scholarly journals Effects of hyperbaric oxygen (HBO), as pre-conditioning in liver of rats submitted to periodic liver ischemia/reperfusion

2013 ◽  
Vol 28 (suppl 1) ◽  
pp. 66-71 ◽  
Author(s):  
Diego Elias da Silva Caldeira ◽  
Maria Eliza Jordani Souza ◽  
Maria Cecília Jordani Gomes ◽  
Maria Aparecida Neves Cardoso Picinato ◽  
Clarice Fleury Fina ◽  
...  
Keyword(s):  
Hyperbaric Oxygen ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Respiratory Control ◽  
Mitochondrial Swelling ◽  
Liver Ischemia ◽  
Respiratory Control Ratio ◽  
Simultaneous Exposure ◽  
Significant Difference

PURPOSE: to assess the effect of hyperbaric oxygen (HBO) as pre-conditioning on periodic liver ischemia/reperfusion injury. METHODS: Thirty-six male Wistar rats were divided into 4 groups (SHAM, I/R , HBO-I/R and CONTROL). The surgical technique consisted of total clamping of the hepatic pedicle for 15 min followed by twice repeated reperfusion for 5 min (unclamping). HBO was applied in a collective chamber (simultaneous exposure of 4 rats) directly pressurized with oxygen at 2 ATA for 60 min. Hepatic mitochondrial function was determined using samples of the median lobe obtained after exactly 5 min of reperfusion for the analysis of mitochondrial respiration based on the determination of states 3 and 4, the respiratory control ratio and the transition of mitochondrial permeability (mitochondrial swelling).Data were analyzed by the Mann-Whitney test and the level of significance was set at p < 0.05. RESULTS: There was a statistically significant difference (p< 0.05) in state 3 between the CONTROL and I/R and HBO-I/R groups, in state 4 between the CONTROL and I/R and HBO-I/R groups; in respiratory control ratio (RCR) between the CONTROL and I/R and HBO-I/R groups and between the CONTROL and Sham groups, and in mitochondrial swelling between the CONTROL and I/R and HBO-/R groups and between the Sham and I/R and HBO-I/R groups. CONCLUSION: In this process of periodic ischemia and reperfusion, hyperbaric pre-conditioning did not improve significantly hepatic mitochondrial function.

scholarly journals Effect of hyperbaric oxygen therapy on liver function during intermittent ischemia

2013 ◽  
Vol 28 (suppl 1) ◽  
pp. 61-65 ◽  
Author(s):  
Leticia Botigeli Baldim ◽  
Ricardo Nejo Jr ◽  
Maria Eliza Jordani Souza ◽  
Maria Cecília Jordani Gomes ◽  
Maria Aparecida Neves Cardoso Picinato ◽  
...  
Keyword(s):  
Liver Function ◽  
Hyperbaric Oxygen ◽  
Mitochondrial Function ◽  
Hyperbaric Oxygen Therapy ◽  
Aspartate Aminotransferase ◽  
Alanine Aminotransferase ◽  
Oxygen Therapy ◽  
Respiratory Control ◽  
Respiratory Control Ratio ◽  
Hepatic Pedicle

PURPOSE: To analyze the effects of hyperbaric oxygen therapy on liver function in rats previously subjected to ischemia and reperfusion. METHODS: A randomly distribution of 23 Wistar rats was conducted into three groups: SHAM, animals subjected to surgical stress without restricting blood flow by clamping the hepatic pedicle, IR, rats underwent hepatic vascular occlusion intermittently for two complete cycles of 15 minutes of ischemia followed by 5 min of reperfusion, IR / HBO, rats underwent hepatic pedicle clamping and thereafter exposed to hyperbaric oxygen pressure of 2 absolute atmospheres for 60 minutes. We evaluated liver function through mitochondrial function, determined by the stages 3 and 4 of respiration, respiratory control ratio (RCR) and mitochondrial permeability transition (Swelling). Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also quantified . We analyzed the results using the Mann-Whitney test and were considered significant all results with p <0.05. RESULTS: There were significant differences between the results of stage 3 in SHAM vs IR group ; of the stage 4 in the groups IR vs SHAM and SHAM vs IR /HBO; of the Respiratory Control Ratio (RCR) in the group IR vs IR / HBO ; of alanine aminotransferase in the groups IR vs SHAM , SHAM vs IR/HBO and IR vs IR / HBO; aspartate aminotransferase in the groups SHAM vs IR and SHAM vs IR / HBO. CONCLUSION: The whole analysis of the mitochondiral function indicators permits us to conclude that the hyperbaric oxygen therapy acted as a protective agent of the mitochondrial function, minimizing the ischemia-reperfusion injury of the hepatic parenchyma.

