山莨菪碱治疗兔缺血性急性肾功能衰竭的实验研究

An experimental study of the anisodamini hydrobromidum treating rabbits ischemic acute renal failure

目的探讨山莨菪碱（６５４－２）治疗缺血性急性肾功能衰竭的机理。方法用新西兰大白兔制作缺血性急性肾功能衰竭模型。观察缺血性急性肾功能衰竭组（简称肾衰组）与山莨菪碱治疗组（简称６５４－２组）肾组织细胞内胞浆游离钙（［Ｃａ２＋］ｉ）和第二信使—三磷酸肌醇（ＩＰ３）的浓度变化及各组肾小管超微病理改变。结果肾衰组［Ｃａ２＋］ｉ为４１２１±４７３ｎｍｏｌ／Ｌ，ＩＰ３为７７６０±６８０ｐｃｍ，较之对照组的［Ｃａ２＋］ｉ（１０６１±１５５ｎｍｏｌ／Ｌ）、ＩＰ３（２９７９±５４３ｐｃｍ）含量明显增高（均为Ｐ＜００１）。６５４－２组［Ｃａ２＋］ｉ为１７０９±３７７ｎｍｏｌ／Ｌ，ＩＰ３为３４０１±２１５ｐｃｍ，两者较肾衰组显著下降（均为Ｐ＜０００１）。肾衰组肾小管病理明显重于对照组，６５４－２组显著轻于肾衰组。结论６５４－２能改善缺血性急性肾功能衰竭时肾小管的损伤，能减轻肾组织细胞内钙超负荷，其作用机理与细胞内ＩＰ３含量降低有关。

Objective To elucidate mechanism of the Anisodamini Hydrobromidum(654-2)treating ischemic acute renal failure. Methods Ischemic acute renal failure models in rabbits were establishd.Concentration of i and IP3 in renal histocytes were measured.The changes of renal tubule were ultrapathomorphologically observed. Results The concentrations of intracellular i 1155 nmol/L),P<001] and IP3pcm), P<0001] were increased in renal failure group compared with the contrasted group,concentration of intracellular 2+]i and IP3 were decresed in 654-2 treating group compared with the renal failure group.The pathomorphological change was aggravated in renal failure group compared with the contrasted group,was mitigated in 654-2 group compared with the renal failure group. Conclusion 654-2 can alleviate Ca2+-overload in renal histocytes.The mechanism was related to the decrease of concentration of intracellular IP3.