Klabunde R E
Am J Physiol. 1983 Feb;244(2):H273-80. doi: 10.1152/ajpheart.1983.244.2.H273.
Postischemic vasodilation (PIVD) was studied in pump-perfused dog gracilis muscles. The hemodynamic responses to 1, 3, and 5 min of ischemia were evaluated in the presence and absence of intraarterial infusions of dipyridamole in concentrations that inhibit cellular transport of adenosine. Dipyridamole infusion produced concentration-dependent reductions in vascular resistance and increased the time for 50% recovery (t0.5) in vascular resistance by 39% following 5 min of ischemia. The t0.5 for PIVD was unaffected by dipyridamole following 1 and 3 min of ischemia. Dipyridamole elevated tissue adenosine content two- to three-fold at 1, 3, and 5 min of ischemia compared with saline controls. Intra-arterial infusions of adenosine deaminase along with dipyridamole completely prevented the dipyridamole-induced increase in tissue adenosine, demonstrating that dipyridamole increases extracellular adenosine during muscle ischemia. The significance of these findings is analyzed using a two-compartment model for the distribution of adenosine. The data indicate that a severalfold increase in interstitial adenosine content does not alter PIVD and that the hemodynamic effects of dipyridamole following 5 min of ischemia may be due to some mechanism other than enhanced accumulation of adenosine.
在泵灌注的犬股薄肌中研究了缺血后血管舒张（PIVD）。在有无动脉内输注双嘧达莫（其浓度可抑制腺苷的细胞转运）的情况下，评估了对1、3和5分钟缺血的血流动力学反应。输注双嘧达莫导致血管阻力呈浓度依赖性降低，并使缺血5分钟后血管阻力恢复50%的时间（t0.5）增加了39%。缺血1分钟和3分钟后，双嘧达莫对PIVD的t0.5没有影响。与生理盐水对照组相比，在缺血1、3和5分钟时，双嘧达莫使组织腺苷含量升高了两到三倍。动脉内输注腺苷脱氨酶与双嘧达莫一起完全阻止了双嘧达莫诱导的组织腺苷增加，表明双嘧达莫在肌肉缺血期间增加了细胞外腺苷。使用腺苷分布的双室模型分析了这些发现的意义。数据表明，间质腺苷含量增加几倍并不会改变PIVD，并且缺血5分钟后双嘧达莫的血流动力学效应可能是由于腺苷积累增强以外的某种机制。
