Effects of the ATP-dependent K ( )-channel effectors pinacidil and glibenclamide on liver tissue in an experimental model of epilepsy: A histopathological study

Abstract

It is known that most of the antiepileptic drugs have negative effects on the liver. Pinacidil is a nonselective opener of KATP channels, including the plasma membrane and mitochondria. Glibenclamide is an ATP -dependent K channel blocker ensuring the intake of calcium. Our aim in this experimental study was to examine the effects of pinacidil and glibenclamide on the liver tissue of rats with focal epilepsy. Method: Sixty male Sprague Dawley rats (2-4 months old, 200-250 gr) were used in the study. The rats were divided into 4 groups, 15 in each group. The groups were divided into control group, penicillin group, penicillin + pinacidil group and penicillin + glibenclamide group. The craniums of the rats in the control group were opened and normal saline was given; Penicillin (2 µl 500 IU) was intracortically administered to other groups and an experimental epilepsy model was created. At the end of the study, liver tissue of rats was taken and evaluated in terms of vacuolar degeneration, lymphocyte infiltration, vascular congestion, sinusoidal dilatation, necrosis, and Kupffer cell proliferation, radial alignment of hepatic cords, central vein and portal vein dilatation in hepatocytes. Results: Venous congestion, cytoplasmic vacuolization, Kupffer cell proliferation, portal vein dilatation and necrosis were distinct in the group to which pinacidil was administered, and distortion was present in the radial sequence (p<0.001). In addition, inflammation, venous congestion and hepatocyte necrosis were found to be lower in the glibenclamide given group compared to the control group (p<0.001). Conclusion: It can be suggested that pinacidil treatment caused negative results in liver histopathological parameters, whereas glibenclamide was more protective by reducing inflammation, venous congestion and hepatocyte necrosis.