literature. With rising health care costs and the appearance of nu- merous technicaladvancements in surgery, it is essential for sur- geons and policymakers to understand opportunity cost and apply it to assessment of new technologies. Methods: To demonstrate the principle of opportunity cost, we developed a simple model based on a hypothetical scenario comparing two competing technologies with equivalent outcomes, one of which lengthened operating time in a hypothetical procedure by 30 minutes (Device A) when compared to its alternative (Device B). The potential value of the extra operating time (opportunity cost) was then calculated based on the value of other surgicalprocedures.In our model, we selected five surgical procedures from five surgicalspecialties that were elective,high volume, had a duration less than 240 minutes, and profitable. Data for these procedures was taken from a university hospital setting in 2007. The outcome measure (opportunity cost) was estimated by dividing the selected procedure’s profit margin by its duration. Re- sults: Opportunity cost varies among surgical specialties (see table). Opportunity cost was highest in otolaryngology:38 dollars per minute. This was calculated using myringotomy as the substitute procedure,chosen because it is of short duration, done in high vol- ume, provides a high profit margin, and is elective. In simulation, a otolaryngology surgeon using the less efficient Device A in perform- ing a hypothetical procedure would incur an opportunity costof $1140 ($38 per minute times 30 minutes). Opportunity cost is lowest in general surgery - 9 dollars a minute - using laparoscopic inguinal hernia repair as the substitute procedure. Under the same simula- tion, the general surgeon using Device A would incur an opportunity cost of $270 ($9 per minute times 30 minutes). Conclusion: Oppor- tunity costs with changes in technology are potentially significant and should be acknowledged when assessing the economic value of new technologies. Five Selected High Volume Elective Procedures DRG Code (s) CPT Code (s) Procedure Name (s) Volume Average Margin per case (S) Average Surgical Time (min) Opportunity Cost (S/min) Urology 335 55866 Laparoscopic Prostectomy 110 4,954 228 22 Otolaryngology 062 69436 Myringotomy with Insertion of Tube 231 1,378 36 38 General Surgery 162 49650 Laparoscopic Femoral/ Inguinal Hernia Repair 127 962 102 9 Plastic Surgery 261 19318 Bilateral Reduction 155 3,423 180 19 Orthopedic Surgery 503 29881 Mammoplasty Knee arthroscopy 362 1,260 54 23 GASTROINTESTINAL AND NUTRITION 1: WOUND HEALING AND INFLAMMATION 33. ADENOVIRUS-MEDIATED OVEREXPRESSION OF HU- MAN T-PA PREVENTS PERITONEAL ADHESION FORMATION/REFORMATION IN RATS. H. M. Atta 1 , A. Al-Hendy 2 , M. A. El-Rehany 1 , S. R. Abdel Raheim 1 , H. M. Abd Elghany 1 , R. Foad 1 , M. Dewerchin 3 ; 1 Minia University, El-Minia, Egypt; 2 Meharry Medical College,Nashville, TN; 3 Vesalius Re- search Center, Leuven, Belgium Background: The use of human recombinant tissue-plasminogen activator (t-PA) has proved successful in the reduction of postoper- ative adhesions.Its short half-life, however,limits its continual fibrinolytic effect within the peritoneal cavity. To overcome this limitation, we delivered adenovirus vector encoding human t-PA gene into the peritoneal cavity to determine its effect in preventing adhesion formation and reformation after adhesiolysis in a rat peri- toneal adhesion model. Material and Methods: Adult male Wistar rats were subjected to peritoneal injury and randomly assigned to a treatment or control group. Two distinct protocols were evaluated. In protocol I, de novo adhesions, adenovirus encoding human t-PA gene (Ad-ht-PA) at a dose of 510 7 pfu was instilled in the peritoneal cavity following peritoneal injury in one group (n22) and the