Abstract
Purpose To evaluate the effects of treatment with Indigo Carmine (IC) on rat livers subjected to ischemia-reperfusion injury.Methods The animals were subdivided into 4 groups: 1.SHAM group(SH) - saline; 2.SHAM group with IC-2mg/Kg(SHIC); 3.IR group - rats submitted to ischemia and reperfusion with saline(IR); 4.IR group with IC-2mg/Kg(IRIC). The IR protocol consists of liver exposure and administration of drug or saline intravenously, followed by 60 minutes of ischemia and 15 of reperfusion. Liver samples were collected for biochemical analysis.Results State 3 of mitochondrial respiration showed a significant worsening of the IRIC group in relation to all others. State 4 showed a difference between IRIC and SHIC. The Respiratory Control Ratio showed statistical decrease in IR and IRIC versus Sham. The osmotic swelling showed significant difference between SHxIR; SHICxIRIC and SHxIRIC. There was a significant increase in ALT in the IRIC group in relation to all the others. Concerning the nitrate dosage, there was a decrease in the group treated with IC(IRxIRIC). There was no difference regarding the dosage of Malondialdehyde.Conclusion IC was not able to protect mitochondria from IR injury and proved to be a potentiating agent, acting in synergy with the IR injury promoting damage to the hepatocyte membranes.
Highlights
When performing liver surgical procedures, such as resections and transplants, blood flow must be interrupted in order to contain bleeding
The use of Indigo Carmine (IC) without performing surgical ischemia (SHIC) did not promote changes with statistically significant differences when compared to the Sham group (SH)
IC when associated with ischemia (IRIC) showed difference statistically significant when compared to the SHAM group with IC – 2mg/Kg (SHIC) group
Summary
When performing liver surgical procedures, such as resections and transplants, blood flow must be interrupted in order to contain bleeding. This control can be achieved through the Pringle Maneuver, which consists of a temporary occlusion of the portal triad composed of the hepatic artery, bile duct and portal vein[1,2]. With oxygen depletion in the tissues, there is a change to anaerobic metabolism, as well as interruption of the electrons transport mechanisms of the respiratory chain, which causes a decrease in ATP levels, impairing the functioning of the Na+ / K+ ATPase pump and culminates in depolarization of the cell, along with calcium overload. Calcium accumulation is part of a metabolic pathway which triggers to activation of phospholipase C enzyme, protein kinase C, and proteases, ATPase, reactive oxygen species (ROS) generation and, hepatocytes apoptotic mechanisms[6]
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