Angioplasty, Balloon, Coronary ; Humans ; Percutaneous Coronary Intervention ; methods ; Tungsten

Objective To probe the safety of performing transradial artery percutaneous coronary intervention (PCI) for Allen test negative patients.Methods One hundred and six patients performed transradial artery PCI were enrolled in the study.The patients were divided into negative group (57 cases) and positive group (49 cases) according to Allen test results.Patients were performed ulnar artery angiography,deep palmar arch angiography and superficial palmar arch angiography.Ulnar artery diameter,deep palmar arch conditions,superficial palmar arch conditions,the frames counting through angiography on the side of ulnar vessel system,and hand ischemia after PCI (follow up for 3 months) was observed.Results There was no significant difference between negative group and positive group in parameters of ulnar artery diameter [(2.02 ±0.18) mm vs.(2.07 ±0.17) mm] and deep palmar arch and superficial palmar arch [85.96％ (49/57) vs.87.76％ (43/49),75.44％ (43/57) vs.81.63％ (40/49)] (P ＞0.05).The frames counting had no significant difference between negative group and positive group [(218.6 ± 63.6) frames vs.(180.8 ± 44.1) frames],but the ratio of the frames counting ≥380 frames had significant difference between negative group and positive group [14.04％(8/57) vs.2.04％(1/49)] (P ＜ 0.05).None of patients had been found to suffer from hand ischemia after PCI.Conclusion Transradial artery PCI is suitable for Allen test negative patients.

Objective To study the sequence of learning and memory loss in the rat after hemispheric irradiation. Methods After Sprague Dawly(SD) female rats were anaesthetized with chloral hydrate, their cerebral hemispheres were irradiated with a single dose of 5,15 or 30?Gy by 4?MeV electron. On D3,D7,D30 and D60, the learning and memorizing ability was measured with the Y maze test. Results On D3 and D7, the learning ability of SD rats was impaired most but partly restored in 1 to 2 months. In observation of memory loss, the intensity of cerebral function damage was in direct proportion to the increase of radiation dose.Conclusion The learning and memorizing ability of rats can be damage by hemispheric irradiation with the severity of impairment and possibility of recruitment depending on the dose.

Objective To observe the effect of depressive disorder on ventricular remodeling and its mechanism in acute myocardial infarction (AMI) rats. Methods Forty-six AMI Wistar rats were randomly divided into sham-operation (n=10), AMI (n=12), depression (n=12), neurostan by open field test, and the detection of angiotensin Ⅱ (Ag Ⅱ ), aldosterone (ALD), malondialdehyde (MDA), superoxide dismutase (SOD) were performed, the pathological sections were observed under light and electron microscopes. Results Compared with sham-operation group, depression group had decreased values of squares crossing times, rearing times and grooming time, increased time of staying in the central square and defecation. Compared with depression group, AMI and neurostan treatment groups had increased values of squares crossing times, rearing times and grooming time,decreased time of staying in the central square and defecation (F=16. 9, 44.56, 71.79, 34.86,29. 18, P＜0.01). At the 4 week of test, the left and right ventricular relative weights (LVRW,RVRW) and thickness of interventricular septum were (1.63±0.15) mg/g, (0. 48±0. 10) mg/g and (1.75 ± 0. 38) mm in sham-operation group, the corresponding data were (2.06±0.21) mg/g,(0.62±0.10) mg/g and (2.25±0.30) mm in AMI group, (2.90±0.47) mg/g, (1.00±0.28) mg/gand (2.58±0.34) mm in depression group, (2.20±0.34) mg/g, (0.67±0.15) mg/g and (2. 25±0.23) mm in neurostan treatment group. Compared with sham-operation group, AMI, depression and neurostan groups had obviously increased values of LVRW, RVRW and thickness of interventricular septum. Compared with depression group, AMI and neurostan groups had decreased LVRW, RVRW and thickness of interventricular septum (F=6.31, 21.9, 115.7, 9.91, P＜0.05). And the depression also could aggravate edema and injury of ultrastructure in myocardial tissue. The values of AgⅡ , ALD, MDA and SOD were (1957.5±662.6) ng/L, (0.453±0.111) ng/L, (16. 00±3.03)nmol/L and (80.57 ± 7.00) U/ml in depression group, the corresponding data were (1143.8± 98.0)ng/L, (0.198±0.087) ng/L, (8.03 ± 0.44 ) nmol/L and (95.20 ± 4.87) U/ml in sham-operated group, (1407.5±255.8) ng/L, (0.295±0.027) ng/L, (11.18±4.30) nmol/L and (87.33±3.51)U/ml in AMI group, (1400.0±239.0) ng/L, (0.326±0.073) ng/L, (11.88±3.36) nmol/L and (89.13 ±0.17) U/ml in neurostan group. After 4 weeks, the values of Ag Ⅱ , ALD and MDA increased in depression group while the level of SOD reduced (F=6.58, 11.9, 11.39, 8. 82, P＜0.05). Conclusions Depressive disorder after AMI in rats can aggravate ventricular remodeling and lower the ability of antioxygen.

