title: Atelectasis causes vascular leak and lethal right ventricular failure in uninjured rat lungs.
abstract: During mechanical ventilation, lung recruitment attenuates injury caused by high VT, improves oxygenation, and may optimize pulmonary vascular resistance (PVR). We hypothesized that ventilation without recruitment would induce injury in otherwise healthy lungs. Anesthetized rats were ventilated with conventional mechanical ventilation (VT 8 ml/kg; respiratory frequency 40 per minute) and 21% inspired oxygen, with or without a recruitment strategy consisting of recruitment maneuvers plus positive end-expiratory pressure, in the presence or absence of a laparotomy. Additional experiments examined the impact of atelectasis on right ventricular function using echocardiography, as well as functional residual capacity and PVR. Lack of recruitment resulted in reduced overall survival (59% nonrecruited vs. 100% recruited, p < 0.05), increased microvascular leak, greater impairment of oxygenation and lung compliance, increased PVR, and elevated plasma lactate. Echocardiography demonstrated that right ventricular dysfunction occurred in the absence of recruitment. Finally, samples from nonrecruited lungs demonstrated ultrastructural evidence of microvascular endothelial disruption. Although such effects clearly do not occur with comparable magnitude in the clinical context, the current data suggest novel mechanisms (microvascular leak, right ventricular dysfunction) whereby derecruitment may contribute to development of lung injury and adverse systemic outcome.
authors.affiliation: The Lung Biology Program, The Research Institute, and the Department of Critical Care Medicine, The Hospital for Sick Children, and the Interdepartmental Division of Critical Care Medicine, University of Toronto, Ontario, Canada.
authors.forename: Michelle
authors.initials: M
authors.lastname: Duggan
authors.forename: Conán L
authors.initials: CL
authors.lastname: McCaul
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: McNamara
authors.forename: Doreen
authors.initials: D
authors.lastname: Engelberts
authors.forename: Cameron
authors.initials: C
authors.lastname: Ackerley
authors.forename: Brian P
authors.initials: BP
authors.lastname: Kavanagh
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D019559:Capillary Leak Syndrome / Q000209:etiology*; D004195:Disease Models, Animal; D004452:Echocardiography; D005652:Functional Residual Capacity; D006323:Heart Arrest / Q000209:etiology / Q000401:mortality; D006333:Heart Failure / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D019344:Lactic Acid / Q000097:blood; D007813:Laparotomy; D008170:Lung Compliance; D008297:Male; D011175:Positive-Pressure Respiration / Q000009:adverse effects* / Q000379:methods; D001261:Pulmonary Atelectasis / Q000150:complications*; D011652:Pulmonary Circulation; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012121:Respiration, Artificial / Q000009:adverse effects* / Q000379:methods; D012128:Respiratory Distress Syndrome / Q000150:complications*; D016019:Survival Analysis; D014655:Vascular Resistance; D018497:Ventricular Dysfunction, Right / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology
chemical_list: D019344:Lactic Acid