Shirai M, Shimouchi A, Kawaguchi A T, Sunagawa K, Ninomiya I
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Suita, Osaka, Japan.
Am J Physiol. 1996 Mar;270(3 Pt 2):H974-80. doi: 10.1152/ajpheart.1996.270.3.H974.
Using an X-ray television system on the in vivo cat lung, we directly measured internal diameter (ID) changes in the small pulmonary arteries and veins (100-1,100 microns ID) in response to 5, 15, and 40 ppm nitric oxide (NO) inhalations. We also measured to what extent 40 ppm NO inhalation can attenuate large ID constrictions at the different serial segments of the small vessels due to unilobar anoxic (0% O2) exposure. Under normoxic conditions, 5-40 ppm NO inhalations significantly increased the ID of both arteries and veins less than approximately 900 microns dose dependently but caused no significant, or only slight, ID increases in the vessels larger than this, if any at all. The ID increase in the serially connected arteries was nonuniform (4-18, 8-28, and 7-35% with 5, 15, and 40 ppm NO inhalations, respectively), whereas that for the veins was relatively uniform (4-9, 6-17, and 7-18% with 5, 15, and 40 ppm NO, respectively). The maximum ID increase occurred in the 200- to 500- and 200- to 700-microns arteries in response to 5-15 and 40 ppm NO, respectively. Unilobar anoxic exposure significantly decreased the ID of the 100- to 700-microns arteries and veins, but not the ID of the other-sized vessels. The ID decrease in the serially connected arteries was nonuniform (13-29%) but relatively uniform in the veins (8-12%). The maximum ID decrease occurred in the 200- to 300-microns arteries. However, adding 40 ppm NO to the lobe completely eradicated the ID decreases at all segments of the arteries and veins and, instead, caused significant ID increase (11-21%) in the arteries and (10-12%) in the veins. The data indicate that, according to dosage, 5-40 ppm NO inhalations cause selective dilation of approximately 100- to 900-microns pulmonary arteries and veins, particularly the 200- to 700-microns arteries. During anoxic exposure, the vasodilator effect of NO is preserved and can completely reverse the marked pulmonary vasoconstriction.
我们使用X射线电视系统对活体猫肺进行研究，直接测量了小肺动脉和静脉（内径100 - 1100微米）在吸入5 ppm、15 ppm和40 ppm一氧化氮（NO）后的内径变化。我们还测量了吸入40 ppm NO能在多大程度上减轻由于单叶缺氧（0%氧气）暴露导致的小血管不同连续节段的大内径收缩。在常氧条件下，吸入5 - 40 ppm NO可使内径小于约900微米的动脉和静脉内径剂量依赖性地显著增加，但对大于此内径的血管，若有变化，也无显著增加或仅有轻微增加。连续连接的动脉内径增加不均匀（吸入5 ppm、15 ppm和40 ppm NO时分别为4 - 18%、8 - 28%和7 - 35%），而静脉内径增加相对均匀（吸入5 ppm、15 ppm和40 ppm NO时分别为4 - 9%、6 - 17%和7 - 18%）。吸入5 - 15 ppm和40 ppm NO时，最大内径增加分别出现在200 - 500微米和200 - 700微米的动脉中。单叶缺氧暴露显著降低了100 - 700微米动脉和静脉的内径，但对其他尺寸血管的内径无影响。连续连接的动脉内径减小不均匀（13 - 29%），但静脉内径减小相对均匀（8 - 12%）。最大内径减小出现在200 - 300微米的动脉中。然而，向肺叶添加40 ppm NO可完全消除动脉和静脉各节段的内径减小，反而使动脉内径显著增加（11 - 21%），静脉内径增加（10 - 12%）。数据表明，根据剂量，吸入5 - 40 ppm NO可使内径约100 - 900微米的肺动脉和静脉选择性扩张，尤其是200 - 700微米的动脉。在缺氧暴露期间，NO的血管舒张作用得以保留，并可完全逆转明显的肺血管收缩。