BACKGROUND: The observation of vascular endothelial growth factor gene expression of cerebrovascular diseases and ultrastructure of cells may be helpful to understand angiogenesis and its relative cellular factors involved in the pathogenesis at cellular and molecular levels. OBJECTIVE: To investigate the method of culture of human cerebral cap illary endothelial cell by separation of capillary fragment in vitro, and to ob serve vascular endothelial growth factor gene expression and ultrastructure of cells. DESIGN: A randomized controlled research on technique and method. SETTING: The neurosurgery department of a general hospital of a military area command of Chinese PLA and the neurosurgery department of a college hospital. PARTICIPANTS: Eighteen patients with arteriovenous malformation of brain(Spetzler Ⅱ-Ⅲ grade), as confirmed by aortocranial angiography before operation, in the Department of Neurosurgery, General Hospital of Shenyang Military Area Command of Chinese PLA were included. The material was obtained from fresh integrated specimen of arteriovenous malfor mation of brain with surrounding fresh brain tissues during the opera tion. Capillary endothelial cell was separated by homogenate, filtration and enzymatic digestion techniques. Cells grew well in culture flask and were divided into 4 groups(hypoxia state for 2, 4, 8 hours groups and control group). Each group contained four flasks.METHODS: Simulation of anoxia condition: volume faction 0.95 N2 and volume fraction 0.05 CO2. Expression of factor Ⅷ related antigen in cells was detected by immunohistochemistry. mRNA expression of vascular endothelial growth factor on endothelial in every group was observed by RT-PCR, protein content of vascular endothelial growth factor in supernatant detected by enzyme-linked immunoadsordent assay, and cellular ultrastructural change observed by transmission electron microscopy.MAIN OUTCOME MEASURES: mRNA expression of vascular endothelial growth factor on endothelial cell and protein content of vascular endothelial growth factor in supernatant in control group and every hypoxia groups; cellular ultrastructural changes.RESULTS: Under phase contrast microscope, cultured living cells had mono-layer pebble-like typical character. More than 90% of were factor Ⅷrelated antigen(FⅧ-RA) staining positive. mRNA and protein expression of vascular endothelial growth factor in hypoxia 4 hours group was 0.98 ±0. 19,( 180. 77 ± 20. 15) ng/L, which was significantly higher than in control group [0, (26. 20 ± 6.33) ng/L, P ＜ 0.01 ]. Eight hours later, expression decreased [(0. 35 ±0.07), (31.68 ±8.34) ng/L]; swollen mitochondrion, dilated endoplasmic reticulum, and lysosome vesiculation were found.CONCLUSION: Humane cerebral capillary endothelial cell can be cultured by separation of capillary fragment, which is easy to operate and the cellular purity is reliable. In the early stage of ischemia and hypoxia, expression of vascular endothelial growth factor is not enough to maintain cellular ultrastructure integrity. Cells may be injured along with the prolong of hypoxia.Zhao MG, Tang T, Gao YZ, Pu PY, Wei XZ. Culture of human cerebral capillary endothelial by separation of capillary fragment and the observation of vascular endothelial growth factor gene expression and cell ultrastructure. Zhongguo Linchuang Kangfu 2005; 9(21):211-3 (China) [www. zglckf. com]

