AIM: To evaluate the role of leptin in the internal disorders during hepatic ischemia/reperfusion injury. METHODS: A rat model of 70% hepatic ischemia/reperfusion injury was established, with groups of shamoperation (...AIM: To evaluate the role of leptin in the internal disorders during hepatic ischemia/reperfusion injury. METHODS: A rat model of 70% hepatic ischemia/reperfusion injury was established, with groups of shamoperation (Sham), 60 min ischemia/60 min reperfusion (I60'R60'), I60'R150', I60'R240' and I60'R360'. Serum leptin was detected by a self-produced radioimmunoassay; serum glucose, total anti-oxidation capacity, myeloperoxidase, alanine transaminase and diamine oxidase were determined by relevant kits, while histologicalalterations and protein levels of leptin in the lung, liver and duodenum were examined by hematoxylin-eosin staining and immunohistochemistry. Spearman's rank correlation between leptin and other variables or grading of tissue impairment were analyzed simultaneously. RESULTS: Serum leptin in I60'R360' was significantly higher than in Sham and I60'R240' groups (both P < 0.05), serum glucose in I60'R360' was higher than in Sham and I60'R150' (both P < 0.05), and serum total anti-oxidation capacity in I60'R240' and I60'R360' were higher than in Sham (both P < 0.05) and I60'R150' groups (both P < 0.01). Serum myeloperoxidase in groups of I60'R240' and I60'R360' were lower than in I60'R150'group (both P < 0.05), serum alanine transaminase in the four reperfusion groups were higher than in the Sham group (all P < 0.05), while serum DAO in I60'R360' was lower than in I60'R60' (P < 0.05). Histological impairment in the lung, liver and duodenum at the early phase of this injury was more serious, but the impairment at the later phase was lessened gradually. Protein levels of leptin in the lung in the four reperfusion groups were significantly lower than in the Sham group (all P < 0.01), decreasing in the order of I60'R150', I60' R60', I60'R360' and I60'R240'; the levels in the liver in I60'R60' and I60'R240' were higher than in the Sham group (both P < 0.01), while the levels in I60'R240' and I60'R360' were lower than in I60'R60' (both P < 0.01); the levels in duodenum in I60'R240' and I60'R360' were higher than in Sham, I60'R60' and I60'R150' (all P < 0.01), while the level in I60'R150' was lower than in I60' R60' (P < 0.05). There was a significantly positive correlation between serum leptin and alanine transaminase (ρ = 0.344, P = 0.021), a significantly negative correlation between the protein level of leptin in the lung and its damage scores (ρ = -0.313, P = 0.036), and a significantly positive correlation between the protein level of leptin in the liver and its damage scores (ρ = 0.297, P = 0.047). CONCLUSION: Endogenous leptin fluctuates in he-patic ischemia/reperfusion injury, exerts a potency to rehabilitate the internal disorders and represents a potential target for supportive therapy.展开更多
AIM To investigate the effect of ischaemia and reperfusion(I/R) injury on the Ca^(2+)-ATPase activation in the intestinal tissue of a rat autologous orthotopic liver transplantation model and to determine if hypoxia p...AIM To investigate the effect of ischaemia and reperfusion(I/R) injury on the Ca^(2+)-ATPase activation in the intestinal tissue of a rat autologous orthotopic liver transplantation model and to determine if hypoxia preconditioning(HP) therapy induces HIF-1α to protect rat intestinal tissue against I/R injury.METHODS Rats received non-lethal hypoxic preconditioning