The impact of different biocompatible coated cardiopulmonary bypass circuits on inflammatory response and oxidative stress

Gourlay, T. and Shedden, L. (2010) The impact of different biocompatible coated cardiopulmonary bypass circuits on inflammatory response and oxidative stress. Perfusion, 25 (6). pp. 427-429. ISSN 0267-6591 (https://doi.org/10.1177/0267659110381453)

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Abstract

Background. The use of DEHP plasticised poly-vinyl-chloride (DEHPPPVC)) in medical devices persists despite evidence suggesting that DEHP migration can be harmful. Researchers have shown that a simple surface sulfonation process can retard the migration of DEHP, which may reduce the associated inflammatory response. The present study is designed to investigate the effects of surface sulfonation on DEHP migration and blood contact activation using in-vitro and rodent models. Methods. The study was carried out in two phases; Phase 1 in which the migration rate of DEHP from DEHPPPVC and sulfonated DEHP plasticised PVC (SDEHPPPVC) was measured. In phase 2 of the study the materials were incorporated into a rat recirculation biomaterial test model and blood samples taken to assess CD11b expression on neutrophils, IL-6 and Factor XIIa. Results. The initial DEHP concentration washed from the surface after storage was 37.19 ± 1.17 mg/l in the PPVC group and 5.89 ± 0.81 mg/l in the SPPVC group (P<0.0001). The post-wash migration rate was 3.07 ± 0.32 mg/l/hour in the PPVC group, compared to 0.46 ± 0.038 mg/l/hour in the SPPVC group (P<0.0001). In phase 2 of the study CD11b expression increased by 228.9% ± 37% over the test period in the PPVC group compared to 118.3% ± 46% in the SPPVC group (p<0.01). IL-6 levels rose from 3.1 ± 1.4 pg/ml to 263 ± 26 pg/ml in the PPVC group and 2.2 ± 1.6 pg/ml to 161 ± 29 pg/ml in the SPPVC group (p<0.01). Factor FXIIa levels rose from 0.22 ± 0.13 ug/ml to 3.7 ± 0.32 ug/ml and 0.28 ± 0.09 to 2.71 ± 0.21 ug/ml in the PPVC and SPPVC groups respectively (p<0.05 at 90 minutes). Conclusions. The simple sulfonation process significantly retards the migration of DEHP and is associated with the moderation of contact activation processes.

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