Please use this identifier to cite or link to this item:
|Type:||Artigo de periódico|
|Title:||Plasma cGMP levels in air embolism-induced acute lung injury|
|Abstract:||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. Copyright (C) 2000 by W.B. Saunders Company.|
|Editor:||W B Saunders Co|
|Appears in Collections:||Unicamp - Artigos e Outros Documentos|
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.