therapy to induce HIF-1α expression. We used an autologous orthotopic liver transplantation model to imitate the I/R injury in intestinal tissue. Then, we detected the microstructure changes in small intestinal tissues, Ca^(2+)-ATPase activity, apoptosis, and inflammation within 48 h postoperatively. RESULTS HIF-1α expression was significantly increased in intestinal tissue at 12 h postoperatively in rats that were exposed to a hypoxic environment for 90 min compared with a non-HP group(HP vs AT, P = 0.0177). Pathological analysis was performed on the intestinal mucosa cells, and the cells in the HP group appeared healthier than the cells in the AT group. The Ca^(2+)-ATPase activity in the small intestinal cells in the AT group was significantly lower after the operation, and the Ca^(2+)-ATPase activity in the HP group recovered faster than that in the AT group at 6 h postoperatively(HP vs AT, P = 0.0106). BCL-2 expression in the HP group was significantly higher than that in the AT group at 12 h postoperatively(HP vs AT P = 0.0010). The expression of the inflammatory factors NO, SOD, IL-6, and TNF-α was significantly lower in the HP group than in the AT group.CONCLUSION Hypoxia-induced HIF-1α could protect intestinal mucosal cells against mitochondrial damage after I/R injury. HP could improve hypoxia tolerance in small intestinal mucosal cells and increase Ca^(2+)-ATPase activity to reduce the apoptosis of and pathological damage to intestinal cells. HP could be a useful way to promote the earlier recovery of intestinal function after graft procedure.展开更多
The last decade saw increased organ donation activity from donors after cardiac death (DCD). This contributed to a signif icant proportion of transplant activity. Despite certain drawbacks, liver transplantation from ...The last decade saw increased organ donation activity from donors after cardiac death (DCD). This contributed to a signif icant proportion of transplant activity. Despite certain drawbacks, liver transplantation from DCD donors continues to supplement the donor pool on the backdrop of a severe organ shortage. Understanding the pathophysiology has provided the basis for modulation of DCD organs that has been proven to be effective outside liver transplantation but remains experimental in liver transplantation models. Research continues on how best to further increase the utility of DCD grafts. Most of the work has been carried out exploring the use of organ preservation using machine assisted perfusion. Both ex-situ and in-situ organ perfusion systems are tested in the liver transplantation setting with promising results. Additional techniques involved pharmacological manipulation of the donor, graft and the recipient. Ethical barriers and end-of-life care pathways are obstacles to widespread clinical application of some of the recent advances to practice. It is likely that some of the DCD offers are in fact probably "prematurely" of-fered without ideal donor management or even prior to brain death being established. The absolute benef its of DCD exist only if this form of donation supplements the existing deceased donor pool; hence, it is worthwhile revisiting organ donation process enabling us to identify counter remedial measures.展开更多
