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Objective: Resistance arteries remain subject to pulsatility, a potent regulator of large elastic artery tone and structure, but the effect is incompletely understood. Extracorporeal circulation during cardiac surgery is often associated with absence of pulsatility, which may affect vascular tone. To define the role of the vascular wall in the inflammatory process that may occur with or without pulsatility, we studied resistance arteries functions ex vivo. We measured vascular reactivity, oxidative stress, and inflammation in the arterial wall., Methods: Isolated rat mesenteric resistance arteries were mounted in an arteriograph and subjected to pulsatility or not in vitro. Arteries were perfused with a physiologic salt solution without circulating cells., Results: After 180 minutes, flow-mediated dilation was higher and pressure-induced myogenic tone lower in arteries subjected to pulsatility. Without pulsatility, reactive oxygen species and markers of inflammation (monocyte chemotactic protein 1 and tumor necrosis factor α) were higher than baseline. In perfused mesenteric beds under similar conditions, tumor necrosis factor α was higher in perfusate after 180 minutes of nonpulsatility (5.7 ± 1.6 pg/mL vs 1.1 ± 0.4 pg/mL; P < .01). In arteries treated with the antioxidant 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl (tempol), flow-mediated dilation and myogenic tone were similar in nonpulsatile and pulsatile arteries; monocyte chemotactic protein 1 and nuclear factor κB expression levels were not increased in tempol-treated nonpulsatile arteries., Conclusions: Absence of pulsatility in resistance arteries increased oxidative stress, which in turn induced inflammation and preferentially altered pressure and flow-dependent tone, which play a key role in control of local blood flow., (Copyright © 2011 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.)

Background: The impact of the postoperative inflammatory response on the central nervous system after cardiac surgery is uncertain. The goal of the study was to evaluate the role of complement activation on cellular brain injury in patients undergoing coronary artery bypass grafting. In addition, neuropsychological functioning was assessed., Methods: We randomly assigned 30 patients to undergo surgery using either standard noncoated or heparin-coated extracorporeal circuits. Closed cardiopulmonary bypass and controlled suctions of pericardial shed blood were standardized in both groups. Complement activation and cellular brain injury were assessed by measuring sC5b-9 and protein s100beta. Neuropsychometric tests were performed at least 2 weeks before operation and at discharge. They served to calculate z scores of cognitive domains and changes in neuropsychological functioning., Results: Peak value of sC5b-9 at the end of cardiopulmonary bypass in the noncoated group was significantly higher than in the heparin-coated group (p = 0.005). Changes in the heparin-coated group were not significant. Glial injury started after initiation of surgery and peaked at the end of cardiopulmonary bypass with significantly higher concentration of s100beta in the noncoated than in the heparin-coated group (p = 0.008). Values of s100beta and of sC5b-9 were significantly correlated (p = 0.03). Although no statistically significant between group difference was detected, z scores of attention and flexibility or executive functions were lowered postoperatively within the noncoated group (p = 0.033 and p = 0.028), whereas z scores were unchanged within the heparin-coated group., Conclusions: Inhibition of complement activation by heparin-coated cardiopulmonary bypass reduced brain cell injury and was associated with preserved neuropsychological functioning after coronary artery bypass grafting.

Previous reports have highlighted the disparity in biocompatibility of two differently engineered heparin coatings during the cardiopulmonary bypass (CPB) procedure. The aim of this prospective study was to evaluate the impact of the difference in haemocompatibility provided by either the Duraflo II equipment or the Carmeda equipment in the terminal inflammatory response observed after coronary artery surgery. Thirty patients were randomly allocated to two groups to be operated on using either Duraflo II equipment (group I) or Carmeda equipment (group 2) for extracorporeal circulation (ECC). Initial inflammatory response was assessed by terminal complement complex activation (SC5b-9). The late inflammatory response observed in the postoperative period was assessed by measuring cytokine production (tumour factor necrosis (TNF alpha), interleukin IL-6, interleukin IL-8) and circulating concentrations of adhesion molecules (ELAM-1, ICAM-1). The release of SC5b-9 after CPB and after protamine administration was lower in group 2 than in group 1 (p = 0.0002 and p = 0.006, respectively). A significant production of cytokines was detected in both groups with peak values observed within the time range of 4-6 h after the start of CPB.