Hamann Jason J, Buckwalter John B, Clifford Philip S
Medical College of Wisconsin, VA Medical Center, Milwaukee, WI 53295, USA.
J Physiol. 2004 Jun 15;557(Pt 3):1013-20. doi: 10.1113/jphysiol.2004.062836. Epub 2004 Apr 8.
There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis we examined the blood flow response to a brief tetanic contraction in which potassium (K(+)) was infused intra-arterially to elevate the K(+) and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs control contractions increased hindlimb blood flow by 97 +/- 14 ml min(-1). During K(+) infusion the hyperaemic response to contraction was 8 +/- 3 ml min(-1). Since the hindlimb blood flow was reduced during K(+) infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion the hyperaemic response to contraction was preserved (89 +/- 23 ml min(-1)). Recovery contractions performed after the discontinuation of the K(+) infusion elicited blood flow responses similar to control (100 +/- 11 ml min(-1)). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs (n= 6) K(+) infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation, there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible for the initial contraction-induced hyperaemia. We conclude that the increase in blood flow immediately following a single muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.
运动开始时，活跃骨骼肌的血流量会迅速增加，但其引发这种增加的机制仍不清楚。我们假设，运动开始时活跃骨骼肌血流量的迅速增加是由于平滑肌超极化导致血管舒张的结果。为了验证这一假设，我们检测了对短暂强直收缩的血流反应，在该实验中通过动脉内注入钾离子（K⁺）来升高细胞外钾离子浓度（[K⁺]o），并钳制骨骼肌血管床内平滑肌的膜电位。在6只麻醉的比格犬中，对照收缩使后肢血流量增加了97±14 ml·min⁻¹。在注入K⁺期间，对收缩的充血反应为8±3 ml·min⁻¹。由于注入K⁺期间后肢血流量减少，注入去氧肾上腺素也产生了类似的基线血流量减少。在注入去氧肾上腺素期间，对收缩的充血反应得以保留（89±23 ml·min⁻¹）。停止注入K⁺后进行的恢复性收缩引发的血流反应与对照相似（100±11 ml·min⁻¹）。在另一个使用杂种犬分离的腓肠肌的实验方案中（n = 6），注入K⁺并未改变骨骼肌产生的力量。我们的数据表明，在没有血管舒张的情况下，血流量几乎没有变化。这一发现的一个启示是，肌肉泵不能解释最初的收缩诱导性充血。我们得出结论，单次肌肉收缩后立即出现的血流量增加是由于血管舒张，推测是平滑肌超极化的结果。
