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1 Departmen of Physiology, Virginia Commonwealth University, Richmond, VA, USA; Department of Emergency Medicine, Virginia Commonwealth University, Richmond, VA, USA
2 Departmen of Physiology, Virginia Commonwealth University, Richmond, VA, USA
* To whom correspondence should be addressed. E-mail: pittman{at}hsc.vcu.edu.
We tested the hypothesis that a deficit in oxygen extraction, or an increase in oxygen demand, following skeletal muscle contraction, leads to delayed recovery of tissue oxygen tension in the skeletal muscle of hypertensive rats in comparison with normotensive rats. Blood flow and the recovery of oxygen tension (PO2) at various sites in the spinotrapezius muscle of the spontaneously hypertensive rat (SHR) were evaluated following a 3-min period of muscle contraction, and compared to the corresponding values in Wistar-Kyoto (WKY) rats. The recovery of tissue PO2 [75 ± 7% (SHR) vs. 99 ± 12% (WKY) of resting values] and venular PO2 [72 ± 13% (SHR) vs. 104 ± 10% (WKY) of resting values] were significantly depressed in the SHR 30 seconds postcontraction. The delayed recovery persisted for 120 s post-contraction for both tissue [86 ± 11% (SHR) vs. 119 ± 13% (WKY) of resting values] and venular [74 ± 2% (SHR) vs. 100 ± 9% (WKY) of resting values] PO2. There was no significant difference in the recovery of arteriolar PO2 between the two groups 30 s post-contraction [95 ± 7% (SHR) vs. 84 ± 8% (WKY) of resting values]. Resting diameter of arcade arterioles in the two groups was not different [52 ± 3 µm (SHR) vs. 51 ± 3 µm (WKY)], but the arteriolar diameter following the 3-min contraction period was greater in the SHR [71 ± 4 µm (SHR) vs. 66 ± 4 µm (WKY)]. Likewise, red blood cell velocity [5.8 ± 0.3 mm/s (SHR) vs. 4.7 ± 0.2 mm/s (WKY)] and blood flow [23.0 ± 0.8 nl/s (SHR) vs. 16.0 ± 1.0 nl/s (WKY)] were significantly greater in the SHR 30 s post-contraction. The delayed recovery of tissue PO2 in the SHR, in comparison with the WKY, can be explained by a decrease in oxygen diffusion from the rarefied microvascular network due to the increased RBC velocity and shorter residence time in the microcirculation and the consequent disequilibrium for oxygen between plasma and RBCs. The delayed recovery of venular PO2 in the SHR 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 following muscle contraction.
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