BACKGROUND: It is reported that mast cells are involved in ischemia-reperfusion (I/R) injury of several organs such as intestine, heart, and brain in rats. However, the roles of mast cells are not known in rat hepatic I/R injury. We determined using genetically mast cell deficient (Ws/Ws) rats whether mast cells participate in the genesis of hepatic I/R injury. METHODS: Isolated livers from male Ws/Ws rats (n = 6), their wild type +/+ rats (n = 6), and Sprague Dawely (SD) rats (n = 12) were perfused portally with diluted blood (Hct 8%) at a constant blood flow. Ischemia was induced at room temperature by occlusion of the inflow line of the portal vein for 1 h, followed by 1-h reperfusion in a recirculating manner. The pre- and post-sinusoidal resistances were determined by measuring the portal venous pressure (Ppv), hepatic venous pressure, blood flow and the sinusoidal pressure, which was assessed by the double occlusion pressure (Pdo). Liver injury was assessed by blood alanine aminotransferase (ALT) levels, bile flow rate and histology of the livers. RESULTS: In the +/+ group, liver injury occurred after reperfusion; blood ALT levels increased from 19 ± 4 (SD) to 71 ± 18 and 135 ± 30 (IU/L) at 30 and 60 min, respectively, and bile flow decreased to 51% ± 6% of the baseline at 60 min after reperfusion. Histologic examination revealed marked hepatic degeneration. Similar changes were observed in the Ws/Ws rats and the SD rats (n = 6), and there were no significant differences in the variables among the Ws/Ws, +/+, and SD groups. In any ischemia groups, immediately after reperfusion, Ppv substantially, but Pdo only slightly, increased, followed by a return towards the baseline, indicating a predominant increase in pre-sinusoidal resistance over post-sinusoidal resistance. Liver weight significantly increased at 60 min after reperfusion. In the control SD rats without I/R (n = 6), no significant changes were observed in the variables. CONCLUSIONS: I/R injury occurs in the absence of hepatic mast cells in the isolated perfused rat liver model of I/R injury.
BACKGROUND: It is reported that mast cells are involved in ischemia-reperfusion (I/R) injury of several organs such as intestine, heart, and brain in rats. However, the roles of mast cells are not known in rat hepatic I/R injury. We determined using genetically mast cell deficient (Ws/Ws) rats whether mast cells participate in the genesis of hepatic I/R injury. METHODS: Isolated livers from male Ws/Ws rats (n = 6), their wild type +/+ rats (n = 6), and Sprague Dawely (SD) rats (n = 12) were perfused portally with diluted blood (Hct 8%) at a constant blood flow. Ischemia was induced at room temperature by occlusion of the inflow line of the portal vein for 1 h, followed by 1-h reperfusion in a recirculating manner. The pre- and post-sinusoidal resistances were determined by measuring the portal venous pressure (Ppv), hepatic venous pressure, blood flow and the sinusoidal pressure, which was assessed by the double occlusion pressure (Pdo). Liver injury was assessed by blood alanine aminotransferase (ALT) levels, bile flow rate and histology of the livers. RESULTS: In the +/+ group, liver injury occurred after reperfusion; blood ALT levels increased from 19 ± 4 (SD) to 71 ± 18 and 135 ± 30 (IU/L) at 30 and 60 min, respectively, and bile flow decreased to 51% ± 6% of the baseline at 60 min after reperfusion. Histologic examination revealed marked hepatic degeneration. Similar changes were observed in the Ws/Ws rats and the SD rats (n = 6), and there were no significant differences in the variables among the Ws/Ws, +/+, and SD groups. In any ischemia groups, immediately after reperfusion, Ppv substantially, but Pdo only slightly, increased, followed by a return towards the baseline, indicating a predominant increase in pre-sinusoidal resistance over post-sinusoidal resistance. Liver weight significantly increased at 60 min after reperfusion. In the control SD rats without I/R (n = 6), no significant changes were observed in the variables. CONCLUSIONS: I/R injury occurs in the absence of hepatic mast cells in the isolated perfused rat liver model of I/R injury.