Objective To observe the mechanism of action of panax quinquefolium diolsaponins (PQDS) on anti-ventricular remodeling in rats. Methods The model of pressure-loading ventricular remodeling was established through the method of rat’s abdominal aorta deligation. The male Wistar rats were divided into 5 groups,including sham operation group,remodeling model group,Benazepril group,and low and high dose groups of PQDS. The rats were treated with PQDS (with dose of 50 and 100 mg?kg-1 i.g) for 6 weeks. The rats in sham operation group and remodeling model group were treated with normal sodium (with dose of 10 mL?kg-1?d-1 i.g) for 6 weeks. The rats in masculine medicine group were treated by Benazepril (with dose of 10 mg?kg-1 i.g) for 6 weeks. After 6 weeks of treatment,myocardial morphological parameters,the content of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) in serum,the contents of prostacycline (PGI2),thromboxane A2 (TXA2),nitric oxide (NO) and angiotensinⅡ (AngⅡ) in plasma were determined. At the same time,the contents of endothelium (ET) in plasma and myocardium were also determined. Results Compared with remodeling model group,the ventricular weight and cardiac coefficient were decreased significantly in the rats treated with PQDS (P0.05). Conclusion PQDS has protective effects on ventricular remodeling through increasing anti-oxidase activity,reducing the damage of free radicals and vasoactive substance on myocardium and correcting disequilibrium of PGI2/TXA2 in ventricular remodeling etc.

Objective To study the role of Bid in simulated ischemia/reperfusion injury in cultured neonatal rat cardiocytes and its possible mechanism.Methods A cell culture model of neonatal rat(born within 3 days) cardiocytes was used to establish simulated ischemia/reperfusion model.Unrelated siRNA or Bid specific siRNA was transfected into rat cardiocytes by Oligofectamine.The activation of Bid and caspase-8 was detected by Western blotting.The apoptotic rate of cardiocytes was determined by flow cytometry.Results Bid and caspase-8 of cardiocytes were activatied in simulated ischemia/reperfusion injury model.The activation of caspase-8 of cardiocytes in Bid-specific siRNA group decreased significantly compared with those in simulated(ischemia/reperfusion) group and unrelated siRNA group;the apoptotic rate of cardrocytes(7.4%) was lower than those in simulated ischemia/reperfusion group(51.2%) and unrelated siRNA group(48.7%)(P

Objective To investigate the gene expression of vascular endothelial growth factor(VEGF) and ultrastructural changes in cultured endothelial cells from human cerebral microvessels under hypoxic conditions.Methods Human cerebral microvessels were isolated from freshly obtained specimens of normal brain adherent to resected cerebral arteriovenous malformations.The expression of factor Ⅷ-relative antigen(FⅧ-RA) in cultured cells was observed with immunocytochemistry.The level of VEGFmRNA in cells and released VEGF protein in cell supernatant were determined by RT-PCR analysis and ELISA respectively when they were exposed to hypoxic conditions(95% N_2,5% CO_2;two hours,four hours,eight hours) or maintained in basal condition.Ultrastructural changes in cells were also observed by electron microscopy.Results In inverted microscope the cultured cells showed contact inhibition and a rounded cobblestone appearance.More than 90% of them were stained strongly with antibodies against FⅧ-RA.Significant VEGF mRNA and protein accumulated when these cells were exposed to hypoxia for 4 hours.However,their VEGF expression was down-regulated after hypoxia for 8 hours and a number of vesicles and swollen mitochondria were present in the cytoplasm.Conclusion The level of VEGF expression may havesignificant relationship with ultrastructural changes in human cerebral endothelial cells under hypoxic conditions.

