RESPONSES OF SEQUENTIALLY BRANCHING MACROVESSELS AND MICROVESSELS DURING REACTIVE HYPEREMIA IN SKELETAL-MUSCLE
RESPONSES OF SEQUENTIALLY BRANCHING MACROVESSELS AND MICROVESSELS DURING REACTIVE HYPEREMIA IN SKELETAL-MUSCLE
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DOI：
10.1016/0026-2862(87)90077-x
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发表时间：
1987-07-01
影响因子：
3.1
通讯作者：
MEININGER, GA
中科院分区：
文献类型：
--
作者：
MEININGER, GA
Small artery and microvascular responses during reactive hyperemia were compared to determine which resistance-bearing vessels played a role in controlling blood flow and resistance for the cremaster skeletal muscle. Using an intravital video microscopy system, measurements of microvessel pressure, flow velocity, and diameter were obtained from cremaster muscles in anesthetized rats. These were compared with measurements of diameter that were obtained from the small arteries feeding the cremaster muscle. After a 60-sec occlusion of the sacral aorta total cremaster blood flow increased approximately 28% and calculated microvascular resistance for the cremaster muscle fell 50%. During the period of occlusion, diameters of small arteries (159-292 .mu.m) decreased despite the presence of smooth muscle tone. Likewise, the diameters of large arterioles (65-117 .mu.m) decreased whereas small arterioles (16-30 .mu.m) dilated. The decrease in diameter of the small arteries and large arterioles was accompanied by a significant fall in intravascular pressure, suggesting that the behavior of these vessels was largely passive. Immediately following the release of occlusion, small arteries and large arterioles returned to their control diameters while small arterioles remained in a dilated state for approximately 2 min. These results indicate that for the cremaster muscle, (1) vascular responses vary along the length of the arterial tree during reactive hyperemia, (2) small but not large artrioles are primarily responsible for the decrease in network resistane and subsequent hyperemia following occlusion, and (3) the small feeder arteries did not dilate during reactive hyperemia but instead acted to set a limit on the decrease in network resistance and the increase in blood flow.
