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Prolonged tissue PO₂ reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats

Virginia Commonwealth University Reanimation Engineering and Shock Center,Physiology and Emergency Medicine, School of Medicine, Virginia Commonwealth University, Richmond, Virginia 23298

Submitted 21 November 2002 ; accepted in final form 13 February 2004

We tested the hypothesis that a deficit in oxygen extraction or an increase in oxygen demand after skeletal muscle contraction leads to delayed recovery of tissue oxygen tension (PO₂) in the skeletal muscle of hypertensive rats compared with normotensive rats. Blood flow and PO₂ recovery at various sites in the spinotrapezius muscle of spontaneously hypertensive rats (SHRs) were evaluated after a 3-min period of muscle contraction and were compared with corresponding values in Wistar-Kyoto rats (WKYs). The recovery of tissue PO₂ [75 ± 7 (SHRs) vs. 99 ± 12% (WKYs) of resting values] and venular PO₂ [72 ± 13 (SHRs) vs. 104 ± 10% (WKYs) of resting values] were significantly depressed in the SHRs 30 s postcontraction. The delayed recovery persisted for 120 s postcontraction for both tissue [86 ± 11 (SHRs) vs. 119 ± 13% (WKYs) of resting values] and venular [74 ± 2 (SHRs) vs. 100 ± 9% (WKYs) of resting values] PO₂ levels. There was no significant difference in the recovery of arteriolar PO₂ between the two groups 30 s postcontraction [95 ± 7 (SHRs) vs. 84 ± 8% (WKYs) of resting values]. Values for resting diameter of arcade arterioles in the two groups were not different [52 ± 3 (SHRs) vs. 51 ± 3 µm (WKYs)], but the arteriolar diameter after the 3-min contraction period was greater in the SHRs (71 ± 4 µm) than the WKYs (66 ± 4). Likewise, red blood cell (RBC) velocity [5.8 ± 0.3 (SHRs) vs. 4.7 ± 0.2 mm/s (WKYs)] and blood flow [23.0 ± 0.8 (SHRs) vs. 16.0 ± 1.0 nl/s (WKYs)] measurements were significantly greater in the SHRs at 30 s postcontraction. The delayed recovery of tissue PO₂ in the SHRs compared with the WKYs can be explained by a decrease in oxygen diffusion from the rarefied microvascular network due to the increased RBC velocity and the shorter residence time in the microcirculation and the consequent disequilibrium for oxygen between plasma and RBCs. The delayed recovery of venular PO₂ in the SHRs is consistent with this explanation, as venular PO₂ is slowly restored to baseline by release of oxygen from the RBCs. This leaves the arterioles in the primary role as oxygen suppliers to restore PO₂ in the tissue after muscle contraction.

hypertension; oxygen tension; hypoxia; microvascular blood flow; rarefaction; phosphorescence quenching microscopy; disequilibrium

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