Hillier S C, Graham J A, Hanger C C, Godbey P S, Glenny R W, Wagner W W
Department of Anesthesia, Indiana University School of Medicine, Indianapolis 46202, USA.
J Appl Physiol (1985). 1997 Apr;82(4):1084-90. doi: 10.1152/jappl.1997.82.4.1084.
Pulmonary microvessels (<70 microm) lack a complete muscular media. We tested the hypothesis that these thin-walled vessels do not participate in the hypoxic pressor response. Isolated canine lobes were pump perfused at precisely known microvascular pressures. A videomicroscope, coupled to a computerized image-enhancement system, permitted accurate diameter measurements of subpleural arterioles and venules, with each vessel serving as its own control. While vascular pressure was maintained constant throughout the protocol, hypoxia caused an average reduction of 25% of microvessel diameters. The constriction was reversed when nitric oxide was added to the hypoxic gas mixture. The nitric oxide reversal, combined with a lack of lobar blood flow redistribution as measured by fluorescent microspheres, shows that the constriction was active. This response suggests the unexpected potential for active intra-acinar ventilation-perfusion matching.
肺微血管（<70微米）缺乏完整的肌性中膜。我们检验了这样一个假说，即这些薄壁血管不参与缺氧升压反应。对离体犬肺叶以精确已知的微血管压力进行泵灌注。一台与计算机图像增强系统相连的视频显微镜能够准确测量胸膜下小动脉和小静脉的直径，每根血管都作为自身的对照。在整个实验过程中血管压力保持恒定，而缺氧导致微血管直径平均减小25%。当向缺氧气体混合物中添加一氧化氮时，这种收缩反应被逆转。一氧化氮的逆转作用，再加上通过荧光微球测量显示的肺叶内血流再分布缺乏，表明这种收缩是主动的。这种反应提示了腺泡内主动通气-灌注匹配存在意想不到的可能性。
