30%. For inferior genicular artery lesions,only balloon angioplasty were carried out. All patients were followed up for 6 months and 12 months to assess of restenosis and clinical efficacy. Results All the patients' therapy was successful,their clinical symptoms were improved or disappeared. The 6-month follow-up showed that restenosis rates were 5.5%,16.7% and 25% respectively in the iliac artery,femoral popliteal artery,and inferior genicular artery. The rates in 12-month follow-up were 11.1%,33.3%,and 75% correspondingly. Conclusion Angioplasty and stent implantation are safe and effective in treatment of lower limb atherosclerosis obliterans. Standardized postoperative anti-platelet,anticoagulant,and anti-lipid therapy is essential to maintain blood vessel recanalization.

Hemodynamic and clinical observations were performed on 15 patients with severe congestive heart failure treated with Chinese-made milrinone.It was found that after treatment with milrinone,cardiac index was significantly increased,pulmonary capillary wedge pressure,systemic vascular resistance,and pulmonary vascular resistance were significantly decreased,and heart rate and myocardialoxygen consumption remained unchanged.Tolerance exercise test was prolonged and plasma cyclic AMP was increased.No thrombocytopenia or pro-arrhythmic effect was observed.The total clinical efficacy of the drug was 86.7%.These facts suggest that the Chinese-made milrinone is the durg of choice for the management of patients with congestive heart failure.

Objective To investigate the effect of brain microvascular endothelial cells (BMECs) on mesenchymal stem cells (MSCs) expressing fetal liver kinase-1(Flk-1) and von Willebrand factor (vWF) under normal and hypoxic conditions. Methods Human bone marrow MSCs and rat BMECs were isolated, cultured and identified. We used direct and indirect co-culture to induce the differentiation of MSCs. The expression of Flk-1 and vWF after induction was observed and analyzed by flow cytometry and immunofluorescence staining. Results Undifferentiated MSCs did not express Flk-1 or vWF. In indirect co-culture group, indirect co-culture under hypoxic conditions induced (7.58?0.58)% (n=6, P=0.034) MSCs to express Flk-1 but not vWF, while in normoxic indirect co-culture, MSCs expressed neither. In direct co-culture group, after 5-day direct co-culture with BMECs under normoxia or hypoxia, MSCs expressing Flk-1 accounted for (13.76?1.67)% (n=6, P

Objective To investigate the expression of MMP-2 in rabbit carotid artery injured by airing drying. Methods Fifty-four rabbits were assigned to normal diet (n=18), fat diet (n=36), 18 of fat diet rabbits underwent airing drying of carotid intima after one-week fat diet. Then fed on fat diet after operation. All animals were sacrificed respectively at 1, 2, 3 months after airing drying (n=6 at each time piont), and MMP-2 expression was evaluated by immunohistochemistry. Results MMP-2 expression was low in the carotid of normal diet group, high in the fat diet group including the rabbits underwent airing drying with significant difference between them (P

AIM:To investigate the paracrine actions of mesenchymal stem cells(MSCs)to brain microvascular endothelial cells(BMECs)in hypoxic conditions.METHODS:Human bone marrow MSCs and rat BMECs were isolated,cultured and identified.The contents of VEGF and MMP-9 were confirmed using ELISA assays of the conditioned media.The transendothelial electrical resistance(TEER)was detected to reflect the permeability of the BMECs monolayer.The effects of different conditioned media on BMECs were investigated in hypoxic conditions.RESULTS:The contents of VEGF and MMP-9 in conditioned media were induced to increase significantly by the hypoxic stress,which were much lower in BMECs conditioned media than that in MSCs conditioned media.Hypoxia induced a significant increase in VEGF and MMP-9 in MSCs conditioned media collected in comparison to those in normal conditions.In hypoxic conditions,MSCs conditioned media enhanced the proliferation(optical density values:0.947?0.103 vs 0.254?0.024,P

Objective To explore the mechanisms of angiotensin Ⅱ (Ang Ⅱ) induced apoptosis of cultured cardiomyocytes of neonatal rats. Methods Cultured neonatal rat cardiomyocytes were divided into three groups. Cells in the control group were incubated in serum-free medium for 2, 6, 12, and 24 h. Cells in Ang Ⅱ group were incubated with Ang Ⅱ at the dose of 10 -7 mol/L for 2, 6, 12, and 24 h. Cells in Ang Ⅱ and Ang Ⅱ type 1 receptor antagonist group were incubated in medium containing 10 -7 mol/ L Ang Ⅱ plus 10 -5 mol/L irbesartan. The apoptotic cells were detected by TUNEL assay. The Bcl-2 protein expression was assessed by immunohistochemistry. Caspase-3 activity was measured by a fluorescent assay kit. Results The number of apoptotic cells in Ang Ⅱ group increased significantly in a time-dependent manner, accompanied by decreased Bcl-2 protein expression but increased activity of caspase-3. Treatment with irbesartan resulted in decreased number of apoptotic cells and decreased activity of caspase-3. Conclusion Angiotensin Ⅱ could induce the apoptosis of neonatal rat cardiomyocytes through the caspase-dependent pathway, which might be mediated by Ang Ⅱ type 1 receptor. Bcl-2 may participate in the regulation.

