PURPOSE: The primary step in postoperative peritoneal adhesion formation involves the exudation of fibrin through permeable mesenteric capillaries. Nicotine, the most potent constituent of cigarette smoke, augments the release of vascular endothelial growth factor (VEGF), which increases vascular permeability. The objective of this study was to evaluate the effect of nicotine on postlaparotomy abdominal adhesions. METHODS: CD-1 mice were randomized to receive, ad libitum, either water alone (as 2% sucrose solution) or water mixed with 100 microg/mL nicotine (to obtain blood levels equivalent to a 1 pack/day smoker) (n = 32 mice per group). After 1 wk, all mice underwent laparotomy to induce adhesion formation using the same experimental method (consisting of laparotomy with cecal abrasion to achieve serosal punctuate hemorrhage). Fourteen days later, all animals were sacrificed for adhesion grading (0 to 3) by a blinded observer. Additionally, peritoneal lavage fluid from separate mice receiving either water or nicotine water before their surgery or else undergoing sham laparotomy was retrieved at 2, 6, and 24 h postoperatively (4 mice per group/time point) and assessed for VEGF concentrations. RESULTS: The nicotine treated group had a mean +/- SEM adhesion score of 2.4 +/- 0.2, which was significantly greater than that of the control group (1.2 +/- 0.2) (P < 0.05, Mann Whitney U test.). This correlated with a significant increase in peritoneal VEGF levels occurring at 6 and 24 h in the nicotine group. CONCLUSION: Peritoneal adhesion formation after surgery is increased in mice receiving nicotine perioperatively. This effect may be mediated through a direct augmentation of peritoneal VEGF release by nicotine with a subsequent increase in mesenteric endothelial permeability. These findings could have significant implications for smokers undergoing intra-abdominal surgical procedures.
PURPOSE: The primary step in postoperative peritoneal adhesion formation involves the exudation of fibrin through permeable mesenteric capillaries. Nicotine, the most potent constituent of cigarette smoke, augments the release of vascular endothelial growth factor (VEGF), which increases vascular permeability. The objective of this study was to evaluate the effect of nicotine on postlaparotomy abdominal adhesions. METHODS: CD-1 mice were randomized to receive, ad libitum, either water alone (as 2% sucrose solution) or water mixed with 100 microg/mL nicotine (to obtain blood levels equivalent to a 1 pack/day smoker) (n = 32 mice per group). After 1 wk, all mice underwent laparotomy to induce adhesion formation using the same experimental method (consisting of laparotomy with cecal abrasion to achieve serosal punctuate hemorrhage). Fourteen days later, all animals were sacrificed for adhesion grading (0 to 3) by a blinded observer. Additionally, peritoneal lavage fluid from separate mice receiving either water or nicotine water before their surgery or else undergoing sham laparotomy was retrieved at 2, 6, and 24 h postoperatively (4 mice per group/time point) and assessed for VEGF concentrations. RESULTS: The nicotine treated group had a mean +/- SEM adhesion score of 2.4 +/- 0.2, which was significantly greater than that of the control group (1.2 +/- 0.2) (P < 0.05, Mann Whitney U test.). This correlated with a significant increase in peritoneal VEGF levels occurring at 6 and 24 h in the nicotine group. CONCLUSION: Peritoneal adhesion formation after surgery is increased in mice receiving nicotine perioperatively. This effect may be mediated through a direct augmentation of peritoneal VEGF release by nicotine with a subsequent increase in mesenteric endothelial permeability. These findings could have significant implications for smokers undergoing intra-abdominal surgical procedures.