Objective: To investigate the association of Glu298Asp polymorphism of theeNOS gene with essential hypertension in elderly people. Methods: Ninety-five cases of essentialhypertension were randomly chosen from outpatie...Objective: To investigate the association of Glu298Asp polymorphism of theeNOS gene with essential hypertension in elderly people. Methods: Ninety-five cases of essentialhypertension were randomly chosen from outpatients and inpatients as the study group, and an equalnumber of sexes, age-matched healthy people as the control group. Their height, weight and bloodpressure were recorded and their fasting plasma lipid concentrations were measured. Glu298Asppolymorphism of the eNOS gene was measured using the methods of PCR and RFLP. Results: Theconstituent ratio of Genotype Glu/Asp in the study group (26.3%) was higher than that in the controlgroup (12.6%, x^2 = 5. 67, P<0.05), the allelic frequency of 298Asp in the study group (13.2%) wassignificantly higher than that in the control group (6.3%, x^2 = 5.06, P<0.05). Conclusion: Glu298Asp variant of the eNOS gene may be an independent predictor in essential hypertension.展开更多
Objective To explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension(PAH) in patients of chronic obstructive pulmonary disease(COPD) associated with chronic cor pulmonale(C...Objective To explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension(PAH) in patients of chronic obstructive pulmonary disease(COPD) associated with chronic cor pulmonale(CCP) during exacerbation.Methods Seventy patients of COPD and CCP with acute exacerbation were randomly and equally divided into control group and treatment group.The control group received standard treatment with antibiotics,antiasthmatic and expectorant medications,and oxygenation;and the ligustrazine treatment group received ligustrazine treatment(80 mg/d;i.v.;for 2 weeks) in addition to the standard treatment.Before and at the end of 2 week treatment,the clinic responses of the two regimens were evaluated,plasma levels of endothelin-1(ET-1) and nitric oxide(NO) were determined;arterial oxygen partial pressure(PaO_2),mean pulmonary arterial pressure(mPAP),outflow tract of right ventricle(RVOT),and internal diameter of right ventricle(RV) were measured.Results Good clinic benefits were achieved in both the standard and ligustrazine regimens,plasma level of ET-1,values of mPAP,RV and RVOT decreased significantly,plasma level of NO and PaO_2 values decreased(all P<0.01 vs pretreatment to all parameters).Compared with the control group,ligustrazine greatly enhanced the clinic efficacy from 77.1%to 97.1%(P<0.05),and also resulted in more significant changes of all these parameters(P<0.01 vs control group for all parameters).For both groups,the levels of plasma ET-1 were positively correlated with values of mPAP,RVOT,and RV(r = 0.710,0.853,and 0.766,respectively,all P = 0.000),and negatively correlated with plasma NO and PaO_2(r =- 0.823,and- 0.752,respectively,all P = 0.000).Conclusion Ligustrazine is effective in treating pulmonary artery hypertension during acute exacerbation of COPD and CCP in patients from the plateau area.The observed changes in the plasma levels of NO and ET-1 in response to ligustrazine treatment suggest that ligustrazine may act through the selective effect on pulmonary blood vessels to enhance the synthesis and release of NO and suppress those of ET-1 from lung vascular endothelial cells,thus reducing pulmonary artery pressure and decreasing pulmonary arterial hypertension.展开更多
To assess the role of oxidative metabolism and nitric oxide synthesis for elucid a ting their pathophysiological mechanisms in a Tibetan patient with essential hyp ertension Methods The serum levels of total supero...To assess the role of oxidative metabolism and nitric oxide synthesis for elucid a ting their pathophysiological mechanisms in a Tibetan patient with essential hyp ertension Methods The serum levels of total superoxide dismutase (T SOD), malondialdehyde (MDA), total antioxidant capacity (T AOC), nitric oxide (NO) and nitric oxide synthase (NOS) were assayed in sixty native Tibetans (thirty hypertensive patients and t hirty healthy volunteers as control) Results The levels of T SOD, T AOC, NO and NOS were significantly lower in the patien t group than in the control group ( P <0 01); MDA was significantly higher in the patient group than in the control group ( P <0 01) The level of MDA ha d a strong negative correlation with T SOD, T AOC, NO and NOS ( r =-0 82, -0 76, -0 79, -0 73, respectively, P <0 001 for all) Conclusion Tibetan patients with essential hypertension (EH) may have underlying oxidative metabolism dysfunction and depressed NO synthesis, both responsible for the hype rtensive process展开更多
