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首页> 外文期刊>American Journal of Physiology >Prolonged tissue PO2 reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats.
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Prolonged tissue PO2 reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats.

机译：自发性高血压大鼠脊髓斜方肌收缩后组织PO2减少时间延长。

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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.
机译：我们测试了以下假设，与正常血压的大鼠相比，骨骼肌收缩后缺氧或缺氧需求增加会导致高血压大鼠骨骼肌组织氧张力（Po（2））的恢复延迟。在3分钟的肌肉收缩期后，评估自发性高血压大鼠（SHRs）斜方肌肌肉各个部位的血流量和Po（2）恢复，并将其与Wistar-Kyoto大鼠（WKYs）的相应值进行比较。组织Po（2）的恢复[75 +/- 7（SHRs）对比静止值的99 +/- 12％（WKYs）]和静脉Po（2）[72 +/- 13（SHRs）对比104收缩后30 s，SHRs静息值的+/- 10％（WKYs）明显降低。两种组织[86 +/- 11（SHRs）相对于静息值的119 +/- 13％（WKYs）]和静脉[74 +/- 2（SHRs）相对于100 + /-静止值的9％（WKYs）Po（2）的水平。两组在收缩后30 s的小动脉Po（2）恢复上无显着差异[95 +/- 7（SHRs）与84 +/- 8％（WKYs）的静息值]。两组的弓形小动脉静息直径值没有差异[52 +/- 3（SHRs）与51 +/- 3 microm（WKYs）]，但是在3分钟的收缩期后，小动脉直径更大。 SHR（71 +/- 4微米）比WKY（66 +/- 4）。同样，红细胞（RBC）速度[5.8 +/- 0.3（SHRs）对4.7 +/- 0.2 mm / s（WKYs）]和血流量[23.0 +/- 0.8（SHRs）对16.0 +/-收缩后30 s，SHRs的测量值[1.0 nl / s（WKYs）]明显更高。与WKYs相比，SHRs中组织Po（2）的延迟恢复可以解释为由于RBC速度增加和在微循环中的停留时间更短，以及氧气的不平衡导致稀疏微血管网络中的氧气扩散减少在血浆和红细胞之间。 SHRs中静脉Po（2）的延迟恢复与该解释一致，因为通过从RBC中释放氧气，静脉Po（2）缓慢恢复到基线。这使小动脉起主要的氧气供应者的作用，在肌肉收缩后恢复组织中的Po（2）。

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