Tyml K, Budreau C H
Department of Biophysics, University of Western Ontario, Canada.
Int J Microcirc Clin Exp. 1988 Aug;7(3):205-21.
The aim of this study was to use the video-microscopic approach to analyze simultaneously, at very low magnification, red cell velocity (VRBC) and density of perfused capillaries (CD) in an entire capillary network of a frog sartorius muscle before and after 3 s, 1 min and 30 min arterial occlusions. In 11 muscles studied, the 3 s occlusion caused a significant increase in the overall peak hyperemic VRBC and CD (from 0.14 +/- 0.08 to 0.28 +/- 0.16 S.D. mm/s, and from 104 +/- 41 to 126 +/- 42 S.D. cap/mm2). All muscles participated in this overall response. On average, 71% of capillaries per network showed hyperemia. The 1 min occlusion also caused significant increases in overall VRBC and CD (from 0.14 +/- 0.08 to 0.34 +/- 0.17 S.D. mm/s, and from 94 +/- 44 to 123 +/- 44 S.D. cal/mm2). In contrast to the 3 s response, only 9 out of 11 muscles participated in this response, with an average capillary participation of 80%. The 30 min occlusion caused a significant increase in overall VRBC (from 0.13 +/- 0.07 to 0.24 +/- 0.17 S.D. mm/s) but no change in CD. Only 6 out of 11 muscles participated in this response, with an average capillary participation of 56%. In terms of these microvascular data, the present study demonstrate for the first time ever (1) an appreciable spatial heterogeneity of responses within the capillary network in a single muscle following all three types of occlusions, and (2) a progressively larger muscle-to-muscle heterogeneity of responses with longer duration of occlusion. Since the spatial heterogeneity (i.e. increase, no change or even decrease in flow) was associated with groups of similarly behaving capillaries supplied by a common arteriole, the existence of a flow-suppressing arteriolar mechanism (in addition to metabolic and myogenic vasodilating mechanisms) is postulated to explain the dramatic heterogeneity of response to ischemia in this muscle.
本研究的目的是采用视频显微镜方法,在非常低的放大倍数下,同时分析蛙缝匠肌整个毛细血管网络在动脉闭塞3秒、1分钟和30分钟前后的红细胞速度(VRBC)和灌注毛细血管密度(CD)。在研究的11块肌肉中,3秒的闭塞导致整体峰值充血VRBC和CD显著增加(从0.14±0.08增加到0.28±0.16标准差mm/s,从104±41增加到126±42标准差cap/mm2)。所有肌肉都参与了这一整体反应。平均而言,每个网络中71%的毛细血管出现充血。1分钟的闭塞也导致整体VRBC和CD显著增加(从0.14±0.08增加到0.34±0.17标准差mm/s,从94±44增加到123±44标准差cal/mm2)。与3秒的反应不同,11块肌肉中只有9块参与了这一反应,平均毛细血管参与率为80%。30分钟的闭塞导致整体VRBC显著增加(从0.13±0.07增加到0.24±0.17标准差mm/s),但CD没有变化。11块肌肉中只有6块参与了这一反应,平均毛细血管参与率为56%。就这些微血管数据而言,本研究首次证明:(1)在所有三种类型的闭塞后,单个肌肉内毛细血管网络内的反应存在明显的空间异质性;(2)随着闭塞时间的延长,肌肉间反应的异质性逐渐增大。由于空间异质性(即血流增加、无变化甚至减少)与由共同小动脉供应的行为相似的毛细血管组相关,因此推测存在一种血流抑制小动脉机制(除代谢和肌源性血管舒张机制外)来解释该肌肉对缺血反应的显著异质性。