is located. Given that O2 flux density is greatest across the skeletal muscle capillary endothelium, any changes in capillary diameter (dc) would be expected to affect O2 diffusing capacity as well as hemodynamic resistance. We used intravital microscopy techniques to study the maximally vasodilated rat (n = 5) spinotrapezius muscle microcirculation in vivo within the physiological sarcomere length range, at high and low mean arterial pressures (MAP) systematically altered by blood withdrawal and infusion. We tested the hypothesis that in vivo capillary diameter alterations in response to changes of MAP would be reduced at extended sarcomere lengths. At 2.4-microm sarcomere length, mean dc (dc) within the spinotrapezius increased from 5.6 +/- 0.1 to 5.9 +/- 0.1 microm (P < 0.01) as MAP increased from 33 to 94 mm Hg. However, there was absolutely no change (i.e., 5.2 +/- 0.1 vs 5.2 +/- 0.1 microm) in dc in response to changes in MAP at 3.2-microm sarcomere length. Furthermore, at sarcomere lengths <2.8 microm there was a significant increase (P < 0.01) in dc (n = 40) as MAP increased, whereas dc (n = 49) remained unchanged with alterations of MAP when sarcomere length was >/=2.8 microm (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 that the MAP-induced increases in capillary luminal diameter at the shorter sarcomere lengths are modest ( approximately 5%) and unlikely to affect O2 diffusing capacity and vascular resistance appreciably.
Published Version
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