The effect of methanol washing of plasticized polyvinyl chloride on biomaterial-contact-mediated CD11b (mac-1) expression in a rat recirculation model.

Our objective was to assess whether using a methanol wash to reduce the level of plasticizer present on the surface of medical-grade polyvinyl chloride (PVC) has a moderating effect on the expression of CD11b (mac-1) on neutrophils in rats undergoing recirculation. The study was carried out on 3 groups of 10 adult male Sprague-Dawley rats weighing between 350 and 450 g. In the 2 test groups, the animals were exposed to 48 cm(2) of di-(2-ethyl-hexyl)-phthalate (DEHP)-plasticized PVC in a parallel plate recirculating test cell through which blood was recirculated at 1.5 ml/min. In the first test group, the PVC was untreated; in the second test group, the PVC was washed in methanol to reduce the level of plasticizer on the surface. The test cell was connected to the right femoral circulation, and recirculation was established for a period of 60 min. Blood samples were taken at 0, 30, and 60 min for assessment of CD11b expression on neutrophils using flow cytometric analysis. In a third group of 10 control experiments, rats underwent the entire surgical procedure, but without recirculation through the test cell. There was statistically significant (p < 0.001) lower Cd11b expression on neutrophils in the blood of rats perfused through the cell containing methanol-washed PVC after 30 min and at 60 min. CD11b expression was significantly (p < 0.001) lower in the control group than in both test groups at both the 30 and 60 min time points and at the 60 min time point on comparison with the group where blood was perfused through methanol-washed PVC. These results demonstrate that the biomaterial-contact-mediated upregulation of CD11b may be significantly reduced by employing a methanol-washing technique on the plasticized PVC. Although this technique does not entirely eliminate the expression of CD11b on neutrophils, the difference is significant and suggests the role of the plasticizer in the development of this inappropriate inflammatory response.