Effect of carbon dioxide pneumoperitoneal pressure on the ultrastructure of implanted endometriotic lesions in a rat model
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Carbon dioxide pneumoperitoneum at 10 mmHg and 20 mmHg significantly damaged the ultrastructure of endometriotic lesions in rats, with higher pressure causing more severe damage.
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Abstract
ObjectiveTo evaluate the effect of carbon dioxide (CO2) pneumoperitonal pressure on the ultrastructure of implanted endometriotic lesions in a rat model.Study designAn endometriotic model was established in Sprague-Dawley rats with peritoneal implantation of their own endometrial tissue to form ectopic endometrial tissue. Thirty rats were divided at random into three groups: control group, 10 mmHg CO2 pneumoperitoneum group and 20 mmHg CO2 pneumoperitoneum group. CO2 inflation lasted for 1 h in both pneumoperitoneum groups. Selected endometriotic lesions were examined by electron microscopy 1 week after CO2 pneumoperitoneum to determine changes in the ultrastructure of cell organelles of glandular and stromal cells.ResultsIn the control group, stromal cells had an orderly arrangement, and the structure of the microvilli was normal. The 10 mmHg and 20 mmHg CO2 pneumoperitoneum groups had increased chromatin margination of glandular epithelial cells, reduced or absent mitochondrial cristae and mitochondrial swelling. Further ultrastructural damage included reduced or absent microvilli, widened or collapsed cell junctions, and stromal cells with a disorderly arrangement. Ultrastructural damage of glandular epithelial cells was more severe in the 20 mmHg group compared with the 10 mmHg group.ConclusionCO2 pneumoperitoneum leads to significant ultrastructural damage of endometriotic lesions. Higher CO2 pneumoperitoneal pressure resulted in more damage than lower CO2 pneumoperitoneal pressure.
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