BACKGROUND Exposure to high sustained +Gz(head-to-foot inertial load) is known to have harmful effects on pilots' body in flight. Although clinical data have shown that liver dysfunction occurs in pilots, the prec...BACKGROUND Exposure to high sustained +Gz(head-to-foot inertial load) is known to have harmful effects on pilots' body in flight. Although clinical data have shown that liver dysfunction occurs in pilots, the precise cause has not been well defined.AIM To investigate rat liver function changes in response to repeated +Gz exposure.METHODS Ninety male Wistar rats were randomly divided into a blank control group(BC group, n = 30), a +6 Gz/5 min stress group(6 GS group, n = 30), and a +10 Gz/5 min stress group(10 GS group, n = 30). The 6 GS and 10 GS groups were exposed to +6 Gz and +10 Gz, respectively, in an animal centrifuge. The onset rate of +Gz was 0.5 G/s. The sustained time at peak +Gz was 5 min for each exposure(for 5 exposures, and 5-min intervals between exposures for a total exposure and non-exposure time of 50 min). We assessed liver injury bymeasuring the portal venous flow volume, serum alanine aminotransferase(ALT)and aspartate aminotransferase(AST), liver tissue malondialdehyde(MDA), Na+-K+-ATPase, and changes in liver histology. These parameters were recorded at 0 h, 6 h, and 24 h after repeated +Gz exposures.RESULTS After repeated +Gz exposures in the 6 GS and the 10 GS groups, the velocity and flow signal in the portal vein(PV) were significantly decreased as compared to the BC group at 0 h after exposure. Meanwhile, we found that the PV diameter did not change significantly. However, rats in the 6 GS group had a much higher portal venous flow volume than the 10 GS group at 0 h after exposure. The 6 GS group had significantly lower ALT, AST, and MDA values than the 10 GS group 0 h and 6 h post exposure. The Na^+-K^+-ATPase activity in the 6 GS group was significantly higher than that in the 10 GS group 0 h and 6 h post exposure.Hepatocyte injury, determined pathologically, was significantly lower in the 6 GS group than in the 10 GS group.CONCLUSION Repeated +Gz exposures transiently cause hepatocyte injury and affect liver metabolism and morphological structure.展开更多
目的:观察大鼠肢体缺血再灌注后肝脏的损伤性变化,以及牛磺酸对肝脏损伤性变化的保护效应,探讨牛磺酸对大鼠肢体缺血再灌注后肝脏功能保护作用的可能机制.方法:实验用W istar大鼠30只,随机分为对照(control,C)组,缺血再灌注(ischem ia r...目的:观察大鼠肢体缺血再灌注后肝脏的损伤性变化,以及牛磺酸对肝脏损伤性变化的保护效应,探讨牛磺酸对大鼠肢体缺血再灌注后肝脏功能保护作用的可能机制.方法:实验用W istar大鼠30只,随机分为对照(control,C)组,缺血再灌注(ischem ia reperfusion,IR)组和牛磺酸+缺血再灌注(taurine+ischem ia reperfusion,TR)组,每组10只.观察缺血4 h再灌注4 h各组大鼠血浆中XOD,LDH,MDA,AST,ALT和SOD的变化;观察肝组织XOD,MDA,ROS,MPO和Ca2+的变化;观察肝线粒体GSH-PX和Ca2+的变化.结果:单纯肢体缺血再灌注组大鼠血浆中LDH[(190.16±13.36)μkat/L],XOD[(758.82±151.53)nkat/L],MDA[(5.19±0.67)nmol/L],ALT[(78.40±6.45)nkat/L],AST[(47.70±4.47)nkat/L]等较正常对照组血浆中LDH[(122.39±14.87)μkat/L],XOD[(543.61±43.51)μkat/kg],MDA[(1.27±0.21)nmol/L],ALT[(20.50±3.70)nkat/L],AST[(25.25±2.98)nkat/L]明显增加,而SOD[(1.30±0.15)μkat/L]较对照组(1.80±0.16)μkat/L明显降低;单纯肢体缺血再灌注组大鼠肝组织XOD[(104.69±12.34)μkat/Kg],MDA[(2.66±0.08)nmol/L],ROS[(771.65±100.69)μkat/L],MPO(0.47±0.04),[Ca2+][(0.248±0.050)mmol/L]较正常对照组肝组织XOD[(59.01±10.50)μkat/kg],MDA[(1.29±0.14)nmol/L],ROS[(606.45±52.01)μkat/L],MPO[(0.28±0.06)],[Ca2+][(0.123±0.014)mmol/L]均明显增加;缺血再灌注组大鼠肝线粒体GSH-Px活性[(20.34±4.67)nkat/L]与正常对照组[(31.17±11.50)nkat/L]比较明显降低,而[Ca2+]浓度[(0.38±0.06)mmol/L]则高于正常对照组[(0.14±0.03)mmol/L].牛磺酸+缺血再灌注组大鼠血浆中LDH[(158.29±4.87)μkat/L],XOD[(758.82±151.53)nkat/L],MDA[(2.81±0.19)nmol/L],ALT[(64.40±9.05)nkat/L],AST[(38.70±8.10)nkat/L]较单纯缺血再灌注组明显降低,而SOD[(1.50±0.17)μkat/L]则增加;肝组织XOD[(94.19±13.50)μkat/L],MDA[(1.67±0.12)nmol/L],ROS[(710.81±55.34)μkat/L],MPO(0.36±0.04),[Ca2+][(0.192±0.426)mmol/L]等指标也较单纯缺血再灌注组明显降低,此外牛磺酸+缺血再灌注组大鼠肝线粒体GSH-Px活性[(22.50±3.17)nkat/L]与单纯肢体缺血再灌注组相比明显增加,而Ca2+浓度[(0.31±0.06)mmol/L]则降低,损伤减轻.结论:牛磺酸可以减轻大鼠肢体缺血4 h再灌注4 h后所致的肝损伤.展开更多
