Lombard J H, Duling B R
Am J Physiol. 1981 Nov;241(5):H748-55. doi: 10.1152/ajpheart.1981.241.5.H748.
To investigate mechanisms of reactive hyperemia, single arterioles of the hamster cheek pouch were occluded for periods of 1 s-3 min. Arteriolar diameters were measured upstream and downstream from the occlusion. O2 availability to the tissue was controlled by equilibrating the suffusate with low (0% O2) or high (10% O2) O2 gas mixtures. After very brief occlusions downstream sites dilated transiently, but upstream diameters did not change. Upstream and downstream diameters both increased during longer occlusions with O%-O2 and 10%-O2 suffusion. Microvascular pressure decreased at downstream sites and increased at upstream sites within 1-2 s of occlusion. During 0%-O2 suffusion tissue and periarteriolar O2 tensions (PO2's) began to decrease within 2 s of occlusion and had decreased halfway to their minimum value by 7 s. PO2's decreased only slightly during 10%-O2 suffusion. Calculated first-order rate constants for arteriolar diameter recovery decreased and total recovery time increased as occlusion duration was prolonged. This study suggests that multiple mechanisms (metabolic, myogenic, and passive) contribute to reactive hyperemia.
为研究反应性充血的机制，将仓鼠颊囊的单个小动脉闭塞1秒至3分钟。在闭塞部位的上游和下游测量小动脉直径。通过用低氧（0%氧气）或高氧（10%氧气）气体混合物平衡灌注液来控制组织的氧气供应。在非常短暂的闭塞后，下游部位短暂扩张，但上游直径没有变化。在使用0%-氧气和10%-氧气灌注进行较长时间的闭塞期间，上游和下游直径均增加。闭塞后1至2秒内，微血管压力在下游部位降低，在上游部位升高。在0%-氧气灌注期间，组织和小动脉周围的氧张力（PO2）在闭塞后2秒内开始下降，到7秒时已降至其最小值的一半。在10%-氧气灌注期间，PO2仅略有下降。随着闭塞持续时间的延长，计算得出的小动脉直径恢复的一级速率常数降低，总恢复时间增加。这项研究表明，多种机制（代谢、肌源性和被动机制）促成了反应性充血。
