Hepatic injury induced by carbon dioxide pneumoperitoneum in experimental rats.

AIM

To observe the hepatic injury induced by carbon dioxide pneumoperitoneum in rats and to explore its potential mechanism.

METHODS

Thirty healthy male SD rats were randomly divided into control group (n = 10), 0 h experimental group (n = 10) and 1 h experimental group (n = 10) after sham operation with carbon dioxide pneumoperitoneum. Histological changes in liver tissue were observed with hematoxylin-eosin staining. Liver function was assayed with an automatic biochemical analyzer. Concentration of malonyldialdehyde (MDA) and activity of superoxide dismutase (SOD) were assayed by colorimetry. Activity of adenine nucleotide translocator in liver tissue was detected with the atractyloside-inhibitor stop technique. Expression of hypoxia inducible factor-1 (HIF-1) mRNA in liver tissue was detected with in situ hybridization.

RESULTS

Carbon dioxide pneumoperitoneum for 60 min could induce liver injury in rats. Alanine aminotransferase and aspartate aminotransferase were 95.7 +/- 7.8 U/L and 86.8 +/- 6.9 U/L in 0 h experimental group, and 101.4 +/- 9.3 U/L and 106.6 +/- 8.7 U/L in 1 h experimental group. However, no significant difference was found in total billirubin, albumin, and pre-albumin in the three groups. In 0 h experimental group, the concentration of MDA was 9.83 +/- 2.53 micromol/g in liver homogenate and 7.64 +/- 2.19 micromol/g in serum respectively, the activity of SOD was 67.58 +/- 9.75 nu/mg in liver and 64.47 +/- 10.23 nu/mg in serum respectively. In 1 h experimental group, the concentration of MDA was 16.57 +/- 3.45 micromol/g in liver tissue and 12.49 +/- 4.21 micromol/g in serum respectively, the activity of SOD was 54.29 +/- 7.96 nu/mg in liver tissue and 56.31 +/- 9.85 nu/mg in serum, respectively. The activity of ANT in liver tissue was 9.52 +/- 1.56 in control group, 6.37 +/- 1.33 in 0 h experimental group and 7.28 +/- 1.45 (10(-9) mol/min per gram protein) in 1 h experimental group, respectively. The expression of HIF-1 mRNA in liver tissue was not detected in control group, and its optical density difference value was 6.14 +/- 1.03 in 0 h experimental group and 9.51 +/- 1.74 in 1 h experimental group, respectively.

CONCLUSION

Carbon dioxide pneumoperitoneum during the sham operation can induce hepatic injury in rats. The probable mechanisms of liver injury include anoxia, ischemia reperfusion and oxidative stress. Liver injury should be avoided during clinical laparoscopic operation with carbon dioxide pneumoperitoneum.