AIM:To investigate endothelin-1 hypo-responsive associated with portal hypertension in order to improve patient treatment outcomes.METHODS:Wild type,e NOS-/-and i NOS-/-mice receivedpartial portal vein ligation surger...AIM:To investigate endothelin-1 hypo-responsive associated with portal hypertension in order to improve patient treatment outcomes.METHODS:Wild type,e NOS-/-and i NOS-/-mice receivedpartial portal vein ligation surgery to induce portal hypertension or sham surgery.Development of portal hypertension was determined by measuring the splenic pulp pressure,abdominal aortic flow and portal systemic shunting.To measure splenic pulp pressure,a microtip pressure transducer was inserted into the spleen pulp.Abdominal aortic flow was measured by placing an ultrasonic Doppler flow probe around the abdominal aorta between the diaphragm and celiac artery.Portal systemic shunting was calculated by injection of fluorescent microspheres in to the splenic vein and determining the percentage accumulation of spheres in liver and pulmonary beds.Endothelin-1 hypo-response was evaluated by measuring the change in abdominal aortic flow in response to endothelin-1 intravenous administration.In addition,thoracic aorta endothelin-1contraction was measured in 5 mm isolated thoracic aorta rings ex-vivo using an ADI small vessel myograph.RESULTS:In wild type and i NOS-/-mice splenic pulp pressure increased from 7.5±1.1 mm Hg and 7.2±1 mm Hg to 25.4±3.1 mm Hg and 22±4 mm Hg respectively.In e NOS-/-mice splenic pulp pressure was increased after 1 d(P=NS),after which it decreased and by 7 d was not significantly elevated when compared to 7 d sham operated controls(6.9±0.6 mm Hg and 7.3±0.8 mm Hg respectively,P=0.3).Abdominal aortic flow was increased by 80%and 73%in 7 d portal vein ligated wild type and i NOS when compared to shams,whereas there was no significant difference in 7 d portal vein ligated e NOS-/-mice when compared to shams.Endothelin-1 induced a rapid reduction in abdominal aortic blood flow in wild type,e NOS-/-and i NOS-/-sham mice(50%±8%,73%±9%and 47%±9%respectively).Following portal vein ligation endothelin-1 reduction in blood flow was significantly diminished in each mouse group.Abdominal aortic flow was reduced by 19%±9%,32%±10%and 9%±9%in wild type,e NOS-/-and i NOS-/-mice respectively.CONCLUSION:Aberrant endothelin-1 response in murine portal hypertension is NOS isoform independent.Moreover,portal hypertension in the portal vein ligation model is independent of ET-1 function.展开更多
基金Supported by the National Science of Foundation of Jiangsu Province(BK 2001162)
文摘Objective: To investigate the association of Glu298Asp polymorphism of theeNOS gene with essential hypertension in elderly people. Methods: Ninety-five cases of essentialhypertension were randomly chosen from outpatients and inpatients as the study group, and an equalnumber of sexes, age-matched healthy people as the control group. Their height, weight and bloodpressure were recorded and their fasting plasma lipid concentrations were measured. Glu298Asppolymorphism of the eNOS gene was measured using the methods of PCR and RFLP. Results: Theconstituent ratio of Genotype Glu/Asp in the study group (26.3%) was higher than that in the controlgroup (12.6%, x^2 = 5. 67, P<0.05), the allelic frequency of 298Asp in the study group (13.2%) wassignificantly higher than that in the control group (6.3%, x^2 = 5.06, P<0.05). Conclusion: Glu298Asp variant of the eNOS gene may be an independent predictor in essential hypertension.
基金supported by the Key scientific and technological project in Qinghai Province,China (2006-N-143)
文摘Objective To explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension(PAH) in patients of chronic obstructive pulmonary disease(COPD) associated with chronic cor pulmonale(CCP) during exacerbation.Methods Seventy patients of COPD and CCP with acute exacerbation were randomly and equally divided into control group and treatment group.The control group received standard treatment with antibiotics,antiasthmatic and expectorant medications,and oxygenation;and the ligustrazine treatment group received ligustrazine treatment(80 mg/d;i.v.;for 2 weeks) in addition to the standard treatment.Before and at the end of 2 week treatment,the clinic responses of the two regimens were evaluated,plasma levels of endothelin-1(ET-1) and nitric oxide(NO) were determined;arterial oxygen partial pressure(PaO_2),mean pulmonary arterial pressure(mPAP),outflow tract of right ventricle(RVOT),and internal diameter of right ventricle(RV) were measured.Results Good clinic benefits were achieved in both the standard and ligustrazine regimens,plasma level of ET-1,values of mPAP,RV and RVOT decreased significantly,plasma level of NO and PaO_2 values decreased(all P<0.01 vs pretreatment to all parameters).Compared with the control group,ligustrazine greatly enhanced the clinic efficacy from 77.1%to 97.1%(P<0.05),and also resulted in more significant changes of all these parameters(P<0.01 vs control group for all parameters).For both groups,the levels of plasma ET-1 were positively correlated with values of mPAP,RVOT,and RV(r = 0.710,0.853,and 0.766,respectively,all P = 0.000),and negatively correlated with plasma NO and PaO_2(r =- 0.823,and- 0.752,respectively,all P = 0.000).Conclusion Ligustrazine is effective in treating pulmonary artery hypertension during acute exacerbation of COPD and CCP in patients from the plateau area.The observed changes in the plasma levels of NO and ET-1 in response to ligustrazine treatment suggest that ligustrazine may act through the selective effect on pulmonary blood vessels to enhance the synthesis and release of NO and suppress those of ET-1 from lung vascular endothelial cells,thus reducing pulmonary artery pressure and decreasing pulmonary arterial hypertension.
