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多囊肾肾动脉血液动力学改变与血压变化的研究

Paired Observation on the Change of Hemodynamics and blood pressure level in Polycystic Kidney Disease
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摘要 目的探讨多囊肾患者的血液动力学改变与血压变化的相关性和敏感性。方法用超声多普勒法(包括频谱多普勒和彩色多普勒)分别测定44例多囊肾患者(多囊肾组)和15例正常人、15例非多囊肾1级高血压患者、15例非多囊肾2级高血压患者、15例非多囊肾3级高血压患者(对照组)的肾主动脉(MRA)、肾段动脉(SRA)、肾叶间动脉(IRA)的收缩期峰值流速(Vman)、最小流速(Vmin)、搏动指数(PI)、阻力指数(RI),并测量血压水平,对其资料进行分析。结果血压正常的多囊肾组三级肾动脉的Vmax、Vmin均低于血压正常对照组(P<0.01),PI、RI明显高于对照组(P<0.01);1级高血压的多囊肾组Vmax、Vmin显著低于1级非多囊肾1级高血压对照组(P<0.01),PI、RI显著高于对照组(P<0.01);2级高血压的多囊肾组Vmax、Vmin显著低于2级非多囊肾1级高血压对照组(P<0.01),PI、RI显著高于对照组(P<0.01、P<0.05)。结论①多囊肾患者的血液动力学改变早于血压变化;②Vmax、Vmin的下降和PI、RI的增高与血压水平呈正相关。 Objective To explore the relativity and sensibility of the change of hemody- namics and blood pressure level in patients with polycystic kidney. Methods 44 patients with polycystic kidney and 60 control subjects were enrolled. The maximam city (Vmin) , pulse index (PI) , resistance index velocity(Vmax) ,minimum velo- (RI) of systole of the main renal artery (MRA) ,segmental renal artery (SRA) , interlobar renal artery (IRA) were measured. The blood pressure of patients were also measured and analyzed in the both groups. Results compared with the control, both the Vmax and Vmin of the three levels renal artery in the patients with polycystic kidney were remarkable lower ( P 〈 0.01) . PI and RI were significant increased. All the same,both the Vmax and the Vmin of the patients with polycystic kidney, whose blood pressure was highter,were significant difference also ( P 〈 0.01) ; compared with the controls ,PI and RI significantly increased ( P 〈 0.01 or P〈0.05 ) Conclusions ① The hemodynamics in the patients with polycystic kidneyvaries has changed before the change of blood pressure . ② The decrease of Vmax and Vmin, and the increase of PI and RI have positive relativity with the blood pressure.
作者 傅增顺
出处 《医学信息》 2008年第9期1580-1583,共4页 Journal of Medical Information
关键词 超声多普勒法 多囊肾 血液动力学 血压 Ultrosound Doppler mothed Polycystic kidney Hemolynamics Blood pressure
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  • 1[1]Wilson PD.Polycystic kidney disease[J].N Engl J Med,2004,350(2):151-164.
  • 2[2]Pazour GJ.Intraflagellar transport and cilia-dependent renal disease:the ciliary hypothesis of polycystic kidney disease[J].J Am Soc Nephrol,2004,15(10):2528-2536.
  • 3[3]Yoder BK,Hou X,Guay-Woodford LM.The polycystic kidney disease proteins,polycystin-1,polycystin-2,polaris,and cystin,are co-localized in renal cilia[J].J Am Soc Nephrol,2002,13(10):2508-2516.
  • 4[4]Pazour GJ,San Agustin JT,Follit JA,et al.Polycystin-2 localizes to kidney cilia and the ciliary level is elevated in orpk mice with polycystic kidney disease[J].Curr Biol,2002,12(11):R378-R380.
  • 5[5]Pazour GJ,Dickert BL,Vucica Y,et al.Chlamydomonas IFT88 and its mouse homologue,polycystic kidney disease gene tg737,are required for assembly of cilia and flagella[J].J Cell Biol,2000,151(3):709-778.
  • 6[6]Praetorius HA,Spring KR.Bending the MDCK cell primary cilium increases intracellular calcium[J].J Membr Biol,2001,184(1):71-79.
  • 7[7]Nauli SM,Alenghat FJ,Luo Y,et al.Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells[J].Nat Genet,2003,33(2):129-137.
  • 8[8]Fischer E,Legue E,Doyen A,et al.Defective planar cell polarity in polycystic kidney disease[J].Nat Genet,2006,38(1):21-23.
  • 9[9]Masyuk AI,Masyuk TV,Splinter PL,et al.Cholangiocyte cilia detect changes in luminal fluid flow and transmit them into intracellular Ca2 + and cAMP signaling[J].Gastroenterology,2006,131 (3):911-920.
  • 10[10]Smith LA,Bukanov NO,Husson H,et al.Development of polycystic kidney disease in juvenile cystic kidney mice:insights into pathogenesis,ciliary abnormalities,and common features with human disease[J].J Am Soc Nephrol,2006,17(10):2821-2831.

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