目的观察大鼠肢体缺血再灌注后肝脏的损伤性变化,以及牛磺酸(taurine)对肝脏损伤性变化的影响,探讨牛磺酸对大鼠肢体缺血再灌注后肝脏功能保护作用及可能机制。方法实验用W istar大鼠30只,随机分为对照(control)组,缺血再灌注(ischem ia...目的观察大鼠肢体缺血再灌注后肝脏的损伤性变化,以及牛磺酸(taurine)对肝脏损伤性变化的影响,探讨牛磺酸对大鼠肢体缺血再灌注后肝脏功能保护作用及可能机制。方法实验用W istar大鼠30只,随机分为对照(control)组,缺血再灌注(ischem ia reperfusion,IR)组和牛磺酸+缺血再灌注(taurine+Ischem ia reperfusion,TR)组(n=10)。分别测定各组动物肝组织黄嘌呤氧化酶(XOD)、丙二醛(MDA)、活性氧(ROS)、髓过氧化物酶(MPO)、Ca2+含量和肝细胞线粒体琥珀酸脱氢酶(SDH),Na+-K+-ATPase,Ca2+-Mg2+-ATPase,Ca2+含量的变化。结果发现大鼠肢体缺血再灌注后肝脏功能明显受损,牛磺酸减轻了由于肢体缺血再灌注引起的肝细胞和线粒体的钙超载及过氧化等损伤。结论牛磺酸可以避免或减轻大鼠肢体缺血再灌注继发的肝脏损伤。展开更多
基金Supported by National Natural Science Foundation of China, No. 30670821National Key Technology R&D Program, No. 2006BAF07B01+1 种基金Special Funds for Key Program of Public Welfare of National Ministry of Science and Technology, No. 2002D1A40019Nursery Fund of Chinese PLA General Hospital, No. 06MP83
文摘AIM: To evaluate the role of leptin in the internal disorders during hepatic ischemia/reperfusion injury. METHODS: A rat model of 70% hepatic ischemia/reperfusion injury was established, with groups of shamoperation (Sham), 60 min ischemia/60 min reperfusion (I60'R60'), I60'R150', I60'R240' and I60'R360'. Serum leptin was detected by a self-produced radioimmunoassay; serum glucose, total anti-oxidation capacity, myeloperoxidase, alanine transaminase and diamine oxidase were determined by relevant kits, while histologicalalterations and protein levels of leptin in the lung, liver and duodenum were examined by hematoxylin-eosin staining and immunohistochemistry. Spearman's rank correlation between leptin and other variables or grading of tissue impairment were analyzed simultaneously. RESULTS: Serum leptin in I60'R360' was significantly higher than in Sham and I60'R240' groups (both P < 0.05), serum glucose in I60'R360' was higher than in Sham and I60'R150' (both P < 0.05), and serum total anti-oxidation capacity in I60'R240' and I60'R360' were higher than in Sham (both P < 0.05) and I60'R150' groups (both P < 0.01). Serum myeloperoxidase in groups of I60'R240' and I60'R360' were lower than in I60'R150'group (both P < 0.05), serum alanine transaminase in the four reperfusion groups were higher than in the Sham group (all P < 0.05), while serum DAO in I60'R360' was lower than in I60'R60' (P < 0.05). Histological impairment in the lung, liver and duodenum at the early phase of this injury was more serious, but the impairment at the later phase was lessened gradually. Protein levels of leptin in the lung in the four reperfusion groups were significantly lower than in the Sham group (all P < 0.01), decreasing in the order of I60'R150', I60' R60', I60'R360' and I60'R240'; the levels in the liver in I60'R60' and I60'R240' were higher than in the Sham group (both P < 0.01), while the levels in I60'R240' and I60'R360' were lower than in I60'R60' (both P < 0.01); the levels in duodenum in I60'R240' and I60'R360' were higher than in Sham, I60'R60' and I60'R150' (all P < 0.01), while the level in I60'R150' was lower than in I60' R60' (P < 0.05). There was a significantly positive correlation between serum leptin and alanine transaminase (ρ = 0.344, P = 0.021), a significantly negative correlation between the protein level of leptin in the lung and its damage scores (ρ = -0.313, P = 0.036), and a significantly positive correlation between the protein level of leptin in the liver and its damage scores (ρ = 0.297, P = 0.047). CONCLUSION: Endogenous leptin fluctuates in he-patic ischemia/reperfusion injury, exerts a potency to rehabilitate the internal disorders and represents a potential target for supportive therapy.
