Remifentanil Preconditioning Attenuates Hepatic Ischemia-Reperfusion Injury in Rats via Neuronal Activation in Dorsal Vagal Complex

Figure 2

Effect of opiate agonist on hepatic ischemia reperfusion when peripheral opioid receptors were antagonized. Rats were divided into 5 groups, and animals were performed with laparotomy and dissection of the portal vein but not clamping in the sham group, or treated with MNTX1 (0.5 mg·kg⁻¹) or MNTX2 (5 mg·kg⁻¹) into the peritoneal cavity, followed by an intravenous injection of 2 μg·kg⁻¹·min⁻¹ of remifentanil or normal saline within 15 minutes. Hepatic ischemia reperfusion (IR) was induced 10 minutes after the treatment above with ischemia for 45 minutes and 120-minute reperfusion. in each treatment group and in the sham group. (a) Hepatic tissue histologic changes were processed with hematoxylin and eosin (H&E) staining for light microscopy examination. Photograph depicts a typical pattern of focal necrosis (black arrows) after ischemic degeneration of hepatocytes around the central venous area. Hepatocyte apoptosis was determined by TUNEL staining. Photograph depicts a typical pattern of apoptotic cells (black arrows). Areas of necrosis and percentage of apoptotic cells were significantly decreased in the remifentanil preconditioning (RPC) groups than in the normal saline (NS) groups (magnification: 200x; versus NS/MNTX1; versus NS/MNTX2). (b) Serum alanine aminotransferase (ALT) was significantly lower in the RPC/MNTX1 groups than in the NS/MNTX1 groups, while serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations were significantly lower in the RPC/MNTX2 groups than in the NS/MNTX2 groups ( versus NS/MNTX1; versus NS/MNTX2). (c) The serum level of TNF-α significantly decreased in the remifentanil preconditioning (RPC) groups than in the NS groups ( versus NS/MNTX1; versus NS/MNTX2).

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