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Ischemia and Reperfusion Increases Susceptibility to Ventilator-induced Lung Injury in Rats

Division of Respiratory Medicine, Department of Medicine, University of Toronto; Interdepartmental Division of Critical Care Medicine, University of Toronto; Departments of Anaesthesiology and Surgery, University of Toronto; and Department of Critical Care Medicine, St. Michael's Hospital, Toronto, Ontario, Canada; Departments of Anesthesiology and Critical Care Medicine, University of Eastern Piedmont, Novara; and Sezione di Anestesiologia e Rianimazione, Dipartimento di discipline Medico-Chirurgiche, Università di Torino, Ospedale S. Giovanni Battista, Torino, Italy

Correspondence and requests for reprints should be addressed to Arthur S. Slutsky, M.D., 30 Bond Street, Room 4-042 Queen Wing, Toronto, ON, M5B 1W8 Canada. E-mail: arthur.slutsky{at}utoronto.ca

Objectives: Hemorrhagic shock followed by resuscitation (HSR) commonly triggers an inflammatory response that leads to acute respiratory distress syndrome.

Hypothesis: HSR exacerbates mechanical stress–induced lung injury by rendering the lung more susceptible to ventilator-induced lung injury.

Methods: Rats were subjected to HSR, and were randomized into an HSR + high tidal volume and zero positive end-expiratory pressure (PEEP) or a HSR + low tidal volume with 5 cm H₂O PEEP. A sham-operated rat + high tidal volume and zero PEEP served as a control.

Results: HSR increased susceptibility to ventilator-induced lung injury as evidenced by an increase in lung elastance and the wet/dry ratio and a reduction in Pa_O2 as compared with the other groups. The lung injury observed in the HSR + high tidal volume group was associated with a higher level of interleukin 6 in the lung and blood, increased epithelial cell apoptosis in the kidney and small intestine villi, and a tendency toward high levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and creatinine in plasma.

Conclusions: HSR priming renders the lung and kidney more susceptible to mechanical ventilation–induced organ injury.

Key Words: inflammation • lung mechanics • multiple organ failure

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