[The effects of chronic alcohol exposure on progression of liver injury in spontaneously hypertensive rats; preliminary study].

Abstract

The association between alcohol intake and blood pressure is well known, and our previous studies indicate that the stimulus of sympathetic nervous system induce the progression of liver injury. In this study, we examined the effects of chronic ethanol treatment on the progression of liver injury using the spontaneously hypertensive rat (SHR). The advantage of using the present strain is to possess sympathetic facilitation without any treatment. Normotensive Wistar-Kyoto rat (WKY) was used as control. 7-week-old male rats were pair-fed with either ethanol- or control-liquid-diet for 49 days and divided into four groups: control liquid-diet-fed WKY and SHR, continuous ethanol liquid diet-fed WKY and SHR. Plasma alanine aminotransferase (ALT) levels, and histological analyses based on Hematoxylin-Eosin (H-E), Oil red O and Sirius red stains of the liver sections were used to assess alcohol-induced liver injury. Chronic ethanol treatment induced the increases in plasma ALT, the accumulation of fatty droplets within hepatocytes and pericellular hepatic fibrosis, particularly in SHR. Between the control group rats of SHR and WKY, SHR showed the increases in accumulation of fatty droplets and pericellular hepatic fibrosis. No significant inflammatory cell infiltration was shown in all groups. These results suggested that chronic ethanol treatment in SHR could induce the more severe liver injuries when compared with WKY. In conclusion, chronic alcohol intake in rats with hypertension could deteriorate the ethanol-induced liver injury via the sympathetic overactivity.