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Published ahead of print on March 27, 2003, doi:10.1164/rccm.200210-1215OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 12, June 2003, 1633-1640

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Submitted on October 24, 2002
Accepted on March 25, 2003

ATELECTASIS CAUSES VASCULAR LEAK AND LETHAL RIGHT VENTRICULAR FAILURE IN UNINJURED RAT LUNGS

Michelle Duggan1, Conan L McCaul1, Patrick J McNamara2, Doreen Engelberts3, Cameron Ackerley4, and Brian P Kavanagh5*

1 The Lung Biology Program, The Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada; Critical Care Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada; Anesthesia, The Hospital for Sick Children, Toronto, Ontario, Canada, 2 Pediatrics, The Hospital for Sick Children, Toronto, Ontario, Canada, 3 The Lung Biology Program, The Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada, 4 Pathology and Laboratory Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada, 5 The Lung Biology Program, The Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada; Critical Care Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada

* To whom correspondence should be addressed. E-mail: brian.kavanagh{at}utoronto.ca.

During mechanical ventilation, lung recruitment attenuates injury caused by high tidal volume, improves oxygenation, and may optimize pulmonary vascular resistance. We hypothesized that ventilation without recruitment would induce injury in otherwise healthy lungs. Anesthetized rats were ventilated with conventional mechanical ventilation (tidal volume 8 mL per 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 pulmonary vascular resistance. Lack of recruitment resulted in reduced overall survival (59% non-recruited versus 100% recruited, P<0.05), increased microvascular leak, greater impairment of oxygenation and lung compliance, increased pulmonary vascular resistance, and elevated plasma lactate. Echocardiography demonstrated that right ventricular dysfunction occurred in the absence of recruitment. Finally, samples from non-recruited lungs demonstrated ultrastructural evidence of microvascular endothelial disruption. While 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.
Key words: Lung Injury, Acute; Vascular Permeability; Functional Residual Capacity; Ventricular Function, Right.




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