A series of in vitro studies were designed to determine whether di-(2-ethyl-hexyl)-phthalate (DEHP)-plasticized polyvinyl chloride (PVC) and DEHP itself initiated an inflammatory response in both human and rat blood. Additionally, the effect of methanol washing of the PVC on the inflammatory response was studied in both blood types. Blood from both species was exposed to first, no material; second, ground DEHP-plasticized PVC; third, methanol-washed ground DEHP-plasticized PVC; and fourth, known concentrations of DEHP. The expression of the integrin CD11b was employed as a marker of the inflammatory response. After 20 minutes' exposure to PVC, CD11b expression increased to 210 +/- 32% of baseline in human blood and to 238 +/- 21.7% in rodent blood. Both blood types showed an increase in CD11b expression with increasing concentrations of DEHP (214 +/- 40.8% of baseline levels in human blood and 237 +/- 14.5% in rodent blood at the highest concentration). Methanol washing resulted in a significant moderation in CD11b upregulation in both blood types; 117 +/- 27% of baseline in human and 150 +/- 14.7% in rodent. These results support the hypothesis that DEHP-plasticized PVC and DEHP itself are proinflammatory in blood from both species, and suggest that the rodent is an appropriate model for studies of this nature.
Leucocytes have been shown to play a fundamental role in the pathophysiology of inflammation. This prospective, randomized, controlled study was designed to identify the most advantageous leucocyte depletion technique in terms of reduction in systemic inflammatory response syndrome and myocardial ischaemia reperfusion injury associated with cardiopulmonary bypass (CPB). Forty consecutive patients undergoing elective coronary artery bypass graft (CABG) surgery were randomly allocated to one of four groups. The four groups consisted of a control group, a systemic leucocyte depletion (SLD) group, a cardioplegic leucocyte depletion (CLD) group and a total leucocyte depletion (TLD) group. There were 10 patients in each group. Lactoferrin (marker of neutrophil activation) and troponin-I (marker of myocardial ischaemia reperfusion injury) were measured at six time points: post induction, 5 min on CPB, 5 min before releasing the aortic crossclamp, 15 min after releasing the clamp and 1 and 24 hours after the discontinuation of CPB. Plasma lactoferrin levels increased rapidly in every group after the commencement of CPB, subsequently reached a peak after releasing the aortic crossclamp and gradually declined after the discontinuation of CPB. The lowest lactoferrin concentration was observed in the TLD (range 2.15-141.9 ng/mL) and CLD groups (7.469-114.6 ng/mL). Regarding myocardial injury, plasma cardiac troponin-I levels did not differ significantly between groups; but troponin-I concentrations rose dramatically after releasing the aortic crossclamp in all groups. Nevertheless, the CLD group had the lowest troponin-I level (1.37-5.55 ng/mL). In conclusion, it is believed that myocardial ischaemia is probably a major contributor to the inflammatory response. Although there is no clear statistical significance shown in this pilot study, the data tend to support the cardioplegic leucocyte depletion strategy as the optimal method for attenuating neutrophil activation and myocardial ischaemia reperfusion injury.
Modern cardiopulmonary bypass (CPB) systems are getting smaller, both in terms of the exposed surface area of biomaterials and the priming volume. In a series of studies utilizing a rat recirculation model, we demonstrated that the magnitude of the inflammatory response seen under these conditions is proportional to the surface area of exposed material, a finding that supports the use of miniature systems in terms of moderating the inflammatory response. However, the second impact of miniature perfusion systems, the reduced priming volume with concomitant reduction in haemodilution, was not investigated with reference to inflammation. The present study was designed to determine whether this change in CPB haematocrit profile has any effect on the inflammatory response. In common with previous studies by this group, we employed the expression of the integrin CD11b on neutrophils as a marker of neutrophil activation, and hence the inflammatory response, in a rat recirculation biomaterial testing model, containing di-(2-ethyl-hexyl)-phthalate plasticized polyvinyl chloride of the type commonly employed in CPB circuits. The results demonstrated that neutrophil activation is influenced by haemodilution. We studied five groups of animals, each with different mean induced haematocrit: Group 1 (41.3 +/- 1.27%); Group 2 (30.93 +/- 2.85%); Group 3 (24.83 +/- 1.36%); Group 4 (20.60 +/- 3.47%); Group 5 (20.48 +/- 1.31%). Groups 1 and 5 animals were controls, neither of which underwent the period of recirculation. Rather, these controls were employed to isolate the noncontact effect of haemodilution on CD11b expression. We found that there were differences in per cent change in CD11b expression from start to end of the recirculation period between Group 1 (109.54 +/- 49.53%), Group 2 (189.1 +/- 18.68%), Group 3 (224.28 +/- 43.97), Group 4 (368.97 +/- 24.28%) and Group 5 (127 +/- 57.8%). There were intergroup statistically significant differences (p < 0.05). These results confirm that there is a relationship between haematocrit level and biomaterial contact-mediated activation of neutrophils. Furthermore, these studies confirm that haemodilution alone has no effect on neutrophil activation. One possible explanation for this outcome is that with higher levels of haemodilution, neutrophils have a greater opportunity to contact surface 'receptor' sites on the biomaterial, resulting in more neutrophil activation. Whatever the mechanism, these data tend to support the modern trend towards lower circuit surface area and higher haematocrit.
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