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Prophylaxis with Ketotifen in Rats with Portal Hypertension: Involvement of Mast Cell and Eicosanoids

机译:在具有门静脉高压的大鼠中具有Ketotifen的预防:肥大细胞和籽梨苷的涉及

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We first studied mast cell infiltration in the ileum and in the mesenteric lymph nodes and serum levels of rat mast cell protease II (RMCP-11) by ELISA. In a second set of experiments Ketotifen, a mast cell stabilizer drug, was administered 24 hours before intervention and prostanoids and leukotrienes were assayed by RIA. Results: 48 hours after intervention RMCP-II (p<0,005), PGE 2 (p<0 001) and LTC 4 serum levels decreased and mast cell number and RMCP-II levels increased in mesenteric lymph nodes in portal hypertensive-rats Prophylactic administration of Ketotifen reduced portal pressure (p<0,001), serum levels of PGE 2 (p<0,001) and RMCP-II (p<0,001) in mesentenc lymph nodes. Conclusion: In acute portal hypertension in rat, mast cell trans-location from intestinal mucosa to mesenteric lymph nodes would represent a defence mechanisms to avoid activation of an acute and massive inflammatory response.
机译:我们首先通过ELISA研究了回肠和肠系膜淋巴结和肠系膜细胞蛋白酶II(RMCP-11)的血清水平的肥大细胞浸润。在第二组实验中,在干预前24小时施用肥大细胞稳定剂药物,通过RIA测定前列腺素和白三烯。结果:干预后48小时,RMCP-II(P <0.005),PGE 2(P <0 001)和LTC 4血清水平降低,患有门间高等大鼠预防性给药的肠系膜淋巴结中的肥大细胞数和RMCP-II水平增加在甲骨颈淋巴结中降低了酮晶的血清压力(P <0℃),PGE 2(P <0.001)和RMCP-II(P <0.001)的血清水平。结论:在大鼠急性门静脉高血压中,从肠粘膜到肠系膜淋巴结的肥大细胞反应将代表一种防御机制,以避免激活急性和巨大的炎症反应。

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