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作 者:王新良[1] 陈晓玲[2] 谢菲[1] 李洪娟[1] 黄善生[2]
机构地区:[1]河北医科大学第二医院儿科,河北石家庄050000 [2]河北医科大学基础医学院病理生理学教研室,河北石家庄050017
出 处:《河北医科大学学报》2005年第6期404-408,共5页Journal of Hebei Medical University
摘 要:目的探讨一氧化氮、过氧亚硝基阴离子对大鼠离体肾缺血再灌注(ischemia reperfusion,I-R)损伤时肾血管反应性的影响。方法应用离体灌流肾(isolated perfused kidney,IPK)技术观察肾I-R后肾血管对去甲肾上腺素(norepinephrine,NE)和乙酰胆碱(acetylcholine,Ach)反应性的改变;观察外源性给予NO、ONOO-后大鼠IPK肾血管对NE和Ach反应性的改变,以及阻断内源性NO生成对肾I-R大鼠IPK肾血管反应性的影响。结果①I-R后IPK肾血管对去甲肾上腺素(norepinephrine,NE)的缩血管反应性和Ach的舒血管反应性都有明显降低,I-R5h较I-R1h进一步降低(P<0.01)。②给予硝普钠(100μmol/L)后大鼠IPK血管对NE的缩血管反应性和Ach的舒血管反应性都未见明显变化(P>0.05)。而ONOO-(40μmol/L)和vehicle相比则显著降低IPK血管对NE和Ach的反应性(P<0.01)。③氨基胍+I-R1h大鼠IPK肾血管对NE和Ach的反应性与NS+I-R1h大鼠相比无显著差异(P均>0.05),AG+I-R5h组大鼠肾血管对NE和Ach的反应性较NS+I-R5h明显增强(P均<0.05)。L-NNA+I-R 1h和5h大鼠肾血管对Ach的反应性有进一步的降低,而对NE的反应性却增强(P均<0.05)。结论NO大量生成后产生的ONOO-在肾I-R所致的肾血管反应性损伤中具有重要的作用。Objective To investigate renal vascular response to nitric oxide (NO) and peroxynitrite in isolated perfused rat kidney(IPK) after renal ischemia reperfusion(I-R). Methods IPK was used to examine the effects of renal I-R and nitropru sside(SNP), ONOO^- on the renal vascular response, and the effects of aminoguanidine on the impaired renal vascular response caused by renal I-R. Results ①Contractile response of renal vascular to norepinephrine(NE) and relaxation responses to acetylcholine(Ach) were both impaired obviously in IPK after renal I-R, and the impaired renal vascular response was more serious in I-Rsh than that in I-R1b( P 〈0.01). ②SNP(100μmol/L) did not impact the renal vascular response to NE and Ach( P 〉0.05) in IPK of health rats, but ONOO^- (40 μmol/L) reduced the renal vascular response to NE and Ach compared with vehicle( P 〈0.01). ③There were no difference of the renal vascular response to NE and Ach between aminogu anidine(AG)+ I-R1b and NS+ I-R1h (P 〉 0.05 ), but the renal vascular response were much better in AG+I-R5h than that in NS+I-R1h( P 〈0.05). The renal vascular response to Ach was further reduced in L-NNA+I-R than that in NS+I-R groups, but the renal vascular response to NE was strengthened in L-NNA + I-R group (P 〈 0.05).Conclusion It is proved that a massive quantity generation of NO and ONOO^- play an important role in renal vascular response damage in IPK rats after renal I-R.
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