High in comparison with low tidal volume ventilation aggravates oxidative stress-induced lung injury

Ventilator settings influence the development and outcome of acute lung injury. This study investigates the influence of low versus high tidal volume (V-t) on oxidative stress-induced lung injury. Isolated rabbit lungs were subjected to one of three ventilation patterns (V-t-positive end-expiratory pressure, PEEP): LVZP (6 ml/kg-0 cm, H2O), HVZP (12 ml/kg-0 cm H2O), LV5P (6 ml/kg-5 cm H2O). These ventilation patterns allowed a comparison between low and high V-t without dependence on peak inspiratory pressure (PIP). Infusion of hypochlorite (1000 nmol/min) or buffer (control) was started at t=0 min. Pulmonary artery pressure (PAP), PIP and weight were continuously recorded. Capillary filtration coefficient [K-fc (10(-4) ml s(-1) cm H2O-1 g(-1))] was gravimetrically determined (- 15/30/60/90/120 min). PIP averaged 5.8 +/- 0.6/13.9 +/- 0.6/13.9 +/- 0.4 cm H2O in the LVZP, HVZP and LV5P groups. PIP, K-f,K-c or PAP did not change in control groups, indicating that none of the ventilation patterns caused lung injury by themselves. Hypochlorite-induced increase in K-f,K-c but not hypochlorite-induced increase in PAP, was significantly attenuated in the LVZP-/LV5P- versus the HVZP-group (K-f,K-c,K-max. 1.0 +/- 0.23/1.4 +/- 0.40 versus 3.2 +/- 1.0*). Experiments with hypochlorite were terminated due to excessive edema (>50 g) at 97 +/- 2.2/94.5 +/- 4.5 min in the LVZP-/LV5P-group versus 82 +/- 3.8 * min in the HVZP-group (*: P < 0.05). Low V-t attenuated oxidative stress-induced increase in vascular permeability independently from PIP and PEEP. (C) 2002 Published by Elsevier science B.V.