Organ crosstalk during acute lung injury, acute respiratory distress syndrome, and mechanical ventilation

被引:50
作者
Quilez, Maria E. [1 ]
Lopez-Aguilar, Josefina [1 ,2 ,3 ]
Blanch, Lluis [1 ,2 ,3 ]
机构
[1] Inst Salud Carlos III, CIBER Enfermedades Resp, Madrid, Spain
[2] Corp Sanitaria, Crit Care Ctr, Sabadell, Spain
[3] Univ Parc Tauli, Sabadell, Spain
关键词
acute lung injury; inflammation; mechanical ventilation; organ crosstalk; VASCULAR FLOW; BRAIN-INJURY; MODEL; PULMONARY; FAILURE; ACTIVATION; PRESSURE; OUTCOMES; SEPSIS; DAMAGE;
D O I
10.1097/MCC.0b013e32834ef3ea
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Purpose of review Multiple organ failure is the main cause of morbidity and mortality in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) patients. Moreover, survivors of both ALI and ARDS often show significant neurocognitive decline at discharge. These data suggest a deleterious organ crosstalk between lungs and distal organs. This article reviews the recent literature concerning the role of this organ crosstalk during ALI, ARDS, and mechanical ventilation, especially focusing on brain-lung communication. Recent findings Numerous pulmonary and extrapulmonary disorders could predispose critically ill patients to ALI and ARDS. Mechanical ventilation, although a lifesaving intervention, could contribute by modulating the mechanisms involved in the pathophysiology of lung damage and their impact on remote organs. Emerging clinical and experimental evidence supports the hypothesis of a multidirectional organ crosstalk between lungs and distal organs. Summary Organ crosstalk is an emerging area of research in lung disease in critically ill patients. The findings of these studies are clinically relevant and show the importance of an integrative approach in the management of critical patients. However, further studies are necessary to understand the complex interactions concurring in these pathologies.
引用
收藏
页码:23 / 28
页数:6
相关论文
共 41 条
[1]   THE AMERICAN-EUROPEAN CONSENSUS CONFERENCE ON ARDS - DEFINITIONS, MECHANISMS, RELEVANT OUTCOMES, AND CLINICAL-TRIAL COORDINATION [J].
BERNARD, GR ;
ARTIGAS, A ;
BRIGHAM, KL ;
CARLET, J ;
FALKE, K ;
HUDSON, L ;
LAMY, M ;
LEGALL, JR ;
MORRIS, A ;
SPRAGG, R ;
COCHIN, B ;
LANKEN, PN ;
LEEPER, KV ;
MARINI, J ;
MURRAY, JF ;
OPPENHEIMER, L ;
PESENTI, A ;
REID, L ;
RINALDO, J ;
VILLAR, J ;
VANASBECK, BS ;
DHAINAUT, JF ;
MANCEBO, J ;
MATTHAY, M ;
MEYRICK, B ;
PAYEN, D ;
PERRET, C ;
FOWLER, AA ;
SCHALLER, MD ;
HUDSON, LD ;
HYERS, T ;
KNAUS, W ;
MATTHAY, R ;
PINSKY, M ;
BONE, RC ;
BOSKEN, C ;
JOHANSON, WG ;
LEWANDOWSKI, K ;
REPINE, J ;
RODRIGUEZROISIN, R ;
ROUSSOS, C ;
ANTONELLI, MA ;
BELOUCIF, S ;
BIHARI, D ;
BURCHARDI, H ;
LEMAIRE, F ;
MONTRAVERS, P ;
PETTY, TL ;
ROBOTHAM, J ;
ZAPOL, W .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 149 (03) :818-824
[2]   Low Tidal Volume Ventilation in a Porcine Model of Acute Lung Injury Improves Cerebral Tissue Oxygenation [J].
Bickenbach, Johannes ;
Zoremba, Norbert ;
Fries, Michael ;
Dembinski, Rolf ;
Doering, Robert ;
Ogawa, Eileen ;
Rossaint, Rolf ;
Kuhlen, Ralf .
ANESTHESIA AND ANALGESIA, 2009, 109 (03) :847-855
[3]   Impact of low pulmonary vascular pressure on ventilator-induced lung injury [J].
Broccard, AF ;
Vannay, C ;
Feihl, F ;
Schaller, MD .
CRITICAL CARE MEDICINE, 2002, 30 (10) :2183-2190
[4]   Consequences of vascular flow on lung injury induced by mechanical ventilation [J].
Broccard, AF ;
Hotchkiss, JR ;
Kuwayama, N ;
Olson, DA ;
Jamal, S ;
Wangensteen, DO ;
Marini, JJ .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1998, 157 (06) :1935-1942
[5]   Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. [J].
Brower, RG ;
Matthay, MA ;
Morris, A ;
Schoenfeld, D ;
Thompson, BT ;
Wheeler, A ;
Wiedemann, HP ;
Arroliga, AC ;
Fisher, CJ ;
Komara, JJ ;
Perez-Trepichio, P ;
Parsons, PE ;
Wolkin, R ;
Welsh, C ;
Fulkerson, WJ ;
MacIntyre, N ;
Mallatratt, L ;
Sebastian, M ;
McConnell, R ;
Wilcox, C ;
Govert, J ;
Thompson, D ;
Clemmer, T ;
Davis, R ;
Orme, J ;
Weaver, L ;
Grissom, C ;
Eskelson, M ;
Young, M ;
Gooder, V ;
McBride, K ;
Lawton, C ;
d'Hulst, J ;
Peerless, JR ;
Smith, C ;
Brownlee, J ;
Pluss, W ;
Kallet, R ;
Luce, JM ;
Gottlieb, J ;
Elmer, M ;
Girod, A ;
Park, P ;
Daniel, B ;
Gropper, M ;
Abraham, E ;
Piedalue, F ;
Glodowski, J ;
Lockrem, J ;
McIntyre, R .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (18) :1301-1308
[6]   Neuroimmune Regulation of Ventilator-induced Lung Injury [J].
dos Santos, Claudia C. ;
Shan, Yuexin ;
Akram, Ali ;
Slutsky, Arthur S. ;
Haitsma, Jack J. .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2011, 183 (04) :471-482
[7]   Ventilator-induced lung injury - Lessons from experimental studies [J].
Dreyfuss, D ;
Saumon, G .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1998, 157 (01) :294-323
[8]   Injurious mechanical ventilation affects neuronal activation in ventilated rats [J].
Elisa Quilez, Maria ;
Fuster, Gemma ;
Villar, Jesus ;
Flores, Carlos ;
Marti-Sistac, Octavi ;
Blanch, Lluis ;
Lopez-Aguilar, Josefina .
CRITICAL CARE, 2011, 15 (03)
[9]   HIGH LUNG-VOLUME INCREASES STRESS FAILURE IN PULMONARY CAPILLARIES [J].
FU, ZX ;
COSTELLO, ML ;
TSUKIMOTO, K ;
PREDILETTO, R ;
ELLIOTT, AR ;
MATHIEUCOSTELLO, O ;
WEST, JB .
JOURNAL OF APPLIED PHYSIOLOGY, 1992, 73 (01) :123-133
[10]   Noninjurious mechanical ventilation activates a proinflammatory transcriptional program in the lung [J].
Gharib, Sina A. ;
Liles, W. Conrad ;
Klaff, Lindy S. ;
Altemeier, William A. .
PHYSIOLOGICAL GENOMICS, 2009, 37 (03) :239-248