other group received PBS and served as control(n24). In protocol II, recurrent adhesion, one group (n15) received Ad-ht-PA at a dose of 510 7 pfu intraperitoneally after adhesiolysis one week following peritonealinjury and the second group (n13) received PBS. All animals were sacrificed one week following treatment and adhesions severity was scored. Human t-PA mRNA was measured in the ad- hesion tissues by RT-PCR. Human t-PA protein was measured in adhesion tissues and in plasma. Additionally, we measured the level of rat PAI-1 antigen and activity, TIMP-1, TGF-â and fibrinogen in adhesion tissues using corresponding ELISA kits. Results: Human tPA mRNA was expressed in adhesion tissues from all animals receiving Ad-htPA but not in the control groups. There was a signif- icant (p0.01, Mann-Whitney U test) reduction in adhesion scores in treatment groups compared with control groups in both experimen- tal protocols. Human tPA protein was detected in adhesions from the treatment groups of protocols I & II (2.90.33 ng/mg and 1.40.41ng/mg, respectively) but not in the control groups. In both protocols,there were significant reductions in PAI-1 antigen and activity, TIMP-1, TGF-â, and fibrinogen in the treatment groups compared with control groups (p0.001, independent sample t-test). Also, in both protocols,there were significant negative correlation (r0.58 and r0.69, respectively;p0.01) between adhesion score and tPA but a significant positive correlation (r0.90, p0.01) between adhesion score and PAI-1 antigen and activity, TIMP-1, TGF-â and fibrinogen. No bleeding complications or abdominal wound dehiscence were encountered. Conclusions: This study dem- onstrates that instillation of adenovirus vector encoding human tPA in the peritoneal cavity following peritoneal injury significantly de- creased the developmentand recurrence of peritonealadhesions without increasing the risk for bleeding or wound complications. 34. A NEUROKININ-1 RECEPTOR ANTAGONIST (NK-1RA) THAT REDUCES INTRAABDOMINAL ADHESION FOR- MATION DOWNREGULATES THE ACTIVATION OF THE TGF- ␤ 1/SMAD2 SIGNALING PATHWAY IN A RAT MODEL. R. Lim, S. Heydrick, D. I. Chu, J. M. Morrill, K. L. Reed, A. F. Stucchi, J. M. Becker; Boston Medical Center, Bos- ton, MA Introduction: Intraabdominal adhesions remain a significant long- term complication of abdominal surgery. An increase in active trans- forming growth factor- ␤ 1 (TGF- ␤ 1) has been shown to play a pivotal role in adhesion formation.TGF- ␤ 1 is synthesized in a latent or inactive form and must be activated prior to becoming a biologically active, pro-fibrotic signaling cytokine. The phosphorylation of Smad2 is a key step in the initiation of intracellular TGF-â1 signal trans- duction and serves as an indicator ofTGF-â1 signaling. Previous data from our laboratory (Reed,et al. PNAS 2004) showed that administration of an NK-1RA that interferes with the binding of substance P to its NK-1 receptor reduces adhesion formation in a rat model;however,the underlying mechanism(s) remain unresolved. The aim of this study was to utilize the NK-1RA to determine if substance P modulates the activation of the active TGF-â1/Smad2 signaling pathway. Methods: Adhesions were created in male Wistar rats via a midline laparotomy by placing 3 ischemic buttons, 1 cm apart on each side of the peritoneum. Rats received either 1 ml saline (operated vehicle control; n6) or 25 mg/kg of NK1RA (CJ- 12,255;Pfizer) in 1 ml saline (n6) which was administered intra- peritoneally as a lavage at the time of surgery. Results from these animals were compared to non-operated controls (n 6). To evaluate the activation of the TGF- ␤ 1/Smad2 signaling pathway,animals were sacrificed at 24 hours and peritoneal tissue collected for the 186 ASSOCIATION FOR ACADEMIC SURGERY AND SOCIETY OF UNIVERSITY SURGEONS—ABSTRACTS