Skeletal muscle blood flow is reduced and O-2 extraction is increased at re
st in chronic heart failure (CHF). Knowledge of red blood cell (RBC) flow d
istribution within the capillary network is necessary for modeling O-2 deli
very and exchange in this disease. Intravital microscopy techniques were us
ed to study the in vivo spinotrapezius muscle microcirculation in rats with
CHF 7 wk after myocardial infarction and in sham-operated controls (sham).
A decrease in mean muscle fiber width from 51.3 +/- 1.9 mu m in sham to 42
.6 +/- 1.4 mu m in CHF rats (P < 0.01) resulted in an increased lineal dens
ity of capillaries in CHF rats (P < 0.05). CHF reduced (P < 0.05) the perce
ntage of capillaries supporting continuous RBC flow from 87 +/- to 66 +/- 5
%, such that the lineal density of capillaries supporting continuous RBC fl
ow remained unchanged. The percentage of capillaries supporting intermitten
t RBC flow was increased in CHF rats (8 and 27% in sham and CHF, respective
ly, P < 0.01); however, these capillaries contributed only 2.3 and 3.3% of
the total RBC flux in sham and CHF rats, respectively. In continuously RBC-
perfused capillaries, RBC velocity (252 +/- 20 and 144 +/- 9 mu m/s in sham
and CHF, respectively, P < 0.001) and flux (21.4 +/- 2.4 and 9.4 +/- 1.1 c
ells/s in sham and CHF, respectively, P < 0.01) were markedly reduced in CH
F compared with sham rats. Capillary "tube" hematocrit remained unchanged (
0.22 +/- 0.02 and 0.19 +/- 0.02 in sham and CHF, respectively, P > 0.05). W
e conclude that CHF causes spinotrapezius fiber atrophy and reduces the num
ber of capillaries supporting continuous RBC flow per fiber. Within these c
apillaries supporting continuous RBC flow RBC velocity and flux are reduced
45-55%. This decreases the potential for O-2 delivery but enhances fractio
nal O-2 extraction by elevating RBC capillary residence time. The unchanged
capillary tube hematocrit suggests that any alterations in muscle O-2 diff
using properties in CHF are mediated distal to the RBC.