Grimminger F, Spriestersbach R, Weissmann N, Walmrath D, Seeger W
Department of Internal Medicine, Justus-Liebig University, Giessen, Germany.
J Appl Physiol (1985). 1995 Apr;78(4):1509-15. doi: 10.1152/jappl.1995.78.4.1509.
Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs. J. Appl. Physiol. 78(4): 1509-1515, 1995.--We investigated the role of nitric oxide (NO) generation in hypoxic pulmonary vasoconstriction in buffer-perfused rabbit lungs. Exhaled NO was detected by chemiluminescence, and intravascular NO release was quantified as perfusate accumulation of nitrite, peroxynitrite, and nitrate (NOx). Under baseline conditions, exhaled NO was 45.3 +/- 4.1 parts per billion (1.8 +/- 0.2 nmol/min), and lung NOx release into the perfusate was 4.1 +/- 0.4 nmol/min. Alveolar hypoxia (alveolar PO2 of approximately 23 Torr) induced readily reproducible pressor responses preceded by a sharp drop in exhaled NO concentration. In contrast, perfusate NOx accumulation was not affected. Vasoconstrictor responses to U-46619 and angiotensin II were not accompanied by a decrease in NO exhalation. NG-monomethyl-L-arginine dose-dependently suppressed NO exhalation and amplified pressor responses to hypoxia > U-46619 and angiotensin II. In conclusion, portions of baseline NO generation originating from sites with ready access to the gaseous space sharply decrease in response to alveolar hypoxia, whereas the intravascular release of NO is unchanged. Such differential regulation of lung NO synthesis in response to hypoxia may suggest a complex role in the regulation or modulation of hypoxic pulmonary vasoconstriction.
缓冲液灌注兔肺中一氧化氮的生成与低氧性肺血管收缩。《应用生理学杂志》1995年第78卷第4期：1509 - 1515页。——我们研究了一氧化氮（NO）生成在缓冲液灌注兔肺低氧性肺血管收缩中的作用。通过化学发光法检测呼出的NO，并将血管内NO释放量量化为灌注液中亚硝酸盐、过氧亚硝酸盐和硝酸盐（NOx）的积累量。在基线条件下，呼出的NO为45.3±4.1十亿分比（1.8±0.2 nmol/分钟），肺向灌注液中释放的NOx为4.1±0.4 nmol/分钟。肺泡低氧（肺泡PO2约为23托）诱导出易于重复的升压反应，在此之前呼出的NO浓度会急剧下降。相比之下，灌注液中NOx的积累不受影响。对U - 46619和血管紧张素II的血管收缩反应并未伴随NO呼出量的减少。NG - 单甲基 - L - 精氨酸剂量依赖性地抑制NO呼出，并增强对低氧、U - 46619和血管紧张素II的升压反应。总之，响应肺泡低氧时，源自易于进入气体空间部位的基线NO生成部分会急剧减少，而血管内NO释放则保持不变。这种低氧时肺NO合成的差异调节可能提示其在低氧性肺血管收缩的调节或调制中具有复杂作用。
