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

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 (CO(2)) 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 CO(2) pneumoperitoneum at IPPs of 2, 8, or 15 mmHg. Over the course of each experiment, the peritoneal tissue-oxygen tension (PitO(2)) was continuously monitored. Experiment 2: On the first day, the mice were divided into three groups according to the following treatments: CO(2) 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 (PitO(2): 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 CO(2) 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.

• Authors: Sachiko Matsuzaki, Kris Jardon, Elodie Maleysson, Francis D'Arpiany, Michel Canis, Jean-Etienne Bazin, Gérard Mage
• Journal: Surgical endoscopy (Surg Endosc) Vol. 24 Issue 11 Pg. 2871-80 (Nov 2010) ISSN: 1432-2218 [Electronic] Germany
• PMID: 20419320 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Hypoxia-Inducible Factor 1
• Nitroimidazoles
• Plant Proteins
• RT-TIP protein, Nicotiana tabacum
• Carbon Dioxide
• pimonidazole
• Oxygen

Topics

• Animals
• Carbon Dioxide (administration & dosage)
• Cell Hypoxia
• Female
• Hypoxia-Inducible Factor 1 (metabolism)
• Immunohistochemistry
• Laparotomy
• Mice
• Mice, Inbred C57BL
• Nitroimidazoles (metabolism)
• Oxygen (metabolism)
• Peritoneal Cavity (physiology)
• Peritoneum (metabolism, surgery)
• Plant Proteins
• Pneumoperitoneum, Artificial
• Pressure
• Respiration, Artificial
• Tissue Adhesions (physiopathology)