Mast cells are not involved in the ischemia-reperfusion injury in perfused rat liver.
Mast cells are not involved in the ischemia-reperfusion injury in perfused rat liver.
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DOI：
10.1016/j.jss.2010.11.900
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发表时间：
2012-05
期刊：
影响因子：
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通讯作者：
T. Shibamoto;M. Tsutsumi;Y. Kuda;Chieko Ohmukai;Wei Zhang;Y. Kurata
中科院分区：
文献类型：
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作者：
T. Shibamoto;M. Tsutsumi;Y. Kuda;Chieko Ohmukai;Wei Zhang;Y. Kurata
研究背景肥大细胞参与了大鼠肠、心、脑等多个器官的缺血再灌注损伤。然而，肥大细胞在大鼠肝I/R损伤中的作用尚不清楚。方法采用肥大细胞缺乏（Ws/Ws）大鼠（n = 6）、野生型+/+大鼠（n = 6）和SD大鼠（n = 12），以恒定血流量经门静脉灌注稀释血（Hct 8%），观察肥大细胞是否参与肝I/R损伤的发生。在室温下通过阻断门静脉的流入线1小时，然后以再循环方式再灌注1小时来诱导缺血。通过测量门静脉压（Ppv）、肝静脉压、血流量和窦压来确定窦前和窦后阻力，窦压通过双闭塞压（Pdo）来评估。观察肝组织病理学改变、胆汁流速、血清丙氨酸氨基转移酶（ALT）水平及肝组织病理学改变。血液ALT水平在30和60 min时分别从19 ± 4（SD）升高至71 ± 18和135 ± 30（IU/L），再灌注60 min时胆汁流量降至基础值的51% ± 6%。组织学检查显示明显的肝变性。在Ws/Ws大鼠和SD大鼠（n = 6）中观察到类似的变化，Ws/Ws、+/+和SD组之间的变量无显著差异。在任何缺血组中，再灌注后即刻，Ppv显著增加，但Pdo仅轻微增加，随后恢复至基线，表明前正弦阻力相对于后正弦阻力的主要增加。再灌注后60 min肝重显著增加。在对照SD大鼠无I/R（n = 6），没有显着的变化，观察到的variables.CONCLUSIONSI/R损伤发生在肝脏肥大细胞的情况下，在离体灌流大鼠肝脏I/R损伤模型。
BACKGROUNDIt 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.METHODSIsolated 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.RESULTSIn 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.CONCLUSIONSI/R injury occurs in the absence of hepatic mast cells in the isolated perfused rat liver model of I/R injury.