基金The Second Hospital of Shandong University Youth Foundation,No.Y2013010033
文摘AIM To investigate the effect of ischaemia and reperfusion(I/R) injury on the Ca^(2+)-ATPase activation in the intestinal tissue of a rat autologous orthotopic liver transplantation model and to determine if hypoxia preconditioning(HP) therapy induces HIF-1α to protect rat intestinal tissue against I/R injury.METHODS Rats received non-lethal hypoxic preconditioning therapy to induce HIF-1α expression. We used an autologous orthotopic liver transplantation model to imitate the I/R injury in intestinal tissue. Then, we detected the microstructure changes in small intestinal tissues, Ca^(2+)-ATPase activity, apoptosis, and inflammation within 48 h postoperatively. RESULTS HIF-1α expression was significantly increased in intestinal tissue at 12 h postoperatively in rats that were exposed to a hypoxic environment for 90 min compared with a non-HP group(HP vs AT, P = 0.0177). Pathological analysis was performed on the intestinal mucosa cells, and the cells in the HP group appeared healthier than the cells in the AT group. The Ca^(2+)-ATPase activity in the small intestinal cells in the AT group was significantly lower after the operation, and the Ca^(2+)-ATPase activity in the HP group recovered faster than that in the AT group at 6 h postoperatively(HP vs AT, P = 0.0106). BCL-2 expression in the HP group was significantly higher than that in the AT group at 12 h postoperatively(HP vs AT P = 0.0010). The expression of the inflammatory factors NO, SOD, IL-6, and TNF-α was significantly lower in the HP group than in the AT group.CONCLUSION Hypoxia-induced HIF-1α could protect intestinal mucosal cells against mitochondrial damage after I/R injury. HP could improve hypoxia tolerance in small intestinal mucosal cells and increase Ca^(2+)-ATPase activity to reduce the apoptosis of and pathological damage to intestinal cells. HP could be a useful way to promote the earlier recovery of intestinal function after graft procedure.
文摘The last decade saw increased organ donation activity from donors after cardiac death (DCD). This contributed to a signif icant proportion of transplant activity. Despite certain drawbacks, liver transplantation from DCD donors continues to supplement the donor pool on the backdrop of a severe organ shortage. Understanding the pathophysiology has provided the basis for modulation of DCD organs that has been proven to be effective outside liver transplantation but remains experimental in liver transplantation models. Research continues on how best to further increase the utility of DCD grafts. Most of the work has been carried out exploring the use of organ preservation using machine assisted perfusion. Both ex-situ and in-situ organ perfusion systems are tested in the liver transplantation setting with promising results. Additional techniques involved pharmacological manipulation of the donor, graft and the recipient. Ethical barriers and end-of-life care pathways are obstacles to widespread clinical application of some of the recent advances to practice. It is likely that some of the DCD offers are in fact probably "prematurely" of-fered without ideal donor management or even prior to brain death being established. The absolute benef its of DCD exist only if this form of donation supplements the existing deceased donor pool; hence, it is worthwhile revisiting organ donation process enabling us to identify counter remedial measures.
文摘BACKGROUND Exposure to high sustained +Gz(head-to-foot inertial load) is known to have harmful effects on pilots' body in flight. Although clinical data have shown that liver dysfunction occurs in pilots, the precise cause has not been well defined.AIM To investigate rat liver function changes in response to repeated +Gz exposure.METHODS Ninety male Wistar rats were randomly divided into a blank control group(BC group, n = 30), a +6 Gz/5 min stress group(6 GS group, n = 30), and a +10 Gz/5 min stress group(10 GS group, n = 30). The 6 GS and 10 GS groups were exposed to +6 Gz and +10 Gz, respectively, in an animal centrifuge. The onset rate of +Gz was 0.5 G/s. The sustained time at peak +Gz was 5 min for each exposure(for 5 exposures, and 5-min intervals between exposures for a total exposure and non-exposure time of 50 min). We assessed liver injury bymeasuring the portal venous flow volume, serum alanine aminotransferase(ALT)and aspartate aminotransferase(AST), liver tissue malondialdehyde(MDA), Na+-K+-ATPase, and changes in liver histology. These parameters were recorded at 0 h, 6 h, and 24 h after repeated +Gz exposures.RESULTS After repeated +Gz exposures in the 6 GS and the 10 GS groups, the velocity and flow signal in the portal vein(PV) were significantly decreased as compared to the BC group at 0 h after exposure. Meanwhile, we found that the PV diameter did not change significantly. However, rats in the 6 GS group had a much higher portal venous flow volume than the 10 GS group at 0 h after exposure. The 6 GS group had significantly lower ALT, AST, and MDA values than the 10 GS group 0 h and 6 h post exposure. The Na^+-K^+-ATPase activity in the 6 GS group was significantly higher than that in the 10 GS group 0 h and 6 h post exposure.Hepatocyte injury, determined pathologically, was significantly lower in the 6 GS group than in the 10 GS group.CONCLUSION Repeated +Gz exposures transiently cause hepatocyte injury and affect liver metabolism and morphological structure.
