Barer G R, Russell P C, Kapeller K
Division of Clinical Sciences, Respiratory Medicine, University of Sheffield, UK.
Eur Respir J. 1998 Aug;12(2):277-83. doi: 10.1183/09031936.98.12020277.
Lung inflation was compared in isolated perfused lungs of control (C) and chronically hypoxic (CH) rats; in the latter, there is muscularization and loss of compliance in the pulmonary arterial system. During ventilation hypoxia, high alveolar pressure (Palv) elevated the pulmonary artery pressure (Ppa) less in C than in CH rats; Ppa fell during sustained inflation, rose on deflation, and after inflation hypoxic vasoconstriction was attenuated. Opposite changes took place in CH rats; Ppa often rose during inflation, fell on deflation, and after inflation hypoxic vasoconstriction was enhanced. Inflation also increased Ppa more in CH than C rats during air ventilation. Ppa/Palv relations measured during incremental inflation revealed normoxic tone in "extra-alveolar" vessels in both rat groups, which usually increased during hypoxia. In CH, but not C rats, there was also evidence for constriction in "alveolar" vessels during hypoxia. The effects of inflation were not changed by NO synthase blockade in either rat group. Pulmonary hypertensive effects of inflation in chronically hypoxic rats can be attributed to vascular remodelling.
在对照(C)大鼠和慢性缺氧(CH)大鼠的离体灌注肺中比较肺膨胀情况;在慢性缺氧大鼠中,肺动脉系统存在肌化且顺应性降低。在通气性缺氧期间,高肺泡压(Palv)使对照大鼠的肺动脉压(Ppa)升高幅度小于慢性缺氧大鼠;在持续充气期间Ppa下降,放气时升高,充气后缺氧性血管收缩减弱。慢性缺氧大鼠则出现相反变化;充气期间Ppa常升高,放气时下降,充气后缺氧性血管收缩增强。在空气通气期间,充气也使慢性缺氧大鼠的Ppa升高幅度大于对照大鼠。在递增充气期间测量的Ppa/Palv关系显示,两组大鼠“肺泡外”血管均存在常氧张力,缺氧时通常升高。在慢性缺氧大鼠而非对照大鼠中,缺氧时“肺泡内”血管也有收缩迹象。两组大鼠中,一氧化氮合酶阻断均未改变充气的效应。慢性缺氧大鼠中充气的肺动脉高压效应可归因于血管重塑。