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作 者:李继承[1] 杨泽然[1] Bruno Tota
机构地区:[1]浙江大学医学院淋巴学研究室,浙江杭州310031 [2]意大利Calabria大学细胞生物学研究所
出 处:《中国病理生理杂志》2002年第9期1034-1037,共4页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目 (No .39970 381) ;意大利教育部研究基金资助项目
摘 要:目的 :研究一氧化氮 (NO)对腹膜淋巴孔的调控作用 ,探讨腹膜透析 (PD)失超滤机理。方法 :①应用Baxter腹透液建立腹膜透析小鼠模型 ;②小鼠腹腔注射NO供体硝普钠 (SNP)和NOS的抑制剂NG-单甲基 -L -精氨酸 (L -NMMA) ;③全自动酶标仪测定血清NO-2 量 ;④腹膜淋巴孔的扫描电镜观察和计算机图像处理。结果 :①随着腹膜透析进行 ,大量巨噬细胞经腹膜淋巴孔游出 ,进入腹膜腔形成乳斑 ;血清NO-2 量逐渐增高 ,腹膜淋巴孔孔径增大、分布密度增高。停止腹膜透析、乳斑减少 ,NO-2 量逐渐降低 ,腹膜淋巴孔渐趋正常。②随SNP剂量增加 ,小鼠血中NO-2 浓度显著提高 ,淋巴孔的直径和密度明显增加。③随着L -NMMA剂量增加 ,小鼠血中NO-2 浓度明显降低 ,腹膜淋巴孔开放数量减少 ,淋巴孔密度降低 ,淋巴孔孔径变小。结论 :NO有调控腹膜淋巴孔的作用 ;长期腹膜透析使血清NO-2 浓度逐渐增高 ,高浓度NO-2 可舒张腹膜淋巴孔 ,使腹膜淋巴孔对腹透液吸收增加 ,导致腹膜透析失超滤。AIM: To study the regulatory effect of nitric oxide on the lymphatic stomata and probe into the mechanism of ultrafiltration failure during long-term peritoneal dialysis (PD). METHODS: ①Sodium nitroprusside(SNP) and N G-monomethyl-L-arginine(L-NMMA) (inhibitor of nitric oxide synthase(NOS)) were injected into the peritoneal cavity of the mouse model of PD. ②NO concentration was measured in serum. ③The lymphatic stomata was studied with SEM and computer image processing.RESULTS: During PD, a lot of macrophages wandered out of the lymphatic stomata to form milky spots on the peritoneal mesothelium, and the diameter and density of the stomata were increased with NO concentration raised. After PD cessation, the stomata was normal gradually and numbers of milky spots reduced with NO concentration fall. The diameter and density of the stomata were increased with a rise in NO concentration as SNP was used, oppositely those were decreased with the increase in NO concentration as L-NMMA was injected intraperitoneally. CONCLUSIONS: The lymphatic stomata might be regulated through increasing the endogenous NO concentration. During PD, NO is increased gradually and the ultrafiltration failure would occur when re-absorption of the stomata was increased from the peritoneal cavity.
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