scholarly journals Effect of liver ischemic preconditioning in cirrhotic rats submitted to hepatic ischemia/reperfusion injury

2006 ◽  
Vol 21 (suppl 1) ◽  
pp. 24-28 ◽  
Author(s):  
Eduardo Garcia Pacheco ◽  
Maria Cecília Jordani Gomes ◽  
Gustavo Ribeiro Rodrigues ◽  
Walter Campos ◽  
Rafael Kemp ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Hepatic Duct ◽  
Ischemia Reperfusion ◽  
Respiratory Control ◽  
Hepatic Tissue ◽  
Control Group ◽  
Liver Ischemia ◽  
Hepatic Ischemia

PURPOSE: The main aim of this study was to determine the influence of ischemic preconditioning (IPC) on rat liver cirrhosis. METHODS: Cirrhosis was induced in Wistar rats by occlusion of the hepatic duct. The animals were divided into four groups of six animals each: non-cirrhotic group (simulated operation only), cirrhotic control group (simulated operation in cirrhotic rats), I/R group (40-minute ischemia without IPC), and IPC group (cirrhotic rats with ischemia, previously submitted to IPC). The IPC procedure consisted of partial hepatic ischemia for five minutes, followed by 10 minutes of reperfusion. In the case of the IPC group, the animals were submitted to liver ischemia for 40 minutes after the preconditioning procedure, followed by 2 hours of reperfusion. Blood samples were collected for measurement of serum aminotransferases (ALT and AST). The respiratory control ratio (RCR), the mitochondrial membrane potential (MMP), and malondialdehyde (MDA) values in the hepatic tissue were analyzed. Nonparametric statistical analysis was used and a value of p<0.05 was considered statistically significant. RESULTS: Ischemia did not induce significant increase in ALT and AST levels. MDA values were significantly higher in cirrhotic animals. MMP did not significantly change in cirrhosis and liver ischemia. Mitochondrial RCR decreased in liver cirrhosis, accentuated upon liver ischemia, and did not significantly change with IPC. CONCLUSION: Ischemic preconditioning does not protect the liver from hepatic injury induced by the ischemia/ reperfusion process.

scholarly journals Hyperbaric oxygen therapy aggravates liver reperfusion injury in rats

2008 ◽  
Vol 23 (4) ◽  
pp. 315-321 ◽  
Author(s):  
Cristiano Xavier Lima ◽  
Marcelo Dias Sanches ◽  
João Baptista de Rezende Neto ◽  
Roberto Carlos de Oliveira e Silva ◽  
Mauro Martins Teixeira ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Hyperbaric Oxygen ◽  
Hyperbaric Oxygen Therapy ◽  
Oxygen Therapy ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ambient Air ◽  
Myeloperoxidase Activity ◽  
Ischemia And Reperfusion ◽  
Liver Ischemia

PURPOSE: To evaluate the effects of hyperbaric oxygen (HO) therapy in the protection against liver ischemia/reperfusion injury. METHODS: Thirty-two male Wistar rats were divided into four groups of eight animals each: group A - laparotomy and liver manipulation, group B - liver ischemia and reperfusion, group C - HO pretreatment for 60 min followed by liver ischemia and reperfusion, and group D - pretreatment with ambient air at 2.5 absolute atmospheres for 60 min followed by liver ischemia and reperfusion. Plasma was assayed for aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH). Intra-arterial blood pressure was monitored continuously. Myeloperoxidase activity in the liver and lung was assessed 30 min after reperfusion. RESULTS: Plasma AST, ALT and LDH increased after reperfusion in all animals. Plasma ALT values and myeloperoxidase activity in the liver parenchyma were higher in HO-pretreated animals than in groups A, B and D. HO had a negative hemodynamic effect during liver reperfusion. CONCLUSION: Liver preconditioning with hyperbaric oxygen therapy aggravated liver ischemia/reperfusion injury in rats as demonstrated by plasma ALT and liver myeloperoxidase activity.

