Phair R D, Sparks H V
Am J Physiol. 1979 Jul;237(1):H1-9. doi: 10.1152/ajpheart.1979.237.1.H1.
If newly formed adenosine is the mediator of active hyperemia in skeletal muscle, tissue adenosine must increase and remain elevated during sustained muscle contraction. We tested this prediction using isolated canine anterior calf muscles. Muscle samples were obtained before and during contraction by punch biopsy and adenosine was measured by spectrophotometric enzyme assay. Tissue adenosine content didnot increase significantly above the precontraction level during either the 2- or 6-Hz contraction. We estimated (by infusing adenosine) that the adenosine concentration required to cause a dilation equal to that observed during 6-Hz contractions was 3.7 X 10(-5) M. We would have detected an increase in tissue adenosine if this concentration were established in as little as 10% of the skeletal muscle interstitium during free flow. These results indicate that adenosine released into the whole interstitial space is not the cause of free-flow exercise hyperemia.
如果新生成的腺苷是骨骼肌主动充血的介质，那么在持续的肌肉收缩过程中，组织中的腺苷必须增加并保持在较高水平。我们使用离体犬小腿前侧肌肉对这一预测进行了测试。通过打孔活检在收缩前和收缩期间获取肌肉样本，并通过分光光度酶法测定腺苷含量。在2赫兹或6赫兹收缩期间，组织腺苷含量并未显著高于收缩前水平。我们（通过输注腺苷）估计，要引起与6赫兹收缩期间观察到的扩张程度相同的扩张所需的腺苷浓度为3.7×10⁻⁵ M。如果在自由流动期间骨骼肌间质中仅有10%达到这一浓度，我们就会检测到组织腺苷增加。这些结果表明，释放到整个间质空间的腺苷不是自由流动运动性充血的原因。
