Plasma cGMP levels in air embolism-induced acute lung injury

Purpose: An impaired generation of cGMP may account for the pulmonary hypertension seen in acute lung injury (ALI). We investigated the hemodynamic changes and the plasma levels of cGMP during air embolism-induced ALI in two different models: venous air infusion (VAI) and massive air embolism (MAE). Materials and Methods: After a baseline hemodynamic evaluation, anesthetized dogs received a VAI (0.2 mL/kg/min, N = 10) or a bolus of air (MAE, 2.5 mL/kg, N = 10) intravenously. A group of control dogs (n = 5) received no further treatment. Hemodynamic evaluation was performed 5 to 60 minutes after the VAI was initiated or after the MAE. Blood samples were drawn for plasma cGMP determinations. Results: The VAI increased the pulmonary artery pressure (by 181%, P < .05) after 15 minutes of air infusion without changing the cardiac index. The MAE increased the pulmonary artery pressure (by 252%) and decreased the cardiac index (by 31%) 5 minutes after the air injection (both P < .05). These variables returned to baseline 15 to 30 minutes thereafter. The cGMP concentrations remained unaltered during the VAI. In contrast, cGMP levels increased 26% (P < .05) by 15 minutes after the MAE and returned to basal levels thereafter. Conclusion: These findings suggest that a lack of increase in the production of the cGMP may account for the pulmonary hypertension seen in air embolisminduced ALI. Additionally, the small increase in cGMP levels after the MAE may reflect the more severe hemodynamic derangement in this setting. Copyright © 2000 by W.B. Saunders Company