2005
DOI: 10.1097/00075198-200502000-00013
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Overview of ventilator-induced lung injury mechanisms

Abstract: The proportion of patients receiving protective ventilatory strategies remains modest. If efforts to minimize the iatrogenic consequences of mechanical ventilation are to succeed, there must be a greater understanding of the signal transduction mechanisms and the development of potential pharmacologic targets to modulate the molecular and cellular effects of lung stretch.

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Cited by 184 publications
(175 citation statements)
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References 47 publications
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“…Thus, further investigation into the mechanisms of acute respiratory distress syndrome remains a top priority for the cardiopulmonary field. The onset of lung injury is characterized by increased vascular permeability and expression of adhesive surface molecules (ICAM-1, VCAM-1, and E-selectin) by activated lung vascular endothelium, which promotes leukocyte adhesion, recruitment to the lung, and inflammatory cytokine production (3)(4)(5).…”
Section: Clinical Relevancementioning
confidence: 99%
“…Thus, further investigation into the mechanisms of acute respiratory distress syndrome remains a top priority for the cardiopulmonary field. The onset of lung injury is characterized by increased vascular permeability and expression of adhesive surface molecules (ICAM-1, VCAM-1, and E-selectin) by activated lung vascular endothelium, which promotes leukocyte adhesion, recruitment to the lung, and inflammatory cytokine production (3)(4)(5).…”
Section: Clinical Relevancementioning
confidence: 99%
“…[1][2][3][4] En la actualidad se acepta que, aunque la asistencia respiratoria mec谩nica (ARM) es muchas veces indispensable para la supervivencia del paciente, tambi茅n es parte del problema del SDRA, ya que datos experimentales y cl铆nicos demuestran que la ventilaci贸n mec谩nica es capaz de generar una lesi贸n histopatol贸gicamente y cl铆ni-camente indiferenciable del SDRA. [5][6][7][8] El cl谩sico estudio de Webb y cols., 9 fue el primero en demostrar, inequ铆vocamente, que la ventilaci贸n mec谩nica puede producir edema pulmonar; y al mismo tiempo, fue una demostraci贸n de que la presi贸n positiva al fin de la espiraci贸n (PEEP), con una estrategia de limitaci贸n del volumen corriente, protege de la lesi贸n pulmonar asociada a la ventilaci贸n mec谩nica. En esta l铆nea de conocimiento, hallazgos como los de Dreyfuss y cols., 10 en estudios experimentales a finales de los ochenta, sobre la relaci贸n entre el empleo de alto volumen corriente y el incremento de la lesi贸n pulmonar; los estudios hechos por el grupo de Gattinoni mediante tomograf铆a axial computarizada y el desarrollo del concepto de baby-lung, 11 que muestran que, en realidad, en el SDRA s贸lo es una peque帽a proporci贸n del pulm贸n la que interviene en el intercambio gaseoso y el resto del 贸rgano se encuentra colapsado o inundado y, por 煤ltimo, los resultados cl铆nicos del estudio de la ARDS Network, 12 que confirm贸 la necesidad de emplear bajo volumen corriente en estos pacientes, fueron sin duda avances importantes en el conocimiento de esta entidad y han influido favorablemente en su pron贸stico.…”
unclassified
“…11 Even with modest tidal volumes and airway pressures, all animal species studied developed a pattern of lung injury which was indistinguishable from human ARDS. More recent studies in man have confirmed that ventilation can exacerbate lung injury in ARDS.…”
Section: Inflammation May Be Beneficialmentioning
confidence: 95%