title: Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle.
abstract: In healthy animals under normotensive conditions (N), contracting skeletal muscle perfusion is regulated to maintain microvascular O2 pressures (PmvO2) at levels commensurate with O2 demands. Hypovolemic hypotension (H) impairs muscle contractile function; we tested whether this condition would alter the matching of O2 delivery (Qo2) to O2 utilization (Vo2), as determined by PmvO2 at the onset of muscle contractions. PmvO2 in the spinotrapezius muscles of seven female Sprague-Dawley rats (280+/-6 g) was measured every 2 s across the transition from rest to 1-Hz twitch contractions. Measurements were made under N (mean arterial pressure, 97+/-4 mmHg) and H (induced by arterial section; mean arterial pressure, 58+/-3 mmHg, P<0.05) conditions; PmvO2 profiles were modeled using a multicomponent exponential fitted with independent time delays. Hypotension reduced muscle blood flow at rest (24+/-8 vs. 6+/-1 ml-1.min-1.100 g-1 for N and H, respectively; P<0.05) and during contractions (74+/-20 vs. 22+/-4 ml-1.min-1.100 g-1 for N and H, respectively; P<0.05). H significantly decreased resting PmvO2 and steady-state contracting PmvO2(19.4+/-2.4 vs. 8.7+/-1.6 Torr for N and H, respectively, P<0.05). At the onset of contractions, H reduced the time delay (11.8+/-1.7 vs. 5.9+/-0.9 s for N and H, respectively, P<0.05) before the fall in PmvO2 and accelerated the rate of PmvO2 decrease (time constant, 12.6+/-1.4 vs. 7.3+/-0.9 s for N and H, respectively, P<0.05). Muscle Vo2 was reduced by 71% at rest and 64% with contractions in H vs. N, and O2 extraction during H averaged 78% at rest and 94% during contractions vs. 51 and 78% in N. These results demonstrate that H constrains the increase of skeletal muscle Qo2 relative to that of Vo2 at the onset of contractions, leading to a decreased PmvO2. According to Fick's law, this scenario will decrease blood-myocyte O2 flux, thereby slowing Vo2 kinetics and exacerbating the O2 deficit generated at exercise onset.
authors.affiliation: Dept. of Kinesiology, Kansas State University, Manhattan, KS 66505-5802, USA.
authors.forename: Brad J
authors.initials: BJ
authors.lastname: Behnke
authors.forename: Danielle J
authors.initials: DJ
authors.lastname: Padilla
authors.forename: Leonardo F
authors.initials: LF
authors.lastname: Ferreira
authors.forename: Michael D
authors.initials: MD
authors.lastname: Delp
authors.forename: Timothy I
authors.initials: TI
authors.lastname: Musch
authors.forename: David C
authors.initials: DC
authors.lastname: Poole
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure; D002199:Capillary Permeability / Q000502:physiology*; D005260:Female; D007022:Hypotension / Q000097:blood / Q000503:physiopathology*; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism*; D018962:Phlebotomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow
chemical_list: D010100:Oxygen