NO IN THE LUNG

被引:62
作者
ADNOT, S [1 ]
RAFFESTIN, B [1 ]
EDDAHIBI, S [1 ]
机构
[1] HOP HENRI MONDOR,INSERM,U296,F-94010 CRETEIL,FRANCE
来源
RESPIRATION PHYSIOLOGY | 1995年 / 101卷 / 02期
关键词
AIRWAYS; (SMOOTH MUSCLE); BLOOD FLOW; (PULMONARY); HYPOXIA; (PULMONARY VASOCONSTRICTION); MEDIATORS; (NO); MUSCLE; (SMOOTH; AIRWAYS); PULMONARY CIRCULATION;
D O I
10.1016/0034-5687(95)00016-7
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
In the lung, nitric oxide (NO) derives from several cellular sources, forming networks of paracrine communication. In pulmonary vessels, NO produced by endothelial cells is a powerful vasodilator. In the airways, NO originates from epithelial cells and from adventitial nerve endings to induce smooth muscle relaxation. Activated macrophages can also produce large quantities of NO during lung immunological reactions. In the normal pulmonary circulation, NO not only mediates vasodilation, but also opposes vasoconstriction, prevents platelet adhesion, controls growth of smooth muscle and influences the composition of the extracellular matrix. During exposure to chronic hypoxia, impaired endothelial NO production contributes to the increased vasomotor tone and vascular remodelling leading to sustained pulmonary hypertension. Exogenous NO gas delivered via the airspaces is a selective pulmonary vasodilator. Inhaled NO is now used as a therapy to treat various forms of pulmonary hypertension and to improve arterial oxygenation during lung injury.
引用
收藏
页码:109 / 120
页数:12
相关论文
共 32 条
  • [1] HEMODYNAMIC AND GAS-EXCHANGE RESPONSES TO INFUSION OF ACETYLCHOLINE AND INHALATION OF NITRIC-OXIDE IN PATIENTS WITH CHRONIC OBSTRUCTIVE LUNG-DISEASE AND PULMONARY-HYPERTENSION
    ADNOT, S
    KOUYOUMDJIAN, C
    DEFOUILLOY, C
    ANDRIVET, P
    SEDIAME, S
    HERIGAULT, R
    FRATACCI, MD
    [J]. AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 148 (02): : 310 - 316
  • [2] LOSS OF ENDOTHELIUM-DEPENDENT RELAXANT ACTIVITY IN THE PULMONARY CIRCULATION OF RATS EXPOSED TO CHRONIC HYPOXIA
    ADNOT, S
    RAFFESTIN, B
    EDDAHIBI, S
    BRAQUET, P
    CHABRIER, PE
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1991, 87 (01) : 155 - 162
  • [3] HYPOXIC PULMONARY VASOCONSTRICTION IS ENHANCED BY INHIBITION OF THE SYNTHESIS OF AN ENDOTHELIUM DERIVED RELAXING FACTOR
    ARCHER, SL
    TOLINS, JP
    RAIJ, L
    WEIR, EK
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 164 (03) : 1198 - 1205
  • [4] AUGMENTATION OF HYPOXIC PULMONARY VASOCONSTRICTION IN THE ISOLATED PERFUSED RAT LUNG BY INVITRO ANTAGONISTS OF ENDOTHELIUM-DEPENDENT RELAXATION
    BRASHERS, VL
    PEACH, MJ
    ROSE, CE
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1988, 82 (05) : 1495 - 1502
  • [5] LOSS OF ENDOTHELIUM-DEPENDENT RELAXATION IN PROXIMAL PULMONARY-ARTERIES FROM RATS EXPOSED TO CHRONIC HYPOXIA - EFFECTS OF IN-VIVO AND IN-VITRO SUPPLEMENTATION WITH L-ARGININE
    CARVILLE, C
    RAFFESTIN, B
    EDDAHIBI, S
    BLOUQUIT, Y
    ADNOT, S
    [J]. JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1993, 22 (06) : 889 - 896
  • [6] BRONCHODILATOR ACTION OF INHALED NITRIC-OXIDE IN GUINEA-PIGS
    DUPUY, PM
    SHORE, SA
    DRAZEN, JM
    FROSTELL, C
    HILL, WA
    ZAPOL, WM
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (02) : 421 - 428
  • [7] L-ARGININE RESTORES ENDOTHELIUM-DEPENDENT RELAXATION IN PULMONARY CIRCULATION OF CHRONICALLY HYPOXIC RATS
    EDDAHIBI, S
    ADNOT, S
    CARVILLE, C
    BLOUQUIT, Y
    RAFFESTIN, B
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (02): : L194 - L200
  • [8] INHALED NITRIC-OXIDE - A SELECTIVE PULMONARY VASODILATOR REVERSING HYPOXIC PULMONARY VASOCONSTRICTION
    FROSTELL, C
    FRATACCI, MD
    WAIN, JC
    JONES, R
    ZAPOL, WM
    [J]. CIRCULATION, 1991, 83 (06) : 2038 - 2047
  • [9] FURCHGOTT RF, 1980, NATURE, V280, P373
  • [10] NITRIC OXIDE-GENERATING VASODILATORS AND 8-BROMO-CYCLIC GUANOSINE-MONOPHOSPHATE INHIBIT MITOGENESIS AND PROLIFERATION OF CULTURED RAT VASCULAR SMOOTH-MUSCLE CELLS
    GARG, UC
    HASSID, A
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1989, 83 (05) : 1774 - 1777