Impaired capillary hemodynamics in skeletal muscle of rats in chronic heart failure

Citation
Ca. Kindig et al., Impaired capillary hemodynamics in skeletal muscle of rats in chronic heart failure, J APP PHYSL, 87(2), 1999, pp. 652-660
Citations number
44
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
87507587 → ACNP
Volume
87
Issue
2
Year of publication
1999
Pages
652 - 660
Database
ISI
SICI code
8750-7587(199908)87:2<652:ICHISM>2.0.ZU;2-I
Abstract
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.