Two clinically relevant pressures of carbon dioxide pneumoperitoneum cause hepatic injury in a rabbit model.

AIM

To observe the hepatic injury induced by carbon dioxide pneumoperitoneum (CDP) in rabbits, compare the effects of low- and high-pressure pneumoperitoneum, and to determine the degree of hepatic injury induced by these two clinically relevant CDP pressures.

METHODS

Thirty healthy male New Zealand rabbits weighing 3.0 to 3.5 kg were randomly divided into three groups (n = 10 for each group) and subjected to the following to CDP pressures: no gas control, 10 mmHg, or 15 mmHg. Histological changes in liver tissues were observed with hematoxylin and eosin staining and transmission electron microscopy. Liver function was evaluated using an automatic biochemical analyzer. Adenine nucleotide translocator (ANT) activity in liver tissue was detected with the atractyloside-inhibitor stop technique. Bax and Bcl-2 expression levels were detected by western blotting.

RESULTS

Liver functions in the 10 mmHg and 15 mmHg experimental groups were significantly disturbed compared with the control group. After CDP, the levels of alanine transaminase and aspartate transaminase were 77.3 ± 14.5 IU/L and 60.1 ± 11.4 IU/L, respectively, in the 10 mmHg experimental group and 165.1 ± 19.4 IU/L and 103.8 ± 12.3 IU/L, respectively, in the 15 mmHg experimental group, which were all higher than those of the control group (P < 0.05). There was no difference in pre-albumin concentration between the 10 mmHg experimental group and the control group, but the pre-albumin level of the 15 mmHg experimental group was significantly lower than that of the control group (P < 0.05). No significant differences were observed in the levels of total bilirubin or albumin among the three groups. After 30 and 60 min of CDP, pH was reduced (P < 0.05) and PaCO₂ was elevated (P < 0.05) in the 10 mmHg group compared with controls, and these changes were more pronounced in the 15 mmHg group. Hematoxylin and eosin staining showed no significant change in liver morphology, except for mild hyperemia in the two experimental groups. Transmission electron microscopy showed mild mitochondrial swelling in hepatocytes of the 10 mmHg group, and this was more pronounced in the 15 mmHg group. No significant difference in ANT levels was found between the control and 10 mmHg groups. However, ANT concentration was significantly lower in the 15 mmHg group compared with the control group. The expression of hepatic Bax was significantly increased in the two experimental groups compared with the controls, but there were no differences in Bcl-2 levels among the three groups. Twelve hours after CDP induction, the expression of hepatic Bax was more significant in the 15 mmHg group than in the 10 mmHg group.

CONCLUSION

A CDP pressure of 15 mmHg caused more substantial hepatic injury, such as increased levels of acidosis, mitochondrial damage, and apoptosis; therefore, 10 mmHg CDP is preferable for laparoscopic operations.