Inhibitory effects of isoproterenol on PAF-induced endothelial cell permeability and morphological changes.
Using a model to study vascular permeability under hydrostatically perfused bovine pulmonary artery endothelial cell (EC) monolayers and a software to automatically analyse cell morphological parameters in a computer image workstation, the effects of isoproterenol (IPN) on platelet-activating factor (PAF)-induced changes in EC monolayer permeability and cell morphological parameters were studied. Albumin has the fortifying effect on endothelial barrier function. After treatment of EC monolayer with 10(-8) mol/L PAF, trans-monolayer permeability increased, cell surface area decreased, and intercellular space enlarged. As pretreatment with 10(-4) mol/L IPN, PAF-induced EC permeability increment and morphological changes were blocked. The results suggest that EC contraction and intercellular gap expansion are important mechanisms for PAF-induced high vascular permeability. IPN inhibits the effects of PAF via stabilization of EC morphology and prevention of intercellular gap formation.
Ding
Z
Z
Department of Pathophysiology, Second Military Medical University, Shanghai, China.
Li
S
S
Wu
Z
Z
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects*; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology*; D007091:Image Processing, Computer-Assisted; D007545:Isoproterenol / Q000494:pharmacology*; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors*; D011651:Pulmonary Artery / Q000166:cytology*
D000318:Adrenergic beta-Agonists; D010972:Platelet Activating Factor; D007545:Isoproterenol