L-arginine in the ischemic phase protects against liver ischemia-reperfusion injury

Taha, Murched Omar; Caricati‐Neto, Afonso; Ferreira, Regiane Miranda; Simões, Manuel de Jesus; Monteiro, Hugo P.; Fagundes, Djalma José

doi:10.1590/s0102-86502012000900005

Cited by 16 publications

(12 citation statements)

References 28 publications

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“…Our studies have shown that the administration of micromolar concentrations of L-arginine or sodium nitroprusside reduces the heart rate and contraction force of the isolated heart ventricle in rats submitted to prolonged tissue hypoxia [81,82,127]. Our studies also showed that administration of L-arginine produces protective actions against lesions by I/R injury in different organs, such as the liver and intestine [128,129]. These findings demonstrate that the L-arginine produces cardioprotective effects.…”

Section: Cardioprotective Strategies Against Myocardial Lesions Camentioning

confidence: 91%

Recent Advances in Pharmacological and Non-Pharmacological Strategies of Cardioprotection

Caricati‐Neto

Errante

Rodrigues

2019

IJMS

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Ischemic heart diseases (IHD) are the leading cause of death worldwide. Although the principal form of treatment of IHD is myocardial reperfusion, the recovery of coronary blood flow after ischemia can cause severe and fatal cardiac dysfunctions, mainly due to the abrupt entry of oxygen and ionic deregulation in cardiac cells. The ability of these cells to protect themselves against injury including ischemia and reperfusion (I/R), has been termed “cardioprotection”. This protective response can be stimulated by pharmacological agents (adenosine, catecholamines and others) and non-pharmacological procedures (conditioning, hypoxia and others). Several intracellular signaling pathways mediated by chemical messengers (enzymes, protein kinases, transcription factors and others) and cytoplasmic organelles (mitochondria, sarcoplasmic reticulum, nucleus and sarcolemma) are involved in cardioprotective responses. Therefore, advancement in understanding the cellular and molecular mechanisms involved in the cardioprotective response can lead to the development of new pharmacological and non-pharmacological strategies for cardioprotection, thus contributing to increasing the efficacy of IHD treatment. In this work, we analyze the recent advances in pharmacological and non-pharmacological strategies of cardioprotection.

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Section: Cardioprotective Strategies Against Myocardial Lesions Camentioning

confidence: 91%

Recent Advances in Pharmacological and Non-Pharmacological Strategies of Cardioprotection

Caricati‐Neto

Errante

Rodrigues

2019

IJMS

Self Cite

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“…Shimamura et al 23 observed a significant increase and maximum of AST levels after 12 hours of reperfusion in a model of hepatic IR, with return to basal level from the 3 rd day of reperfusion. Other authors also evidenced a significant increase in aminotransferases levels after hepatic IR 22,24,25 .…”

Section: Discussionmentioning

confidence: 81%

“…The L-arginine/NO pathway seems to be relevant during the IR process in several organs such as the liver 9 , kidney 14 , heart 15 , skeletal muscle 16 , intestine 17 L-NAME) [19][20][21][22] . The basic design of those studies is the previous use of those drugs and subsequent analysis about the treatment response in several indicators of hepatic tissue injury after IR.…”

Section: Discussionmentioning

confidence: 99%

Effects of L-arginine and L-NAME on ischemia-reperfusion in rat liver

Lucas

Rhoden

et al. 2015

Acta Cir. Bras.

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PURPOSE:To evaluated the effects of L-arginine (a NO donor) and L-NAME (N w -nitro-L-arginine methyl ester -a NOS inhibitor)on ischemia-reperfusion in rat livers. METHODS:One hundred fifty two male Wistar rats were divided into four groups: control (simulated surgery); hepatic IR; pretreatment with L-arginine plus hepatic IR; and L-NAME plus hepatic IR. The hepatocellular damage was evaluated at the first, third and seventh days after the procedures through the alanine-aminotransferase (ALT) and aspartate-aminotransaminase (AST) levels, as well as histopathological features: vascular congestion (VC); steatosis (STE); necrosis (NEC); and inflammatory infiltration (INF). The mortality rate was also evaluated. RESULTS:The pretreatment with L-NAME significantly worsened the AST levels after hepatic IR (p<0.05) at first day and L-arginine demonstrated an attenuating effect on ALT levels at seventh day (p<0.05). Furthermore, the administration of L-arginine was able to reduce the VC and STE in the seventh day after hepatic IR (p<0.05). The analysis of the mortality rates did not demonstrate any difference between the groups. Nevertheless, there was not effect of L-arginine and L-NAME on the mortality of the animals.CONCLUSION: L-arginine/NO pathway has a role in the hepatic IR because the pretreatment with L-arginine partially had attenuated the hepatocellular damage induced by hepatic IR in rats.

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“…63,64 Vacuolization of the liver hepatocyte after I/R is well studied. 65,66 The appearance of vacuoles in the cytoplasm of hepatocytes has already been reported to be induced by anoxia, as described in the morphogenesis of postmortem hepatocyte vacuolation. 67 Histological alterations and the extent of parenchymal vacuolation, in particular, reflected the severity of hepatocellular damage induced by WI and reperfusion.…”

Section: Discussionmentioning

confidence: 98%

Temporal changes in hepatic antioxidant enzyme activities after ischemia and reperfusion in a rat liver ischemia model

et al. 2014

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This study investigated the hypothesis that administration of tilapia fish oil diet would attenuate warm liver ischemia/reperfusion injury (IRI) and whether fish oil modulates prooxidant/antioxidant status. Male Wistar rats were subjected to 30 min of approximately 70% hepatic ischemia followed by 1, 12, and 24 h reperfusion. Rats were randomly divided into three groups: sham-operated group (SO), control–warm hepatic ischemia (WI) group, and Oil–WI group given tilapia oil for 3 weeks followed by liver IRI. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured in the plasma. Levels of thiobarbituric acid reactive substances (TBARS) and antioxidant enzymes as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities were measured in liver fractions. In the sham group, there was no enzymatic or histological change. I/R caused significant increase in serum AST, ALT, and tissue TBARS levels. As compared to the control group, animals treated with tilapia oil experienced a significant decrease ( p < 0.05) in AST and ALT levels in reperfusion periods. Tissue TBARS levels in Oil–WI group were significantly ( p < 0.05) reduced as compared to control group at 60 min after reperfusion. After ischemia, 1, 12, and 24 h of reperfusion, CAT, SOD, and GPx values were the lowest in the Oil–WI group and highest in the control group and were statistically significant ( p < 0.05). Histological analysis also revealed that fish oil provided some protection compared with the control group. Tilapia oil exerts a protective effect during the early phase of reperfusion, and it modulates prooxidant/antioxidant status of rat liver subjected to warm IRI.

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L-arginine in the ischemic phase protects against liver ischemia-reperfusion injury

Cited by 16 publications

References 28 publications

Recent Advances in Pharmacological and Non-Pharmacological Strategies of Cardioprotection

Recent Advances in Pharmacological and Non-Pharmacological Strategies of Cardioprotection

Effects of L-arginine and L-NAME on ischemia-reperfusion in rat liver

Temporal changes in hepatic antioxidant enzyme activities after ischemia and reperfusion in a rat liver ischemia model

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