Objectives: There is no consensus on the use or benefit of extracorporeal circulation (EC) during descending thoracic (DTA) or thoracoabdominal aneurysm (TAA) repair. We evaluated the role of EC during DTA or TAA repair using U.S. Medicare data.Methods: Medicare (2004Medicare ( -2007 patients undergoing intact open DTA or TAA repair were identified by ICD-9 code; specific exclusions included ascending/arch and hypothermic circulatory arrest (DHCA) operations. The impact of EC (ICD-9 39.61) on early and late outcomes was analyzed using standard statistical methods.Results: A total of 4230 patients had DTA or TAA repair, with EC used in 2433 (57%). Differences in baseline clinical features are presented in the Table . The 30-day mortality, any complication, and systemic complications were significantly reduced with EC use (Table ). EC patients had shorter length of stay of 13.5 Ϯ 13 vs 17.2 Ϯ 18 days (P Ͻ .01

Oxidative stress has been implicated in intra-abdominal adhesion formation. Substance P, a neurokinin-1 receptor (NK-1R) ligand, facilitates leukocyte recruitment and reactive oxygen species (ROS) generation. We have shown in a rat model of adhesion formation that intraperitoneal administration of a NK-1R antagonist at the time of abdominal operation reduces postoperative adhesion formation. Thus we determined the effects of NK-1R antagonist administration on peritoneal leukocyte recruitment and oxidative stress within 24 h of surgery. Adhesions were induced in Wistar rats randomly assigned to receive the antagonist or vehicle intraperitoneally. Peritoneal tissue was isolated at 2, 4, 6, and 24 h after surgery for analysis of the oxidative stress biomarkers 8-isoprostane (8-IP), protein carbonyl, NADPH oxidase, myeloperoxidase (MPO), and ICAM-1 and VCAM-1 mRNAs. Total antioxidant capacity of peritoneal fluid was also determined. MPO, NADPH oxidase, 8-IP, and protein carbonyl were elevated (P < 0.05) by 6 h. ICAM-1 mRNA was elevated (P < 0.05) by 2 h, whereas VCAM-1 levels decreased (P < 0.05) at 24 h. The NK-1R antagonist delayed the MPO rise and reduced (P < 0.05) 8-IP levels by 6 h and ICAM-1 mRNA, VCAM-1 mRNA, and protein carbonyl at 2 h. The antagonist also increased (P < 0.05) the antioxidant capacity of peritoneal fluid at all time points. These data further support a role for oxidative stress in adhesion formation and suggest that the NK-1R antagonist may limit adhesions, in part, by reducing postoperative oxidative stress through an inhibition of neutrophil recruitment and an increase in peritoneal fluid antioxidant capacity.

When administered during laparoscopic LOA, an NK-1RA significantly upregulates peritoneal fibrinolytic activity and decreases adhesion reformation.

These data suggest that aprepitant maybe a useful pharmacologic agent for reducing adhesion formation clinically.