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Plasma cGMP levels in air embolism-induced acute lung injury
J E Tanus-Santos1, W M Gordo, M Cittadino
1Department of Pharmacology, Faculty of Medical Sciences, State University of Campinas, Sao Paulo, Brazil.
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 embolism-induced ALI. Additionally, the small increase in cGMP levels after the MAE may reflect the more severe hemodynamic derangement in this setting.