JOURNAL ARTICLE
Dibutyryl cAMP prevents increased vascular permeability caused by air embolism in isolated rat lungs.
Aviation, Space, and Environmental Medicine 1997 September
BACKGROUND AND HYPOTHESIS: Venous gas bubbles are routinely detected in astronauts undergoing extravehicular activities at lower suit pressure. Venous air embolism increases the pulmonary arterial pressure and the vascular permeability leading to acute lung injury. In the present study we evaluated the protective effect of dibutyryl cAMP, aminophylline, and pentoxifylline on the pulmonary vasculatures after air embolism.
METHOD: In isolated and perfused rat lungs, we induced air embolism by introducing air bubbles into the pulmonary artery. We measured the pulmonary arterial pressures and capillary pressure. Vascular permeability was determined by measuring the filtration coefficient (Kf) and the protein concentration in the lung lavage fluid.
RESULTS: Air infusion caused pulmonary hypertension and increased vascular permeability, resulting in pulmonary edema. The Kf (in g.min-1.cm H2O-1.100 g-1) increased from 0.44 +/- 0.05 at baseline to 2.98 +/- 0.47 after air infusion. Pretreatment with DBcAMP prevented the increase in Kf (0.63 +/- 0.09) caused by air embolism without altering the hemodynamics. Aminophylline and pentoxifylline did not prevent lung injury induced by air embolism. Although aminophylline did not alter the response of pulmonary arterial pressure to air infusion, it elevated the capillary pressure to 5.1 +/- 0.4 mmHg, which was significantly greater than that in the lung receiving air infusion alone.
CONCLUSION: Our results suggest that DBcAMP prevents the increase in vascular permeability caused air embolism. The ineffectiveness of aminophylline and pentoxifylline on the prevention of air embolism-induced lung injury remains for further investigation.
METHOD: In isolated and perfused rat lungs, we induced air embolism by introducing air bubbles into the pulmonary artery. We measured the pulmonary arterial pressures and capillary pressure. Vascular permeability was determined by measuring the filtration coefficient (Kf) and the protein concentration in the lung lavage fluid.
RESULTS: Air infusion caused pulmonary hypertension and increased vascular permeability, resulting in pulmonary edema. The Kf (in g.min-1.cm H2O-1.100 g-1) increased from 0.44 +/- 0.05 at baseline to 2.98 +/- 0.47 after air infusion. Pretreatment with DBcAMP prevented the increase in Kf (0.63 +/- 0.09) caused by air embolism without altering the hemodynamics. Aminophylline and pentoxifylline did not prevent lung injury induced by air embolism. Although aminophylline did not alter the response of pulmonary arterial pressure to air infusion, it elevated the capillary pressure to 5.1 +/- 0.4 mmHg, which was significantly greater than that in the lung receiving air infusion alone.
CONCLUSION: Our results suggest that DBcAMP prevents the increase in vascular permeability caused air embolism. The ineffectiveness of aminophylline and pentoxifylline on the prevention of air embolism-induced lung injury remains for further investigation.
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