Intrahepatic arterioportal fistula(IAPF)can be caused by many secondary factors.We report four cases of portal hypertension that were eventually determined to be caused by congenital hepatic arterioportal fistula.The ...Intrahepatic arterioportal fistula(IAPF)can be caused by many secondary factors.We report four cases of portal hypertension that were eventually determined to be caused by congenital hepatic arterioportal fistula.The clinical manifestations included ascites,variceal hemorrhage and hepatic encephalopathy.Computed tomography scans from all of the patients revealed the early enhancement of the portal branches in the hepatic arterial phase.All patients were diagnosed using digital subtraction angiography(DSA).DSA before embolization revealed an arteriovenous fistula with immediate filling of the portal venous radicles.All four patients were treated with interventional embolization.The four patients remained in good condition throughout follow-up and at the time of publication.IAPF is frequently misdiagnosed due to its rarity;therefore,clinicians should consider IAPF as a potential cause of non-cirrhotic portal hypertension.展开更多
Objective To explore the relationship between endogenous ouabain and the pathogenesis of hypertension. Methods ① Sixteen Sprague Dawley (SD) rats were selected and randomly divided into two groups, and then the rats ...Objective To explore the relationship between endogenous ouabain and the pathogenesis of hypertension. Methods ① Sixteen Sprague Dawley (SD) rats were selected and randomly divided into two groups, and then the rats were injected with ouabain in dosage of 20μg/kg.d and normal saline (NS), respectively. The indirect systolic blood pressure of all the rats were recorded once a week. ② Twenty five 1k1c (one kidney and one clipped) hypertensive rats were established and injected randomly with anti ouabain antibody, normal rabbit IgG and normal saline, respectively. The direct blood pressure of all the 1klc hypertensive rats were recorded by cannulated carotid artery for 3h after administration. Results The systolic blood pressure of rats injected with ouabain began to increase 2 weeks after ouabain administration and increased significantly at 6 weeks compared with NS group (17.7±1.2)kPa vs (15.4±1.1)kPa, P <0.01).Anti ouabain antibody could significantly decrease the blood pressure of 1k1c rats, while the normal rabbit IgG could not. Conclusion The results of this study indicate that endogenous ouabain might be one of the pathogenetic factors of hypertension.展开更多
Objective To access the prevalence and risk factors for hypertension after heart transplantation(HT),and the impact of post-transplant hypertension on mediumterm survival among HT patients.Methods Data from 265
目的观察依那普利对肾性与自发性高血压大鼠左心室α-烯醇化酶(α-enolase,Eno1)及谷胱甘肽-s-转移酶,μ2(glutathione-s-transferase,μ2,GSTM2)表达的影响。方法实验共分5组:(1)对照组;(2)两肾两夹高血压大鼠组;(3)两肾两夹高血压大鼠...目的观察依那普利对肾性与自发性高血压大鼠左心室α-烯醇化酶(α-enolase,Eno1)及谷胱甘肽-s-转移酶,μ2(glutathione-s-transferase,μ2,GSTM2)表达的影响。方法实验共分5组:(1)对照组;(2)两肾两夹高血压大鼠组;(3)两肾两夹高血压大鼠+依那普利组;(4)自发性高血压大鼠组;(5)自发性高血压大鼠+依那普利组。检测各组大鼠血压及左室重量指数,行超声心动图检查,并运用Western blot检测各组大鼠左心室Eno1、GSTM2及β-肌球蛋白重链(β-myosin heavy chain,β-MHC)的表达情况。结果两肾两夹及自发性高血压大鼠血压与左室重量指数均明显高于对照组,依那普利治疗后,其左心室肥厚均得到明显逆转。与两肾两夹组相比,Eno1在自发性高血压大鼠中的表达明显上调;与对照组相比,GSTM2在自发性高血压大鼠中的表达明显下调,而两肾两夹组无变化,经依那普利治疗后,二者的表达变化均未得到明显逆转;β-MHC在两种模型中的表达均上调,而依那普利治疗后,β-MHC在二者中的表达均明显下调。结论依那普利能明显逆转β-MHC在两种模型中的差异表达,但不能逆转Eno1和GSTM2在二者中的差异表达。展开更多
