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), ...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.展开更多
The effects of hepatic ischemia/reperfusion (I/R) injuries on hepatocellular viability and store-operated calcium current (Isoc) in isolated rat hepatocytes and the effects of 2-APB on store-operated calcium current (...The effects of hepatic ischemia/reperfusion (I/R) injuries on hepatocellular viability and store-operated calcium current (Isoc) in isolated rat hepatocytes and the effects of 2-APB on store-operated calcium current (Isoc) in isolated rat hepatocytes after hepatic ischemia/reperfusion injuries were studied. Hepatic ischemia and reperfusion injury model was established and whole cell patch-clamp techniques were used to investigate the effects of 2-APB on Isoc. The results showed that ischemia/reperfusion injuries could significantly reduce hepatocellular viability and further increase Isoc in hepatocytes and 2-APB (20, 40, 60, 80, 100 μmol/L) produced a concentration-dependent decrease of Isoc with IC 50 value of 64.63±10.56 μmol/L (n=8). It was concluded that ischemia/reperfusion injuries could reduce hepatocellular viability, probably through increased Isoc in hepatocytes and 2-APB had a protective effect on ischemia/reperfusion-induced liver injury, probably though inhibiting Isoc.展开更多
基金Supported by The Eleventh-five Medical Science Fund of Chengdu Military Command Area,NoMB07011
文摘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.
基金This project was supported by the National Natural Sci ence Foundation of China (No. 30270532), the Trans Cen tury Excellent Talent Development Plan Fund of Ministry ofEducation of China (Official Letter No. 2002 48) and Shu guang Program Project of Shanghai Educational Committee(No. 02SG20).
文摘The effects of hepatic ischemia/reperfusion (I/R) injuries on hepatocellular viability and store-operated calcium current (Isoc) in isolated rat hepatocytes and the effects of 2-APB on store-operated calcium current (Isoc) in isolated rat hepatocytes after hepatic ischemia/reperfusion injuries were studied. Hepatic ischemia and reperfusion injury model was established and whole cell patch-clamp techniques were used to investigate the effects of 2-APB on Isoc. The results showed that ischemia/reperfusion injuries could significantly reduce hepatocellular viability and further increase Isoc in hepatocytes and 2-APB (20, 40, 60, 80, 100 μmol/L) produced a concentration-dependent decrease of Isoc with IC 50 value of 64.63±10.56 μmol/L (n=8). It was concluded that ischemia/reperfusion injuries could reduce hepatocellular viability, probably through increased Isoc in hepatocytes and 2-APB had a protective effect on ischemia/reperfusion-induced liver injury, probably though inhibiting Isoc.