高尿酸血症诱导高血压发病的实验研究  

Experiment study of high uric acid lead to Hypertension

作　　者：滕志涛[1] 陈聪[1] 赵培勇[1] 汤金霞[1] 李妍枚 郭志勇[1] 孙鹏[1] 

机构地区：[1]威海市立医院心血管中心,威海264200 [2]威海市经区医院

出　　处：《滨州医学院学报》2015年第2期119-120,共2页Journal of Binzhou Medical University

摘　　要：目的研究高尿酸血症对大鼠氧化氮产物影响及在高血压发病的实验研究。方法通过饲喂尿酸酶抑制剂在实验大鼠体内制造高尿酸血症。饮水方式服用别嘌呤醇作为阻断剂来拮抗高尿酸血症。将48只大鼠随机分对照组、别嘌呤醇组、氧嗪酸钾盐组(尿酸酶抑制剂)和联合用药组(别嘌呤醇加尿酸酶抑制剂)(每组各12只)。于实验的第1、8天断头处死各组6只大鼠,并检测其血清尿酸及氧化氮产物(亚硝酸盐/硝酸盐)水平。结果氧嗪酸钾盐可以诱导高尿酸血症,在第8天联合用药组与氧嗪酸钾盐组比较,血清尿酸明显下降(0.72比1.70mg/L),氧化氮产物(1.55比0.97mmol/L,P均<0.01)升高。与对照组比较,氧嗪酸钾盐组大鼠第1天氧化氮产物(1.33比1.59mmol/L),第8天(0.99比1.58mmol/L)减少,差异有统计学意义(P<0.05)。结论尿酸酶抑制剂氧嗪酸钾盐可以诱导大鼠产生高尿酸血症,进一步导致血清一氧化氮水平降低,并出现收缩压升高,这种作用可以通过应用别嘌呤醇降低尿酸水平得到改善。Objective Hyperuricemia has been linked to hypertension ,possibly through the generation of reactive oxygen spe‐cies （ROS） and subsequent endothelial dysfunction .Methods Hyperuricemia was induced in WISTAR rats with an uricase in‐hibitor .Allopurinol was placed in drinking water to block hyperuricemia .Rats were randomly divided into four groups ：（1） con‐trol ,（2） allopurinol only ,（3） oxonic acid only ,and （4） oxonic acid ＋ allopurinol .Six rats were sacri ？ ced at 1 and 8 days , and their serum analyzed for serum uric acid and nitrites /nitrates concentrations .Results Oxonic acid can lead to hyperuricemia in rats .Uric acid in oxonic acid ＋ allopurinol group is lower than allopurinol group at 8th day （0.72 ：1.70 mg/L ） ,Nitrates （NOX）（1.55 ：0.97mmol/L ,P 〈 0.01） .Nitrates in allopurinol group were reduced than control group at both first day （1.33 mmol/L VS 1.59 mmol/L）and 8 th days（0.99 mmol/L VS 1.58 mmol/L）（P〈 0.05） .Conclusion Oxonic acid can lead to hy‐peruricemic in rats ,have a decrease in serum nitric oxide which is reversed by lowering uric acid levels in using allopurinol .Hy‐peruricemic rats have high blood pressure .

关 键 词：一氧化氮 高尿酸血症 高血压 内皮功能损伤 

分 类 号：R544.1[医药卫生—心血管疾病]