Hofman W F, Ehrhart I C
Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912.
J Appl Physiol (1985). 1990 Nov;69(5):1828-35. doi: 10.1152/jappl.1990.69.5.1828.
Hemodynamics and vascular permeability were studied during acute alveolar hypoxia in isolated canine lung lobes perfused at constant flow with autogenous blood. Hypoxia was induced in the presence (COI + Hypox, n = 6) or absence (Hypox, n = 6) of cyclooxygenase inhibition (COI) with indomethacin or meclofenamate. Hypoxic ventilation reduced blood PO2 from 143 to 25-29 Torr without a change in PCO2. During hypoxia a capillary filtration coefficient (Kf) was obtained gravimetrically as an index of vascular permeability to water. In COI + Hypox, pulmonary arterial pressure (Pa) increased from 11.5 +/- 0.7, post-COI normoxia, to a peak of 22.1 +/- 2.3 during hypoxia (P less than 0.01) without a change in capillary pressure (Pc). In contrast, hypoxia changed neither Pa nor Pc in Hypox relative to an untreated normoxic control group (Normox, n = 6, P greater than 0.05). Kfs (means +/- SE in ml.min-1.Torr-1.100 g-1) for Normox (0.070 +/- 0.014), Hypox (0.082 +/- 0.024), and COI + Hypox (0.057 +/- 0.017) did not differ from one another (P greater than 0.05). Although COI markedly enhanced the pressor response to acute alveolar hypoxia, hypoxia increased neither Pc nor vascular permeability regardless of COI.
在以自体血液恒流灌注的离体犬肺叶中，研究了急性肺泡缺氧期间的血流动力学和血管通透性。在存在（COI + Hypox，n = 6）或不存在（Hypox，n = 6）用吲哚美辛或甲氯芬那酸进行环氧化酶抑制（COI）的情况下诱导缺氧。低氧通气使血氧分压从143降至25 - 29托，而二氧化碳分压无变化。在缺氧期间，通过重量法获得毛细血管滤过系数（Kf），作为血管对水通透性的指标。在COI + Hypox组中，肺动脉压（Pa）从COI后常氧时的11.5±0.7升高至缺氧时的峰值22.1±2.3（P＜0.01），而毛细血管压（Pc）无变化。相比之下，与未处理的常氧对照组（Normox，n = 6，P＞0.05）相比，缺氧对Hypox组的Pa和Pc均无影响。Normox组（0.070±0.014）、Hypox组（0.082±0.024）和COI + Hypox组（0.057±0.017）的Kfs（以ml·min⁻¹·Torr⁻¹·100 g⁻¹表示的均值±标准误）彼此无差异（P＞0.05）。尽管COI显著增强了对急性肺泡缺氧的升压反应，但无论是否存在COI，缺氧均未增加Pc或血管通透性。
