Proctor K G, Duling B R
Am J Physiol. 1982 Apr;242(4):H688-97. doi: 10.1152/ajpheart.1982.242.4.H688.
Striated muscle arteriolar responses to 1.5 min of 1-Hz contraction and/or increased tissue O2 partial pressure (PO2) were observed during exposure of the tissue interstitial space to adenosine deaminase (ADA) to evaluate the role of adenosine (ADO) as a regulator for blood flow. The microvasculature of the hamster cremaster muscle was continuously superfused with a bicarbonate buffer containing 11 micrograms ADA/ml and equilibrated with 5% CO2 and various O2 concentrations. Arterioles (resting diameter less than 30 micrometers) constricted a maximum of 55% when the superfusate gas tension was increased from 0 to 95% O2, but ADA had no effect on this behavior. Arterioles dilated during exercise, but the diameter change was decreased 20-25% during exercise with ADA treatment at both normal and elevated tissue PO2. As ADA had no effect on either the vasodilation to 2-chloroadenosine or resting arteriolar diameter, it was probably specific in its action. Assuming that all extracellular ADO was accessible to ADA and that ADA neutralized most newly formed ADO, we conclude that ADO is one component of a multifactor system mediating short periods of free-flow exercise hyperemia and that the release of ADO is not necessarily dependent on tissue hypoxia.
在将组织间隙暴露于腺苷脱氨酶（ADA）的过程中，观察了横纹肌小动脉对1赫兹收缩1.5分钟和/或组织氧分压（PO2）升高的反应，以评估腺苷（ADO）作为血流调节因子的作用。用含有11微克ADA/毫升的碳酸氢盐缓冲液持续灌注仓鼠提睾肌的微脉管系统，并用5%二氧化碳和各种氧浓度进行平衡。当灌注液气体张力从0增加到95%氧气时，小动脉（静息直径小于30微米）最大收缩55%，但ADA对这种行为没有影响。小动脉在运动期间扩张，但在正常和升高的组织PO2条件下，用ADA处理的运动期间直径变化减少20 - 25%。由于ADA对2 - 氯腺苷引起的血管舒张或静息小动脉直径均无影响，其作用可能具有特异性。假设所有细胞外ADO均可被ADA作用，且ADA中和了大多数新形成的ADO，我们得出结论，ADO是介导短时间自由流动运动性充血的多因素系统的一个组成部分，并且ADO的释放不一定依赖于组织缺氧。
