The effect of prostacyclin infusion on increased pulmonary vascular permeability following microembolization in dogs.
Prostacyclin (PG I2) generated by vascular endothelium is a strong antiaggregating substance. As platelet aggregation and release of humoral factor(s) have been reported to be crucial in the pathogenesis of acute lung injury following pulmonary microembolization, prostacyclin could have a protective effect against microembolic lung vascular injury. Following unilateral microembolization, the filtration coefficient in the nonembolized lung increased significantly to 0.14 +/- 0.02 from the base line value of 0.07 +/- 0.01 ml/min/mmHg/100g. Prostacyclin as measured as 6-keto PG F1 alpha in arterial blood increased significantly to 4.15 +/- 1.76 at 30 min from the base line value of 1.90 +/- 0.45 ng/ml and increased further to 5.67 +/- 1.49 ng/ml at 60 min following microembolization. Exogenously administered PG I2 methylester (20 ng/kg/min) prevented completely the increase in the filtration coefficient without any effects on hemodynamics, although the effects of PG I2 methylester did not depend on its action on platelet aggregation. Based on these results, we conclude that prostacyclin could play an important role in preserving cell integrity of the lung and prevention of increased lung vascular permeability following pulmonary microembolization.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects*; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology* / Q000031:analogs & derivatives; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D007700:Kinetics; D008168:Lung / Q000098:blood supply; D008297:Male; D010976:Platelet Count; D011453:Prostaglandins / Q000494:pharmacology*; D011655:Pulmonary Embolism / Q000473:pathology / Q000503:physiopathology*
D011453:Prostaglandins; D015121:6-Ketoprostaglandin F1 alpha; C038499:prostaglandin I2 methyl ester; D011464:Epoprostenol