Author:
Adelman B,Stemerman M B,Handin R I
Abstract
Following aortic balloon deendothelialization, rabbits develop a neointima composed of smooth muscle cells and extracellular connective tissue. Injury of this neointima with a balloon catheter results in the accumulation of platelet aggregates and fibrin on the vessel surface. We studied platelet attachment and secretion following injury of the neointima and also the effect of prostaglandin I2 (PGI2) and heparin on these events. Platelet factor 4 was detected within the neointima by indirect immunofluorescence 30 minutes after neointimal injury. By using 51Cr-labeled platelets, it was possible to quantitate total platelet attachment following neointimal injury. When animals were sacrificed 30 minutes after reinjury, there were 4.46 X 10(6) platelets/cm2 of aortic surface in animals injured 10 days after initial balloon deendothelialization, and 3.75 X 10(6) platelets/cm2 of aortic surface in animals injured 29 days after initial injury. In these two groups, infusion of 850 ng/kg/min PGI2, along with a single infusion of 2500 units of heparin, inhibited fibrin deposition and reduced platelet attachment by 71% and 76%, respectively. Although infusion of heparin alone prevented fibrin deposition, neither heparin nor PGI2 individually reduced platelet attachment as profoundly as did their combined use.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine
Cited by
20 articles.
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