Pathogenesis of pulmonary edema: Learning from high-altitude pulmonary edema

被引:43
作者
Sartori, Claudio [1 ]
Allemann, Yves [2 ]
Scherrer, Urs [1 ]
机构
[1] CHU Vaudois, Botnar Ctr Extreme Med, Dept Internal Med, CH-1011 Lausanne, Switzerland
[2] Swiss Cardiovasc Ctr Bern, Inselspital, Bern, Switzerland
关键词
pulmonary edema; high-altitude; hypoxia; capillary stress failure; HAPE;
D O I
10.1016/j.resp.2007.04.006
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Pulmonary edema is a problem of major clinical importance resulting from a persistent imbalance between forces that drive water into the airspace of the lung and the biological mechanisms for its removal. Here, we will review the fundamental mechanisms implicated in the regulation of alveolar fluid homeostasis. We will then describe the perturbations of pulmonary fluid homeostasis implicated in the pathogenesis of pulmonary edema in conditions associated with increased pulmonary capillary pressure, namely cardiogenic pulmonary edema and high-altitude pulmonary edema (HAPE), with particular emphasis on the latter that has provided important new insight into underlying mechanisms of pulmonary edema. We will provide evidence that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent a central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction, and, in turn, capillary stress failure and alveolar fluid flooding. We will then demonstrate that exaggerated pulmonary hypertension, while possibly a prerequisite, may not always be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we will outline, how this new insight gained from studies in HAPE, may be translated into the management of pulmonary edema and hypoxemia related disease states in general. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:338 / 349
页数:12
相关论文
共 101 条
[1]   Simultaneous selection of the wild-type genotypes of the G894T and 4B/4A polymorphisms of NOS3 associate with high-altitude adaptation [J].
Ahsan, A ;
Norboo, T ;
Baig, MA ;
Pasha, MAQ .
ANNALS OF HUMAN GENETICS, 2005, 69 :260-267
[2]   ENOS allelic variants at the same locus associate with HAPE and adaptation [J].
Ahsan, A ;
Charu, R ;
Pasha, MAQ ;
Norboo, T ;
Charu, R ;
Afrin, F ;
Ahsan, A ;
Baig, MA .
THORAX, 2004, 59 (11) :1000-1002
[3]   Patent Foramen ovale and high-altitude pulmonary edema [J].
Allemann, Yves ;
Hutter, Damian ;
Lipp, Ernst ;
Sartori, Claudio ;
Duplain, Herve ;
Egli, Marc ;
Cook, Stephane ;
Scherrer, Urs ;
Seiler, Christian .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2006, 296 (24) :2954-2958
[4]  
Barker D.J. P., 1994, MOTHERS BABIES DIS L
[5]   PREVENTION OF HIGH-ALTITUDE PULMONARY-EDEMA BY NIFEDIPINE [J].
BARTSCH, P ;
MAGGIORINI, M ;
RITTER, M ;
NOTI, C ;
VOCK, P ;
OELZ, O .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (18) :1284-1289
[6]   INTERACTION OF P-NUBARO2 WITH PAO2 ON HYPOXIC PULMONARY VASOCONSTRICTION [J].
BENUMOF, JL ;
PIRLO, AF ;
JOHANSON, I ;
TROUSDALE, FR .
JOURNAL OF APPLIED PHYSIOLOGY, 1981, 51 (04) :871-874
[7]   Hypoxia impairs systemic endothelial function in individuals prone to high-altitude pulmonary edema [J].
Berger, MM ;
Hesse, C ;
Dehnert, C ;
Siedler, H ;
Kleinbongard, P ;
Bardenheuer, HJ ;
Kelm, M ;
Bärtsch, P ;
Haefeli, WE .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2005, 172 (06) :763-767
[8]   Endothelium-derived nitric oxide regulates systemic and pulmonary vascular resistance during acute hypoxia in humans [J].
Blitzer, ML ;
Loh, E ;
Roddy, MA ;
Stamler, JS ;
Creager, MA .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1996, 28 (03) :591-596
[9]   Oxidative stress in severe pulmonary hypertension [J].
Bowers, R ;
Cool, C ;
Murphy, RC ;
Tuder, RM ;
Hopken, MW ;
Flores, SC ;
Voelkel, NF .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2004, 169 (06) :764-769
[10]   PERMEABILITY OF LUNG CAPILLARIES TO MACROMOLECULES IN FOETAL AND NEW-BORN LAMBS AND SHEEP [J].
BOYD, RDH ;
HILL, JR ;
HUMPHREYS, PW ;
NORMAND, ICS ;
REYNOLDS, EO ;
STRANG, LB .
JOURNAL OF PHYSIOLOGY-LONDON, 1969, 201 (03) :567-+