Objective To analyze the change of the shear stress in atherosclerotic carotid artery of rabbits and its effect on the plaque and intimia-media pathological morphology. Methods Totally 36 male Japanese White rabbits were randomly divided into blank control group (n=6), sham operation control group (n=6) and the surgery group (n=24). The blank control group was fed by normal diet. The sham operation control group was fed by the high-cholesterol diet. The surgery group was fed by high-cholesterol diet and treated by air-drying. In the 2nd, 4th, 8th and 12th week after operation, the hemodynamic parameters were measured using Color Doppler Flow Imaging. Blood viscosity was determined and the degree of artery stenosis was showed by digital subtraction angiography (DSA). The stenosis rate, mean shear stress, intimia-media ratio and mean integrated optical densities (IOD) of media smooth muscle cells (SMC) were calculated respectively. Results The typical atherosclerotic plaque was presented in surgery group. The thickness of media and mean IOD of SMC were increased at the 2nd week after operation. However, following the increase of the stenosis rate and shear stress, the flow field was changed on the stenotic artery. The pathological morphology showed the character of vulnerable plaque such a large lipid core, thin fibrous cap, and plaque rupture at 4th, 8th week after operation. The media showed atrophy and became thin, mean IOD of SMC was decreased. Statistic analysis showed significant difference in the 2 week group compared with other group. Conclusion Following the increase in the degree of stenosis, the flow shear stress is increased, turbulent flow presents, and flow field changes on the stenotic artery. Thus the plaque become unstable , and the vessel occurs remodeling.

Objective To investigate the bilateral flow-mediated dilation of brachial artery (BA-FMD) and nitroglycerin mediated dilation (BA-NMD) in patients with cerebral infarct, and to find out if the vasodilation of internal catotid artery after sublingual administration of nitroglycerin can be detected as a more direct way to reflect the vasodilation in patients with cerebral vascular diseases. Methods High resolution ultrasonic system was used to measure 13 patients with acute cerebral infarction. The diameter of brachial artery, internal carotid artery and common carotid artery was measured at relaxation, reactive congestion in the brachial artery and after sublingual administration of nitroglycerin. Meanwhile, the intima media thickness (IMT) and plaques of carotid artery was detected. Results Paralysis did not lead to differences in vasodilation of brachial artery (r=0.52, P=0.07). There was a correlation between ICA-NMD and BA-NMD (r=0.83, P=0.01). Conclusion There were no significant differences between brachial vasodilation in paretic and non-paretic limbs of patients with acute cerebral infarction. Ultrasonic measurement of ICA-NMD can be a more direct measure of the vasodilation of patients with cerebral infarction.

Objective To investigate the role of angiotensin Ⅱ receptors in metabolism of m yocardial collagen. 　Methods The collagen volume fraction(CVF), perivascular circumferential area(PVCA), hydroproline concentration(HC), ratio o f collagen type Ⅰto type Ⅲ(Ⅰ/Ⅲ),angiotensin Ⅱ(AngⅡ) content and the maximal binding capaci ty (Bmax) of ATRs were studied. The methods of radioimmunoassay(RIA),biochemistry assay, and pathological examin ation were used. 　Results Ventricular myocardial CVF, PVCA, HC, Ⅰ/Ⅲ, AngⅡ and B max of ATRs in WKY rats were significantly higher than those in sham -operation(SO)(P<0.05 or P<0.01),suggesting the collagen was abnormal ly accumulated in rats heart muscles. AngⅡ was positivily correlated with HC(r1=0.9045, P<0.01). After treament of Irbesartan, All above parameter were reduced significantly(P<0.05 or P<0.01), abnormally accumulated collagen was disap peared. While after treament of CGP42112A,an ATR2 antagonist, Bmax of ATRs was markedly decreased(P<0 .01), but CVF, PVCA, HC,Ⅰ/Ⅲ, AngⅡ showed little changes(P >0.05). 　Conclusion Obvious hyperplasia of myocardial collagens and remode ling of collagen network occurred after pressure overload. Local produced AngⅡ involves in the process,it's effects is mainly mediated by angiotensin Ⅱ 1 type receptor(ATR1)

AIM: To investigate the mechanism of vascular smooth muscle cells (VSMC) apoptosis after balloon injury. METHODS: VSMCs apoptosis, Bax protein and Bcl-2 protein was measured by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and immunohistochemical technique after balloon injury.RESULTS: VSMCs apoptosis occurred in vascular media at 3 days after balloon injury and reached a peak in media and intima where apoptosis was mainly present at 7 days, then decreased. At 28 days after balloon injury, only a few apoptosis cells were in intima. Irbesartan significantly increased VSMCs apoptosis ( P