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Increased expression of P-cadherin mRNA in the mouse peritoneum after carbon dioxide insufflation.

BACKGROUND: Although systemic responses to carbon dioxide (CO(2)) pneumoperitoneum have been studied, there have been few reports of local responses within the peritoneum. We investigated the expression of mRNA for adhesion molecules involved in cell-cell interactions, including ICAM-1, VCAM-1, CD44, E-cadherin, P-cadherin, and N-cadherin, after the induction of a CO(2) pneumoperitoneum in mice. METHODS: Mice were treated with CO(2) pneumoperitoneum (4-6 mmHg for 30 min) and then killed after 24 h, 48 h, and 72 h. The peritoneum of the abdominal wall was resected, and total RNA was extracted by the acid guanidinium thiocyanate-phenol-chloroform extraction procedure, cDNA were synthesized by reverse transcription. Expression of the mRNA for each gene was normalized to that of b-actin for semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The expression of P-cadherin mRNA was significantly increased at 48 h (p = 0.007) and returned to the control level by 72 h after CO(2) pneumoperitoneum. The expression of CD44 increased gradually, reaching a peak at 48 h and returning to the control value by 72 h after CO(2) pneumoperitoneum. Expression of ICAM-1 mRNA was not changed significantly after the application of CO(2). CONCLUSION: The expression of P-cadherin mRNA in the peritoneum can be induced to repair injuries to mesothelial cells caused by CO(2) pneumoperitoneum.

Actins↗

Laparoscopic insufflation with room air causes exaggerated interleukin-6 response.

BACKGROUND: The gut is a central organ in the postoperative stress reaction. We previously reported that measuring gut-mucosal cytokines may more accurately reflect the response to operative stress. Additionally, we have shown that the gut demonstrates a blunted cytokine response after laparoscopy as compared with laparotomy. METHODS: To further investigate whether this differential response is caused by exposure of the peritoneal cavity to general atmospheric air during laparotomy, 80 A/J mice were randomized equally into four groups: CD (carbon dioxide [CO2] pneumoperitoneum), RA (room air pneumoperitoneum), AP (anesthesia and port insertion only), and PC (pure control, no intervention). Pneumoperitoneum was established and maintained at 3 mmHg for 60 min. All the mice were killed 4 h after the intervention. Jejunal mucosa and serum samples were collected and analyzed for interleukin-6 (IL-6) levels. Results were analyzed by analysis of variance (ANOVA). RESULTS: Gut-mucosal IL-6 in the RA group was significantly higher than in all other groups: RA, 1,354.5 +/- 117.9* vs. CD, 964.3 +/- 114.0 vs. AP, 960.2 +/- 86.2 vs. PC, 908.0 +/- 83.6; *p < 0.05. The CD group did not show a significant increase in gut-mucosal IL-6 as compared with the AP and PC groups. Similarly, RA resulted in significant increases in serum IL-6 as compared with AP and PC, whereas CD showed no significant difference: RA, 161.3 +/- 66.2* vs. 95.1 +/- 1 vs. AP, 10.6 +/- 5.3 vs. PC, undetectable; *p < 0.05. There was no difference in serum IL-6 level between CD or any of the other groups. CONCLUSIONS: Exposure of the peritoneal cavity to atmospheric air, independently of the trauma of abdominal access, causes an exaggerated serum and gut mucosal IL-6 response 4 h after intervention. The beneficial effect of CO2 laparoscopy may be caused by the exclusion of general atmospheric air from the peritoneal cavity.

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