Aquaporin channels may modulate ventilator-induced lung injury

Adult Respiratory Distress Syndrome is a disease with functional lung heter ogeneity and thus a ventilator-delivered breath may over-distend non-involv ed areas. In rats we examined ventilator-delivered tidal volume (TV) breath s of 7 and 20 ml/kg on lung water as evidence of lung injury. We examined t he role of aquaporins on ventilator-induced lung injury (VILI) by infusing HgCl2 which inhibits aquaporins by binding cysteine. Wet to dry lung weight ratio (W/D) as evidence of lung water was 4.47 +/- 0.1 SEM in controls, 4. 6 +/- 0.1 and 5.5 +/- 0.2 (P < 0.05) in rats ventilated at 7 and 20 ml/kg, respectively. Pulmonary artery pressure (PAP) rose from 23 +/- 1 to 26 +/- 1 mmHg (P < 0.05, n = 7) and cardiac output fell from 104 +/- 2 to 67 +/- 3 ml/min (P < 0.05) in rats ventilated at 30 ml/kg. Left ventricular end dia stolic pressure (n = 3) was unchanged. Evans Blue dye, an albumin marker, i ncreased from a control 37 +/- 11 to 97 +/- 41 mg/g wet lung in TV 20 rats (P < 0.05). HgCl2 infused slowly by tail vein did not significantly raise P AP, but did increase W/D to 6 +/- 0.2 (P < 0.05) in rats ventilated at 20 m l/kg but not at 7 ml,kg. Equimolar cysteine: infusions prevented the HgCl2 from increasing the W/D above that seen with TV 20 ml/kg. Thus ventilation with TV of 20 ml/kg produced a protein-rich lung edema. Aquaporin channels may have a protective effect in VILI. (C) 2001 Elsevier Science B.V. All ri ghts reserved.