Smith Lane M, Barbee R Wayne, Ward Kevin R, Pittman Roland N
Department of Physiology, Virginia Commonwealth University Reanimiation Engineering and Shock Center, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298-0551, USA.
Am J Physiol Heart Circ Physiol. 2004 Jul;287(1):H401-7. doi: 10.1152/ajpheart.00980.2002. Epub 2004 Feb 26.
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 (Po(2)) in the skeletal muscle of hypertensive rats compared with normotensive rats. Blood flow and Po(2) 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 Po(2) [75 +/- 7 (SHRs) vs. 99 +/- 12% (WKYs) of resting values] and venular Po(2) [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] Po(2) levels. There was no significant difference in the recovery of arteriolar Po(2) 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 microm (WKYs)], but the arteriolar diameter after the 3-min contraction period was greater in the SHRs (71 +/- 4 microm) 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 Po(2) 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 Po(2) in the SHRs is consistent with this explanation, as venular Po(2) 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 Po(2) in the tissue after muscle contraction.
与正常血压大鼠相比，高血压大鼠骨骼肌收缩后氧摄取不足或氧需求增加会导致骨骼肌组织氧分压（Po₂）恢复延迟。在对自发性高血压大鼠（SHR）斜方肌不同部位进行3分钟肌肉收缩后，评估其血流和Po₂恢复情况，并与Wistar - Kyoto大鼠（WKY）的相应值进行比较。收缩后30秒，SHR组的组织Po₂恢复情况[为静息值的75±7%（SHR）vs. 99±12%（WKY）]和微静脉Po₂恢复情况[为静息值的72±13%（SHR）vs. 104±10%（WKY）]均显著降低。收缩后120秒，组织[为静息值的86±11%（SHR）vs. 119±13%（WKY）]和微静脉[为静息值的74±2%（SHR）vs. 100±9%（WKY）]的Po₂水平仍持续存在延迟恢复。收缩后30秒，两组小动脉Po₂恢复情况无显著差异[为静息值的95±7%（SHR）vs. 84±8%（WKY）]。两组弓状小动脉的静息直径值无差异[52±3（SHR）vs. 51±3微米（WKY）]，但在3分钟收缩期后，SHR组的小动脉直径（71±4微米）大于WKY组（66±4微米）。同样，收缩后30秒，SHR组的红细胞（RBC）速度[5.8±0.3（SHR）vs. 4.7±0.2毫米/秒（WKY）]和血流[23.0±0.8（SHR）vs. 16.0±1.0纳升/秒（WKY）]测量值显著更高。与WKY组相比，SHR组组织Po₂恢复延迟可解释为：由于RBC速度增加和在微循环中停留时间缩短，导致从稀疏微血管网络的氧扩散减少，进而导致血浆和RBC之间的氧失衡。SHR组微静脉Po₂恢复延迟与这一解释一致，因为微静脉Po₂通过RBC释放氧而缓慢恢复至基线。这使得小动脉在肌肉收缩后作为氧供应者在恢复组织Po₂方面起主要作用。
