Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle
Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle
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DOI：
10.1152/japplphysiol.00388.2005
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发表时间：
2006-03-01
影响因子：
3.3
通讯作者：
Poole, DC
中科院分区：
文献类型：
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作者：
Behnke, BJ;Padilla, DJ;Poole, DC
在正常血压条件下 (N) 的健康动物中，收缩骨骼肌灌注受到调节，以将微血管 O-2 压力 (PmvO(2)) 维持在与 O-2 需求相称的水平。低血容量性低血压（H）损害肌肉收缩功能；我们测试了这种情况是否会改变 O-2 输送 (Qo(2)) 与 O-2 利用 (Vo(2)) 的匹配，由肌肉收缩开始时的 PmvO(2) 确定。在从休息到 1 Hz 抽搐收缩的过渡过程中，每 2 秒测量 7 只雌性 Sprague-Dawley 大鼠（280 +/- 6 g）的斜方肌中的 PmvO(2)。测量在N（平均动脉压，97+/-4mmHg）和H（动脉切片诱导；平均动脉压，58+/-3mmHg，P<0.05）条件下进行； PmvO(2) 曲线使用具有独立时间延迟的多分量指数进行建模。低血压会减少静息时的肌肉血流量（N 和 H 分别为 24 +/- 8 与 6 +/- 1 ml(-1) (.) min(-1) (.) 100 g(-1)；P < 0.05）和收缩期间（N 和 H 为 74 +/- 20 与 22 +/- 4 ml(-1) (.) min(-1) (.) 100 g(-1)，分别;P<0.05)。 H 显着降低静息 PmvO(2) 和稳态收缩 PmvO2（N 和 H 分别为 19.4 +/- 2.4 与 8.7 +/- 1.6 Torr，P < 0.05）。在收缩开始时，H 减少了 PmvO(2) 下降之前的时间延迟（N 和 H 分别为 11.8 +/- 1.7 与 5.9 +/- 0.9 s，P < 0.05），并加速了 PmvO(2) 下降的速率（N 和 H 的时间常数分别为 12.6 +/- 1.4 与 7.3 +/- 0.9 s，P < 0.05）。 0.05）。与 N 相比，H 时肌肉 V. O-2 在休息时减少 71%，收缩时减少 64%，H 时 O-2 提取量在休息时平均减少 78%，收缩时平均减少 94%，而 N 时分别为 51% 和 78%。这些结果表明，H 限制了骨骼肌 Qo(2) 相对于收缩开始时 Vo(2) 的增加，导致 PmvO(2) 降低。根据菲克定律，这种情况将减少血肌细胞 O-2 通量，从而减慢 Vo(2) 动力学并加剧运动开始时产生的 O-2 赤字。
In healthy animals under normotensive conditions (N), contracting skeletal muscle perfusion is regulated to maintain microvascular O-2 pressures (PmvO(2)) at levels commensurate with O-2 demands. Hypovolemic hypotension (H) impairs muscle contractile function; we tested whether this condition would alter the matching of O-2 delivery (Qo(2)) to O-2 utilization (Vo(2)), as determined by PmvO(2) at the onset of muscle contractions. PmvO(2) 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; PmvO(2) 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 PmvO(2) 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 PmvO(2) and accelerated the rate of PmvO(2) decrease ( time constant, 12.6 +/- 1.4 vs. 7.3 +/- 0.9 s for N and H, respectively, P < 0.05). Muscle V. O-2 was reduced by 71% at rest and 64% with contractions in H vs. N, and O-2 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 Qo(2) relative to that of Vo(2) at the onset of contractions, leading to a decreased PmvO(2). According to Fick's law, this scenario will decrease blood-myocyte O-2 flux, thereby slowing Vo(2) kinetics and exacerbating the O-2 deficit generated at exercise onset.