基金Supported by National Nature Science Foundation of China No.81000968,No.81101540,No.81101637,No.81172273,No.81272388,No.81301820 and No.81472673Doctoral Fund of Ministry of Education of China No.20120071110058The National Clinical Key Special Subject of China
文摘Intrahepatic arterioportal fistula(IAPF)can be caused by many secondary factors.We report four cases of portal hypertension that were eventually determined to be caused by congenital hepatic arterioportal fistula.The clinical manifestations included ascites,variceal hemorrhage and hepatic encephalopathy.Computed tomography scans from all of the patients revealed the early enhancement of the portal branches in the hepatic arterial phase.All patients were diagnosed using digital subtraction angiography(DSA).DSA before embolization revealed an arteriovenous fistula with immediate filling of the portal venous radicles.All four patients were treated with interventional embolization.The four patients remained in good condition throughout follow-up and at the time of publication.IAPF is frequently misdiagnosed due to its rarity;therefore,clinicians should consider IAPF as a potential cause of non-cirrhotic portal hypertension.
基金This project was supported by the National Medicine Technique Innovation Foundation of ChinaNo.98-B-0 7
文摘Objective To explore the relationship between endogenous ouabain and the pathogenesis of hypertension. Methods ① Sixteen Sprague Dawley (SD) rats were selected and randomly divided into two groups, and then the rats were injected with ouabain in dosage of 20μg/kg.d and normal saline (NS), respectively. The indirect systolic blood pressure of all the rats were recorded once a week. ② Twenty five 1k1c (one kidney and one clipped) hypertensive rats were established and injected randomly with anti ouabain antibody, normal rabbit IgG and normal saline, respectively. The direct blood pressure of all the 1klc hypertensive rats were recorded by cannulated carotid artery for 3h after administration. Results The systolic blood pressure of rats injected with ouabain began to increase 2 weeks after ouabain administration and increased significantly at 6 weeks compared with NS group (17.7±1.2)kPa vs (15.4±1.1)kPa, P <0.01).Anti ouabain antibody could significantly decrease the blood pressure of 1k1c rats, while the normal rabbit IgG could not. Conclusion The results of this study indicate that endogenous ouabain might be one of the pathogenetic factors of hypertension.
文摘Objective To access the prevalence and risk factors for hypertension after heart transplantation(HT),and the impact of post-transplant hypertension on mediumterm survival among HT patients.Methods Data from 265
文摘目的观察依那普利对肾性与自发性高血压大鼠左心室α-烯醇化酶(α-enolase,Eno1)及谷胱甘肽-s-转移酶,μ2(glutathione-s-transferase,μ2,GSTM2)表达的影响。方法实验共分5组:(1)对照组;(2)两肾两夹高血压大鼠组;(3)两肾两夹高血压大鼠+依那普利组;(4)自发性高血压大鼠组;(5)自发性高血压大鼠+依那普利组。检测各组大鼠血压及左室重量指数,行超声心动图检查,并运用Western blot检测各组大鼠左心室Eno1、GSTM2及β-肌球蛋白重链(β-myosin heavy chain,β-MHC)的表达情况。结果两肾两夹及自发性高血压大鼠血压与左室重量指数均明显高于对照组,依那普利治疗后,其左心室肥厚均得到明显逆转。与两肾两夹组相比,Eno1在自发性高血压大鼠中的表达明显上调;与对照组相比,GSTM2在自发性高血压大鼠中的表达明显下调,而两肾两夹组无变化,经依那普利治疗后,二者的表达变化均未得到明显逆转;β-MHC在两种模型中的表达均上调,而依那普利治疗后,β-MHC在二者中的表达均明显下调。结论依那普利能明显逆转β-MHC在两种模型中的差异表达,但不能逆转Eno1和GSTM2在二者中的差异表达。