Glutathione protects mitochondrion and alleviates liver ischemia-reperfusion injury in rats

2015 ◽  
Vol 36 (12) ◽  
pp. 1300
Author(s):  
Lin-lin CAI ◽  
Hai-long FU ◽  
Qing-qing ZHANG ◽  
Yong-hua LI ◽  
Qiu-feng ZHU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia

Arrb1 Ameliorates Liver Ischemia/Reperfusion Injury Via Interacting with TRAF6 in Hepatocytes

2019 ◽  
Author(s):  
Xiaoliang Xu ◽  
Zechuan Zhang ◽  
Yijun Lu ◽  
Qikai Sun ◽  
Yang Liu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia

Beneficial effects of natural compounds on experimental liver ischemia-reperfusion injury

2021 ◽  
Author(s):  
Camila Dossi ◽  
Romina Vargas ◽  
Rodrigo Valenzuela ◽  
Luis Videla
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Natural Compounds ◽  
Liver Ischemia ◽  
Hepatic Surgery ◽  
Beneficial Effects ◽  
Underlying Mechanisms ◽  
Experimental Liver

Liver ischemia-reperfusion injury (IRI) is a phenomenon inherent to hepatic surgery that severely compromises the organ functionality, whose underlying mechanisms involve cellular and molecular interrelated processes leading to the development...

scholarly journals Tanshinone IIA combined with CsA inhibit myocardial cell apoptosis induced by renal ischemia-reperfusion injury in obese rats

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
He Tai ◽  
Xiao-lin Jiang ◽  
Zhi-ming Lan ◽  
Yue Li ◽  
Liang Kong ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Cell Apoptosis ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Abdominal Cavity ◽  
Myocardial Cell ◽  
Renal Ischemia ◽  
Tanshinone Iia ◽  
Obese Rats

Abstract Background Acute myocardial injury (AMI), which is induced by renal ischemia-reperfusion (IR), is a significant cause of acute kidney injury (AKI)-related associated death. Obesity increases the severity and frequency of AMI and AKI. Tanshinone IIA (TIIA) combined with cyclosporine A (CsA) pretreatment was used to alleviate myocardial cell apoptosis induced by renal IR, and to determine whether TIIA combined with CsA would attenuate myocardial cell apoptosis by modulating mitochondrial function through the PI3K/Akt/Bad pathway in obese rats. Methods Male rates were fed a high fat diet for 8 weeks to generate obesity. AKI was induced by 30 min of kidney ischemia followed 24 h of reperfusion. Obese rats were given TIIA (10 mg/kg·d) for 2 weeks and CsA (5 mg/kg) 30 min before renal IR. After 24 h of reperfusion, the rats were anaesthetized, the blood were fetched from the abdominal aorta and kidney were fetched from abdominal cavity, then related indicators were examined. Results TIIA combined with CsA can alleviate the pathohistological injury and apoptosis induced by renal IR in myocardial cells. TIIA combined with CsA improved cardiac function after renal ischemia (30 min)-reperfusion (24 h) in obese rats. At the same time, TIIA combined with CsA improved mitochondrial function. Abnormal function of mitochondria was supported by decreases in respiration controlling rate (RCR), intracellular adenosine triphosphate (ATP), oxygen consumption rate, and mitochondrial membrane potential (MMP), and increases in mitochondrial reactive oxygen species (ROS), opening of the mitochondrial permeability transition pore (mPTP), mitochondrial DNA damage, and mitochondrial respiratory chain complex enzymes. The injury of mitochondrial dynamic function was assessed by decrease in dynamin-related protein 1 (Drp1), and increases in mitofusin1/2 (Mfn1/2), and mitochondrial biogenesis injury was assessed by decreases in PPARγ coactivator-1-α (PGC-1), nucleo respiratory factor1 (Nrf1), and transcription factor A of mitochondrial (TFam). Conclusion We used isolated mitochondria from rat myocardial tissues to demonstrate that myocardial mitochondrial dysfunction occurred along with renal IR to induce myocardial cell apoptosis; obesity aggravated apoptosis. TIIA combined with CsA attenuated myocardial cell apoptosis by modulating mitochondrial function through the PI3K/Akt/Bad pathway in obese rats.

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