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作 者:姚咏明[1] 于燕 彭志齐[2] 董宁 常国友 盛志勇
机构地区:[1]解放军第三○四医院创伤外科中心,北京100037 [2]南京解放军军事理工大学医院
出 处:《中华外科杂志》2000年第6期462-464,共3页Chinese Journal of Surgery
基 金:国家重点基础研究发展规划项目!(G1 9990 542 0 3);国家自然科学基金!资助项目 (39870 2 86);军队杰出中青年人才专项基金!资助项目
摘 要:目的 观察己酮可可碱 (PTX)对内毒素休克家兔休克时生物喋呤诱生的影响。 方法 2 8只大耳白兔 ,随机分为 3组 ,对照组 (8只 )、内毒素休克组 (10只 )、PTX治疗组 (10只 )。制作内毒素休克模型 ,观察血浆生物喋呤、肿瘤坏死因子及组织三磷酸鸟苷环水解酶I活性的变化 ,同时监测全身血流动力学改变。 结果 内毒素休克大鼠早期给予PTX治疗 ,可显著降低血浆生物喋呤及肿瘤坏死因子水平 ,与对照组及休克组比较 ,差异有显著性意义 (P <0 0 5 ,P <0 0 1) ;不同程度地抑制肝、肺、心等组织三磷酸鸟苷环水解酶I活性 (P <0 0 5 ) ;与此同时 ,治疗组平均动脉压、心输出量及外周血管阻力均比休克组明显提高 ,差异有显著性意义 (P <0 0 5 ,P <0 0 1)。 结论 PTX能有效抑制内毒素休克时体内生物喋呤的合成与释放 ,明显减轻全身血流动力学障碍。Objective[WT5”BZ] To observe the potential effect of pentoxifylline on endotoxin mediated biopterin (tetrahydrobiopterin and more oxidized species) formation and systemic hemodynamics. [WT5”HZ]Methods[WT5”BZ] Rabbits were subjected to endotoxic shock induced by a bolus intravenous injection of E.coli O26B6 lipopolysaccharide (400 μg/kg). 28 animals were divided into sham operation group ( n =8), endotoxic shock group ( n =10), and pentoxifylline treated group ( n =10). Plasma biopterin and tumor necrosis factor α (TNF) levels, and guanosine triphosphate cyclohydrolase I (GTP CHI) activity in tissues were determined at various intervals. [WT5”HZ]Results[WT5”BZ] Treatment with pentoxifylline significantly decreased plasma biopterin and TNF levels at 2 to 8 hours after endotoxin challenge ( P <0 05, P <0 01), and inhibited GTP CHI activities in the liver, lung, and myocardial tissues ( P <0 05). Meanwhile, systemic hemodynamic parameters, including mean arterial pressure, cardiac output, and total peripheral resistance, in the treatment group were much higher than those in the endotoxic shock group. [WT5”HZ]Conclusions[WT5”BZ] These data suggest that early treatment with pentoxifylline can effectively inhibit endotoxin induced biopterin synthesis and release, and markedly improve systemic hemodynamics during septic shock. [WT5”HZ]
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