文摘目的:观察大鼠肢体缺血再灌注后肝脏的损伤性变化,以及牛磺酸对肝脏损伤性变化的保护效应,探讨牛磺酸对大鼠肢体缺血再灌注后肝脏功能保护作用的可能机制.方法:实验用W istar大鼠30只,随机分为对照(control,C)组,缺血再灌注(ischem ia reperfusion,IR)组和牛磺酸+缺血再灌注(taurine+ischem ia reperfusion,TR)组,每组10只.观察缺血4 h再灌注4 h各组大鼠血浆中XOD,LDH,MDA,AST,ALT和SOD的变化;观察肝组织XOD,MDA,ROS,MPO和Ca2+的变化;观察肝线粒体GSH-PX和Ca2+的变化.结果:单纯肢体缺血再灌注组大鼠血浆中LDH[(190.16±13.36)μkat/L],XOD[(758.82±151.53)nkat/L],MDA[(5.19±0.67)nmol/L],ALT[(78.40±6.45)nkat/L],AST[(47.70±4.47)nkat/L]等较正常对照组血浆中LDH[(122.39±14.87)μkat/L],XOD[(543.61±43.51)μkat/kg],MDA[(1.27±0.21)nmol/L],ALT[(20.50±3.70)nkat/L],AST[(25.25±2.98)nkat/L]明显增加,而SOD[(1.30±0.15)μkat/L]较对照组(1.80±0.16)μkat/L明显降低;单纯肢体缺血再灌注组大鼠肝组织XOD[(104.69±12.34)μkat/Kg],MDA[(2.66±0.08)nmol/L],ROS[(771.65±100.69)μkat/L],MPO(0.47±0.04),[Ca2+][(0.248±0.050)mmol/L]较正常对照组肝组织XOD[(59.01±10.50)μkat/kg],MDA[(1.29±0.14)nmol/L],ROS[(606.45±52.01)μkat/L],MPO[(0.28±0.06)],[Ca2+][(0.123±0.014)mmol/L]均明显增加;缺血再灌注组大鼠肝线粒体GSH-Px活性[(20.34±4.67)nkat/L]与正常对照组[(31.17±11.50)nkat/L]比较明显降低,而[Ca2+]浓度[(0.38±0.06)mmol/L]则高于正常对照组[(0.14±0.03)mmol/L].牛磺酸+缺血再灌注组大鼠血浆中LDH[(158.29±4.87)μkat/L],XOD[(758.82±151.53)nkat/L],MDA[(2.81±0.19)nmol/L],ALT[(64.40±9.05)nkat/L],AST[(38.70±8.10)nkat/L]较单纯缺血再灌注组明显降低,而SOD[(1.50±0.17)μkat/L]则增加;肝组织XOD[(94.19±13.50)μkat/L],MDA[(1.67±0.12)nmol/L],ROS[(710.81±55.34)μkat/L],MPO(0.36±0.04),[Ca2+][(0.192±0.426)mmol/L]等指标也较单纯缺血再灌注组明显降低,此外牛磺酸+缺血再灌注组大鼠肝线粒体GSH-Px活性[(22.50±3.17)nkat/L]与单纯肢体缺血再灌注组相比明显增加,而Ca2+浓度[(0.31±0.06)mmol/L]则降低,损伤减轻.结论:牛磺酸可以减轻大鼠肢体缺血4 h再灌注4 h后所致的肝损伤.
文摘目的观察大鼠肢体缺血再灌注后肝脏的损伤性变化,以及牛磺酸(taurine)对肝脏损伤性变化的影响,探讨牛磺酸对大鼠肢体缺血再灌注后肝脏功能保护作用及可能机制。方法实验用W istar大鼠30只,随机分为对照(control)组,缺血再灌注(ischem ia reperfusion,IR)组和牛磺酸+缺血再灌注(taurine+Ischem ia reperfusion,TR)组(n=10)。分别测定各组动物肝组织黄嘌呤氧化酶(XOD)、丙二醛(MDA)、活性氧(ROS)、髓过氧化物酶(MPO)、Ca2+含量和肝细胞线粒体琥珀酸脱氢酶(SDH),Na+-K+-ATPase,Ca2+-Mg2+-ATPase,Ca2+含量的变化。结果发现大鼠肢体缺血再灌注后肝脏功能明显受损,牛磺酸减轻了由于肢体缺血再灌注引起的肝细胞和线粒体的钙超载及过氧化等损伤。结论牛磺酸可以避免或减轻大鼠肢体缺血再灌注继发的肝脏损伤。