文摘To assess the role of oxidative metabolism and nitric oxide synthesis for elucid a ting their pathophysiological mechanisms in a Tibetan patient with essential hyp ertension Methods The serum levels of total superoxide dismutase (T SOD), malondialdehyde (MDA), total antioxidant capacity (T AOC), nitric oxide (NO) and nitric oxide synthase (NOS) were assayed in sixty native Tibetans (thirty hypertensive patients and t hirty healthy volunteers as control) Results The levels of T SOD, T AOC, NO and NOS were significantly lower in the patien t group than in the control group ( P <0 01); MDA was significantly higher in the patient group than in the control group ( P <0 01) The level of MDA ha d a strong negative correlation with T SOD, T AOC, NO and NOS ( r =-0 82, -0 76, -0 79, -0 73, respectively, P <0 001 for all) Conclusion Tibetan patients with essential hypertension (EH) may have underlying oxidative metabolism dysfunction and depressed NO synthesis, both responsible for the hype rtensive process
基金Supported by Indiana University department of surgery and Lilly INGEN research fund provided support for the Research performed in this manuscript
文摘AIM:To investigate endothelin-1 hypo-responsive associated with portal hypertension in order to improve patient treatment outcomes.METHODS:Wild type,e NOS-/-and i NOS-/-mice receivedpartial portal vein ligation surgery to induce portal hypertension or sham surgery.Development of portal hypertension was determined by measuring the splenic pulp pressure,abdominal aortic flow and portal systemic shunting.To measure splenic pulp pressure,a microtip pressure transducer was inserted into the spleen pulp.Abdominal aortic flow was measured by placing an ultrasonic Doppler flow probe around the abdominal aorta between the diaphragm and celiac artery.Portal systemic shunting was calculated by injection of fluorescent microspheres in to the splenic vein and determining the percentage accumulation of spheres in liver and pulmonary beds.Endothelin-1 hypo-response was evaluated by measuring the change in abdominal aortic flow in response to endothelin-1 intravenous administration.In addition,thoracic aorta endothelin-1contraction was measured in 5 mm isolated thoracic aorta rings ex-vivo using an ADI small vessel myograph.RESULTS:In wild type and i NOS-/-mice splenic pulp pressure increased from 7.5±1.1 mm Hg and 7.2±1 mm Hg to 25.4±3.1 mm Hg and 22±4 mm Hg respectively.In e NOS-/-mice splenic pulp pressure was increased after 1 d(P=NS),after which it decreased and by 7 d was not significantly elevated when compared to 7 d sham operated controls(6.9±0.6 mm Hg and 7.3±0.8 mm Hg respectively,P=0.3).Abdominal aortic flow was increased by 80%and 73%in 7 d portal vein ligated wild type and i NOS when compared to shams,whereas there was no significant difference in 7 d portal vein ligated e NOS-/-mice when compared to shams.Endothelin-1 induced a rapid reduction in abdominal aortic blood flow in wild type,e NOS-/-and i NOS-/-sham mice(50%±8%,73%±9%and 47%±9%respectively).Following portal vein ligation endothelin-1 reduction in blood flow was significantly diminished in each mouse group.Abdominal aortic flow was reduced by 19%±9%,32%±10%and 9%±9%in wild type,e NOS-/-and i NOS-/-mice respectively.CONCLUSION:Aberrant endothelin-1 response in murine portal hypertension is NOS isoform independent.Moreover,portal hypertension in the portal vein ligation model is independent of ET-1 function.
基金The project supported by Provinicial Natural Science Foundation of Anhui Province(070413124)the Fresh Start Foundation of Wannan Medical College(BK00010804)~~
