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 eects olow-and high-pressure pneumoperitoneum,and to determine the degree o 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 ollowing 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 unction 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 bywestern 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 or 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 prealbumin 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 fa CO2 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.

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 hematoxylineosin 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 60 min could induce liver pneumoperitoneum for 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 μmol/g in liver homogenate and 7.64 ± 2.19 μmol/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 μmol/g in liver tissue and 12.49 ±4.21 μmol/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 7.2 8±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.