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


CONCLUSIONS
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.
Matsuzaki
Sachiko
S
CHU Clermont-Ferrand, Polyclinique de l'Hôtel Dieu, Gynécologie Obstétrique et Médecine de la Reproduction, Boulevard Léon Malfreyt, 63058, Clermont-Ferrand, France. sachikoma@aol.com
Jardon
Kris
K
Maleysson
Elodie
E
D'Arpiany
Francis
F
Canis
Michel
M
Bazin
Jean-Etienne
JE
Mage
Gérard
G
D000818:Animals; D002245:Carbon Dioxide / Q000008:administration & dosage*; D015687:Cell Hypoxia; D005260:Female; D051793:Hypoxia-Inducible Factor 1 / Q000378:metabolism; D007150:Immunohistochemistry; D007813:Laparotomy; D051379:Mice; D008810:Mice, Inbred C57BL; D009593:Nitroimidazoles / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010529:Peritoneal Cavity / Q000502:physiology*; D010537:Peritoneum / Q000378:metabolism* / Q000601:surgery; D010940:Plant Proteins; D011028:Pneumoperitoneum, Artificial; D011312:Pressure; D012121:Respiration, Artificial; D000267:Tissue Adhesions / Q000503:physiopathology
D051793:Hypoxia-Inducible Factor 1; D009593:Nitroimidazoles; D010940:Plant Proteins; C077187:RT-TIP protein, Nicotiana tabacum; D002245:Carbon Dioxide; C033815:pimonidazole; D010100:Oxygen