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AIM To establish the method for quality control of Qiwei Ketenzi Pill (Semen Entadae, Semen Nigellae, Fructus Piperis, ect). METHODS Semen Nigellae was identified by TLC, and vitexicarpin was determined by HPLC. RESULTS TLC spots developed were fairly clear, and the bland test showed no interference. vitexicarpin in Qiwei Ketenzi Pill showed a good linear relation in the concentration range of 0.106 5 - 2.130 0 ?g and the average recovery was up to 101.4 % , RSD was 1.34 T《B》 % . CONCLUSION The method is effecive for the quality control of Qiwei Ketenzi Pills.

AIM To explore the roles of vascular endothelial growth factor (VEGF) in hypoxia pulmonary hypertension and effects of suramin. METHODS Thirty SD rats were randomly divided into normal control group (N), hypoxia hypercapnia group(F), hypoxia hypercapnia +suramin group (S). The levels of VEGF in serum and in lung tissue were measured by ELISA, the ultrastructure of pulmonary arterioles was observed by electron microscopy, the expression of VEGF was observed by immunohistochemistry, the expression of VEGFmRNA was observed by in situ hybirdization. RESULTS ①Mean pulmonary arterial pressure(mPAP), weight ratio of RV to LV+S, the leves of VEGF in serum and in lung tissue of group F were significantly higher than that of group N and group S (P

AIM: To investigate the changes of vascular endothelial growth factor (VEGF) in the pulmonary circulation of rats with different hypoxia and hypercapnia duration. METHODS: Forty SD rats were randomly divided into normol control group (N), exposed to hypoxia hypercapnia for 2 weeks group (T), for 4 weeks group (F), for 8 weeks group (E). The levels of VEGF were measured and the ultrastructure of pulmonary arterioles was observed by electron microscopy. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum and lung tissue, the expression of VEGF and VEGF mRNA in group T, F, E were significantly higher than that in group N. With the prolong duration, base of endothelial cell was narrowed, proliferation of smooth muscle cells and collagenous fibers of pulmonary arterioles in rats were increased gradually. CONCLUSIONS: Hypoxia and hypercapnia increase the expression of VEGF mRNA and synthesis of VEGF. VEGF may play an important role in the pathogenesis of hypoxia pulmonary hypertension and reconstruction of pulmonary artery.

Aim To explore the effects of Puerarin on the Apelin and its receptor APJ of lung tissue in rats with hypoxia pulmonary hypertension.Methods Thirty SD rats were randomly divided into normal control group(N),and hypoxia hypercapnia group(F),and hypoxia hypercapnia+Puerarin group(P).The levels of Apelin-36 in serum and in lung tissue were measured by radioimmunity,the expressions of Apelin and APJ in pulmonary tissuse were observed by RT-PCR.Results ①Mean pulmonary arterial pressure(mPAP),weight ratio of RV to LV+S,the levels of Apelin in serum and in lung tissue of group F were significantly higher than those of group N(P

AIM: To explore the roles of vascular endothelial growth factor (VEGF) in hypoxia pulmonary hypertension and effects of SHENYI Capsule. METHODS: Thirty SD rats were randomly divided into normal control group (N), hypoxia hypercapnia group (F), and hypoxia hypercapnia+SHENYI Capsule group (S). The levels of VEGF in serum and lung tissue are measured by ELISA, the ultrastructure of pulmonary arterioles was observed by electron microscopy, and the expression of VEGFmRNA was observed by in situ hybirdization. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum, and lung tissue of group F were significantly higher than those of group N and group S (P

AIM:To investigate rat Urotensin-II(ra t U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmon ary artery was dissected from the male Sprague -Dawley rats and artery ring width was 3-4 mm. Concentration-response curves wer e gene rated to rat U-II(0 03 nmol/L-30 nmol/L).Inhibitor of MAPK,PD 98059(0 1 ?mol/ L -10 ?mol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoc onstriction had reached plateau to construct the relaxant concentration-respons e curves and their EC 50 and E max . RESULTS: Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries [EC 50 =7 95?0 4 0, E max =(14 28?6 34)% of the response to 60 mmol/L KCl]; PD 98059 caused c oncentration-dependent relaxations of rat U-II precontracted arteries [EC 50 =5 91?0 45, E max =(81 39?13 65)%]. CONCLUSION: Rat U- II was a potent vasoconstrictor of rat main pulmonary arteries and this response was med iated through MAPK.

Aim To study the effect of puerarin on reperfusion injury after thrombolytic therapy in acute pulmonary thromboembolism and its mechanism. Methods Thirty-two Japanese rabbits were randomly divided into sham operation group (group S),Thrombolysis-only group(group T), and Puerarin group(group Pur). Acute pulmonary thromboembolism models of rabbits were established with injection of autologous blood clots through the right heart catheters,haemodynamic monitoring was performed by introducing heart catheter through right jugular vein.The activity of plasma superoxide dismutase (SOD) and content of plasma malondialdehyde (MDA) were detected before embolization,2 h after embolization,2 h and 4 h after thrombolysis. At the end,the rabbits were sacrificed and their lung,removed for histopathologic and electron microscopic investigations. Results ①Pulmonary arterial mean pressure (PAMP) were decreased at 1 hour after thrombolysis both in group T and group Pur(P

AIM: To study the effect of ligustrazine on pulmonary hypertensive rats induced by hypoxic hy- percapnia. METHODS: Thirty rats were randomly divided into three groups: control group(A), hypoxic hypercapnic group (B), hypoxic hypercapnia+ligustrazine (lig. ) group(C). RESULTS: (1) Mean pulmonary axterial pressure (mPAP)of group B was significantly higher than that of group A and mPAP of group C was significantly lower than that of group B(P0.05); (2)Electron microscopy and immunohistochemistry showed ligustrazing could inhibit the diposition of col- lagenous fiber(collagen type Ⅰ )in pulmonary arterioles induced by hypoxic hypercapnia; (3) Plasma endothelin level of group C was significantly lower than that of group B (P

AIM: To study the expression and distribution of osteopontin (OPN) in lungs and pulmonary arteries in pulmonary hypertensive rats induced by hypoxia-hypercapnia, and to explore the role of OPN in pathogenesis of pulmonary hypertension. METHODS: Forty-eight male Sprague-Dawley rats (Weight 180 g-220 g) were randomly divided into four groups: normal control group (NC), hypoxic hypercapnia 1-week,2-week and 4-week group (1HH, 2HH and 4HH). The expressions of OPN mRNA and protein in lungs and pulmonary arteries were detected by RT-PCR and immunohistochemistry. ELISA was used to detect the concentration of OPN in lung homogenates. The content of OPN in pulmonary arteries was detected by Western blotting. RESULTS: ① The mean pulmonary artery pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum [RV/(LV+S)] in all hypoxic hypercapniac groups were higher than those in normal control group (P0.05). ② The expression of OPN mRNA was significantly increased in pulmonary arteries and lung tissues in hypoxic hypercapnic groups compared with normal control group (P