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Carbon dioxide pneumoperitoneum, intraperitoneal pressure, and peritoneal tissue hypoxia: a mouse study with controlled respiratory support

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Abstract

Background

Animal experiments have suggested that the laparoscopic peritoneal environment is hypoxic. This study aimed to investigate whether peritoneal tissue is hypoxic on a cellular level during a carbon dioxide (CO2) pneumoperitoneum at different intraperitoneal pressures (IPPs) and to determine the short-term effects of surgical injury on the hypoxia status of peritoneal tissue in the injured peritoneum and the distant noninjured peritoneum at cellular and molecular levels.

Methods

Experiment 1: Mice were divided into five groups according to the following treatments: anesthesia alone, laparotomy, and CO2 pneumoperitoneum at IPPs of 2, 8, or 15 mmHg. Over the course of each experiment, the peritoneal tissue-oxygen tension (PitO2) was continuously monitored. Experiment 2: On the first day, the mice were divided into three groups according to the following treatments: CO2 pneumoperitoneum at an IPP of either 2 or 8 mmHg or laparotomy. The bilateral caudal epigastric arteries and uterine horns then were coagulated using a bipolar cautery device. On day 7, peritoneal tissue samples were collected for real-time reverse transcriptase–polymerase chain reaction (RT-PCR) and immunohistochemistry. In both experiments, pimonidazole hydrochloride was used to detect tissue hypoxia at a cellular level.

Results

Experiment 1: Peritoneal hypoxia at both tissue and cellular levels was detected only in the groups treated with an IPP of 15 mmHg (PitO2: 5.2 ± 1.0 mmHg, mean ± SEM). Experiment 2: The percentage of pimonidazole immunostained mesothelial and stromal cells from the distant noninjured peritoneum was significantly higher in the group treated with an IPP of 8 mmHg than in the other groups. Hypoxia-inducible factor 1 alpha subunit mRNA expression in the distant noninjured peritoneum of the group treated with an IPP of 8 mmHg was significantly higher than in the control group (anesthesia alone).

Conclusion

The CO2 pneumoperitoneum itself did not cause peritoneal hypoxia at either a tissue or a cellular level in a mouse model when a low IPP was used.

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Acknowledgments

We are grateful to the anesthesiology staff at CHU Clermont-Ferrand for their invaluable discussions. We are indebted to all the staff at le Centre International de la Chirurgie Endoscopique (Clermont-Ferrand, France) and the technicians in the Department of Anatomie et cytologie pathologiques, CHU Clermont-Ferrand, Hôtel-Dieu, for technical support. We are indebted to Karl Storz Endoscopy & GmbH (Tuttlingen, Germany) for providing laparoscopic equipment and Organon (Paris, France) for providing vecuronium bromide. This study was supported in part by Karl Storz Endoscopy & GmbH (Tuttlingen, Germany) and le Conseil Régional d’Auvergne (Recherche et Innovation Technologique) (Clermont-Ferrand, France).

Disclosures

Sachiko Matsuzaki, Kris Jardon, Elodie Maleysson, Francis D’Arpiany; Michel Canis, Jean-Etienne Bazin and Gérard Mage have no conflicts of interest or financial ties to disclose.

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Correspondence to Sachiko Matsuzaki.

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Matsuzaki, S., Jardon, K., Maleysson, E. et al. Carbon dioxide pneumoperitoneum, intraperitoneal pressure, and peritoneal tissue hypoxia: a mouse study with controlled respiratory support. Surg Endosc 24, 2871–2880 (2010). https://doi.org/10.1007/s00464-010-1069-z

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  • DOI: https://doi.org/10.1007/s00464-010-1069-z

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