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肝前型门静脉高压症大鼠高动力循环状态 被引量:4

Hyperdynamic status in a partial portal vein ligated(PVL)rat’s portal hypertension model
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摘要 作者应用同位素标记的微球技术检测实验性门静脉部分结扎肝前型门静脉高压症(PVL)大鼠全身、内脏血液动力学变化和门体分流情况,PVL大鼠门静脉压力增高(1.75±0.24vs.1.23±0.13kPa;P<0.001),大量门-体分流(93%),门静脉血流量增加50%,内脏血管阻力下降40%,心脏指数增高50%,末稍血管阻力下降40%,门静脉阻力未见明显升高。说明肝前型门静脉高压症门静脉压力持续增高的主要因素是高动力的门静脉灌流,直接支持“前向性血流”观点。长期门静脉高压可产生高度的门林分流,内脏血管扩张可能是内脏高动力循环的发生因素,全身血液动力学改变继发于内脏高动力循环。 AbstractThe splanchnic and systemic hemodynamics weremeasured by radioactive microsphere techniques in aPVL rat’s model with portal hypertension.The por- tal-hypertensive rats(1.75±0. 24 vs。1. 23±0. 13 kPa,P<0. 001 ) with greater than 93% portal-systemicshunting had an increase in portal venous inflow by50%(8. 97±0. 8 vs.6. 03±0. 28ml. min ̄(-1).100gBW ̄(-1);P<0. 001)and a concomitant decrease by 40% in splanchnic arteriolar resistance (0. 27 ± 0. 05vs. 0. 42±0. 05kPa·ml ̄(-1)·min ̄(-1)·100gBW ̄(-1); P<0. 01) compared with control rats. Cardiac index (54.6±4.4vs.36.5±3. 0ml· min ̄(-1)· 100gBW ̄(-1)) was ele-vated by 50%(P< 0. 001),and total peripheral resis-tance ( 0.052±0.006 vs.O.084±0.009kPa. ml ̄(-1)·min ̄(-1) . 100gBW ̄(-1) ) was decreased by 40%(P<0.001). The resistance to portal blood flow in portalvein-stenotic rats(0. 087±0.011kPa . ml ̄(-1) .min ̄(-1))was sim11ar to that in control rats(0.076±0.01kPa·ml ̄(-1)·min ̄(-1)),indicating that the hyperdynamic portalvenous inflow, not resistance, was the mainstay of theelevated portal venous pressure。 Which is in favor ofthe forward flow theory of portal hypertension, Thesystemic hemodynamic parameters were secondary tothe splanchnic hemodynamic changes.
出处 《中华外科杂志》 CAS CSCD 北大核心 1994年第9期573-575,共3页 Chinese Journal of Surgery
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同被引文献12

  • 1王承泰,邝耀麟,陈治平,曾民德,袁济民.肝内型门静脉高压症大鼠内脏高动力循环状态[J].中华消化杂志,1995,15(4):209-211. 被引量:5
  • 2Juan G Abraldes,Marcos Pasarín,Juan Carlos García-Pagán.Animal models of portal hypertension[J].World Journal of Gastroenterology,2006,12(41):6577-6584. 被引量:14
  • 3Garcia- Pagan JC, Bosch J, Rodes J. The role of vasoactive mediators in portal hypertension. Semin Gastrointest Dis, 1995, 6:140~ 147.
  • 4Lautt WW, Greenway CV, Legare DJ, et al. Localization of intrahepatic portal vascular resistance. Am J Physiol , 1986, 251:G375~G381.
  • 5Zhang JX, Bauer M, Clemens MG, et al. Vessel - and target cell- specific actions of endothelin - 1 and endothelin - 3 in rat liver. Am J Physiol, 1995, 269: G269~G277.
  • 6Rochey DC & Chung JJ. Reduce nitricoxide production by endothelial celld in cirrhotic rat liver: Endothelial dysfunction in portal hypertension. Gastrienterology 1998, 114: 344~351.
  • 7Vorobioff J, Bredfeldt JE, Groszmann RJ. Increased blood flow through the portal system in cirrhotic rats. Gastroenterology,1984,87:1120~ 1126.
  • 8Ros J, Jienez W, Lamas S, et al. Nitric oxide production in arterial vessels of cirrhotic rats. Hapatology 1995;21:554~560.
  • 9Cahill PA, Foster C, Redmond EM, et al. Enhanced nitric oxide synthase in the hyperdynamic circulation of portal hypertensive rats. Gastroenterology 1995,108:1487~ 1495.
  • 10王承泰 邝耀麟 陈治平 等.抑制NO的生物合成对肝前型门静脉高压症大鼠血液动力学的影响[J].中华实验外科杂志,1994,11:23-25.

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