Objeetive To investigate protective effect of trimetazidine on myocardial ischemia/reperfusion injury (MIRI) in rats.Methods Forty Wistar rats were randomly divided into MIRI group (n =10 rats),trimetazidine high-dosage group (n =10 rats; 20 mg/kg),trimetazidine low-dosage group (n=10 rats; 10 mg/kg),and the normal control group (n =10 rats).After MIRI,hemodynamic changes were observed,the concentration of IL-6 and TNF-α was determined,and the cardiac muscle histology under the microscope was observed.Results Hemodynamic studies:Compared to the indices LVSP(198 ±35.5) mmHg,LVEDP (17 ±9.18) mmHg,+ dp/dt max (11050 ± 1517.4) mmHg/s,and-dp/dtmax (9175± 1900) mmHg/s] in the sham-operated group,the indices [LVSP (143 ± 24.5) mmHg,LVEDP (37.5 ±7.16)mmHg,+ dp/dtmax (7450 ± 1755.1) mmHg/s,and-dp/dtmax (6075 ± 1641) Hg/S] in the MIRI group,the indices [LVSP (154.5 ± 31.1) mmHg,LVEDP (31.3 ± 12.6) mmHg,± dp/dtmax (8527.7 ±2251.5) mmHg/s,and-dp/dtmax (6694 ± 2242.2) mmHg/s] in the trimetazidine low-dosage (10 mg/kg)group,the indices[LVSP (168.3 ± 17.6) mmHg,LVEDP (28 ± 10.05) mmHg,+ dp/dtmax (9213.6 ±1747) mmHg/s,and-dp/dtmax (7568 ± 1462.4) mmHg/s] in the trimetazidine high-dosage (20 mg/kg)group,left ventricular remodeling end diastolic pressure (LVEDP),left ventricular systolic pressure (LVSP),and left ventricular pressure maxial rate of rise and fall (± dp/dtmax) were significantly decreased.Compared to the MIRI group,LVSP and ± dp/dtmax in the trimetazidine high-dosage (20 mg/kg)group were significantly increased (P ＜ 0.01),and myocardial damage of MIRI group was more severe in microscope.Compared to the sham-operated group [IL-6 (2556.5 ± 662.9) ng/ml,and TNF-α (134 ± 73.7)ng/ml],the corresponding indices [IL-6 (3664.0 ± 995.7) ng/ml,and TNF-α (443 ± 22.1) ng/ml] in the MIRI group,[IL-6 (3692.8 1545.2) ng/ml,and TNF-α (295 ± 24.2) ng/ml] in the trimetazidiue low-dosage (10 mg/kg) group,and[IL-6(2654.8 ±681.7) ng/ml,and TNF-α(230 ±7.8) ng/ml]in the trimetazidine high-dosage (20 mg/kg) group,the levels of IL-6 and TNF-α were significantly increased.Compared to the MIRI group,the levels of IL-6 and TNF-α were significantly decreased in the trimetazidine high-dosage (20 mg/kg) group (P ＜ 0.01).Conclusions The high-dosage (20 mg/kg) of trimetazidine had a protective effect on myocardial ischemia-reperfusion injury.

ObjectiveTo investigate the protective effects of panax quinquefolium 20s-protopanaxtriol saponins (PQTS) on ventricular remodeling in rats with pressure overloaded hypertrophic myocardium.Methods Wister rats were randomly divided into operation,model,positive captopril,and low,moderate,high PQTS groups.The model of pressure overload-induced ventricular remodeling was established through the method of rat's abdominal aorta deligation.After 6 weeks of PQTS treatment ( 12.5,25.0 and 50.0 mg · kg-1 · d-1,i.p),myocardial morphological and hemodynamic parameters were determined.The content of malondialdehyde (MDA) and activity of superoxide dismutase (SOD)in serum,and the concentrations of prostacycline (PGI2),thromboxane A2 (TXA2),endothelium (ET) and angiotensin Ⅱ( Ang Ⅱ ) in plasma were also determined.ResultsCompared with remodeling group,PQTS could inhibit myocardial pathological changes,decrease significantly ventricular weight and cardiac coefficient,increase significantly systolic blood pressure,diastolic blood pressure,mean arterial pressure,left ventricular systolic pressure and the maximum left ventricular pressure rising and dropping rates(dp/dtmax),reduce the heart rate and left ventricular end-diastolic pressure in ventricular remodeling rats.PQTS could also decrease the content of MDA and enhance significantly activity of SOD in serum.In addition,PQTS could decline the contents of ET,Ang Ⅱ and TXA2 in plasma while increase significantly the content of PGI2 in plasma and PGI2/TXA2 ratio(P＜0.05 or P＜0.01).ConclusionsPQTS has protective effects on ventricular remodeling through improving systolic and diastolic function in ventricular remodeling rats,increasing anti-oxidase activity,reducing the damage of free radicals and vasoactive substance onmyocardium,and correcting disequilibrium of PGI2/TXA2 in ventricular remodeling rats.