早熟大粒无核葡萄新品种‘超级无核’

 ‘超级无核’葡萄系从美国引进葡萄新品种‘Superior Seedless’优选单株培育出的优良品种。无核、大粒、早熟、优质、早实、丰产、生长势强健、耐病、耐不利栽培条件, 是适合高温、高湿、少日照地区栽培的无核葡萄新品种。     

Effects of matrix metalloproteinases on ventricular remodelingfollowing myocardial ischemia in the rat

AIM:To examine the relationship between the activity of matrix metallproteinases(MMPs) and ventricular remodeling following myocardial ischemia in the rat.METHODS:The model of myocardial ischemia(MI) in the rat was established by isoprenaline(ISP). The activity of MMPs was measured by zymography and collagen concentration was assessed by the method of chloramine T, so did I/III collagen ratio by immunohistochemical staining. The microstructure of myocardium was also observed by electron microscope.RESULTS:The activity of MMP-2 in myocardial ischemia group (group M) increased by 5.8 folds at 1 st week(P＜0.01), 2.3 folds at 2 nd week(P＜0.01) and 1.7 flods at 4 th week(P＜0.05) compared with control group (group C) and MMP-9's activity in group M increased by 4.9 folds (P＜0.01), 1.9 flods(P＜0.01) and 1.4 folds(P＜0.05), respectively. Collagen amount and I/III collagen ratio in group M increased compared with that in group C at 2 nd week and 4 th week. It showed that cardiac myocytes in group M were necrosed and collagen grew abundantly in interstitium under electron microscope.CONCLUSION:The activity of MMPs in the myocardial interstitium increased following myocardial ischemia, then collagen amount and I/III collagen ratio increased, which may be the major causes of ventricular remodeling.     

Experimental study on induction of atherosclerotic plaque instability in rabbits after transfer of wild-type p53 gene

AIM: To study the apoptotic role of wild-type p53 in induction of plaque instability in atherosclerotic rabbits. METHODS: Fifty-four New Zealand White rabbits underwent balloon-induced abdominal aortic wall injury and then were fed on a diet of 1% cholesterol. At the end of the eighth week, the rabbits were randomly divided into two groups: group A and group B. Recombinant adenovirus carrying p53 and β-galactosidase (LacZ) genes were injected in group A and B, respectively. Two weeks later, 10 rabbits each in group A and B was killed and the remaining rabbits all underwent pharmacological triggering with injection of Chinese Russell's viper venom and histamine. RESULTS: Compared with group B, p53 gene over-expression in group A resulted in a marked increase in number of positive apoptotic cells (2.5%±0.8% vs 1.0%±0.3%, P<0.05) and a significant decrease in vascular smooth muscle cells (47.5%±6.8% vs 80.4%±10.6%, P<0.01), the thickness of the fibrous cap ［(132.9±56.7）μm vs （181.8±59.7） μm, P<0.05］ and the cap/intima-media ratio (0.20±0.18 vs 0.21±0.11, P<0.05). CONCLUSION: Transfer of human wild-type p53 genes effectively promotes apoptosis of VSMCs in atherosclerotic plaques, which makes the plaques vulnerable to rupture.     

Effects of high hydrostatic pressure on ADMA metabolism in human vascular endothelial cells and the role of RAS

AIM:To observe the effects of high hydrostatic pressure on asymmetric NG, NG-dimethyl-L-arginine (ADMA) metabolism of human vascular endothelial cells (HUVECs), and the role of renin-angiotensin system (RAS). METHODS:Cultured HUVECs of 3-6th passage were exposed to atmosphere (0 mmHg, APC), 120 mmHg (MPC), 180 mmHg (HPC). There were three groups in each pressure condition, one as control, the other two were interfered with captopril （Cap, 10 μmol/L or 100 μmol/L） or irbesartan （Irb, 10 μmol/L or 100 μmol/L） respectively. Cell proliferation was quantified by determining hexosaminidase activity at 12 h. Concentration of ADMA in conditioned medium was measured by high performance liquid chromatography (HPLC) at 12 h. RESULTS:Compared with APC group, ADMA concentration increased prominently in MPC and HPC (4.69±0.37 and 4.48±0.39 vs 0.75±0.05，P<0.01), but no difference was found between MPC and HPC group. ADMA concentration was not influenced by Cap and Irb in APC, but obviously reduced in MPC and HPC in a dose-dependent manner. CONCLUSION:ADMA is upregulated by high hydrostatic pressure and RAS is involved.     

Contributions of cardiotrophin-1 to cardiac fibroblast proliferation

AIM: To investigated the role of CT-1 in the hypertensive ventricular remodeling. METHODS: The cardiac fibroblasts in 3-4 passages were cultured in vitro, and divided into eight groups according to the different intervention factors: group C (control); group DM: dimethyl sulphoxide (DMSO); group P: cultured under high hydrostatic pressure (160 mmHg); group ASODN: interfered with CT-1 antisense oligodeoxynucleotides (10 μmol/L); group SODN: incubated with CT-1 sense oligodeoxynucleotides (10 μmol/L); group AG: interfered with AG490 (25 μmol/L); group PD: interfered with PD98059 (20 μmol/L); group LY: interfered with LY 294002 (10 μmol/L). Western blotting was employed to assess the expression of STAT3, ERK1/2 and PI3-K respectively at protein level. Cell proliferation was quantified by MTT. RESULTS: High hydrostatic pressure stimulated the proliferation of cardiac fibroblasts, upregulated the expression of CT-1. CT-1ASODN inhibited the proliferation of cardiac fibroblasts (0.132±0.013 vs 0.154±0.011, P<0.05). ASODN extensively inhibited the expression of STAT3, ERK1/2 and PI3-k respectively at protein level (2.09±0.25 vs 2.47±0.28, P<0.05), (1.13±0.19 vs 1.61±0.22, P<0.05), (1.25±0.23 vs1.71±0.25, P<0.05). AG490, a JAK-STAT3 inhibitor, reversed the increase in the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure and the expression of ERK1 phosphorylation (0.118±0.018 vs 0.155±0.010, P<0.05). PD98059, a MAPK-ERK1/2 inhibitor, increased the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure (0.185±0.011 vs 0.155±0.010, P<0.05) and the expression of STAT3 phosphorylation (1.83±0.23 vs 1.58±0.22, P<0.05). LY294002, a PI3-K inhibitor, had no effect on the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure (0.157±0.015 vs 0.155±0.010, P>0.05). No difference of the expression of the above factors was observed in SOND (0.151±0.010 vs 0.154±0.011, P>0.05) and DMSO (0.141±0.017 vs 0.155±0.010, P>0.05) groups as compared with the control group. CONCLUSION: Under high hydrostatic pressure, the proliferation of cardiac fibroblasts is essentially mediated by STAT3, independent of PI3-K and the action is negatively regulated by ERK1/2 via inhibiting STAT3.The interaction between STAT3 and ERK1/2 may assist CT-1 in developing adequate cardiac fibroblast proliferation.     

Significance of soluble CD40 ligand in the vulnerability of coronary atherosclerotic plaque

AIM: To evaluate the significance of serum soluble CD40 ligand (sCD40L) in the vulnerability of coronary atherosclerotic plaque, the relationship between the level of sCD40L and the stenosis degree of the coronary artery by the coronary angiography (CAG), and other inflammatory factors. METHODS: According to WHO diagnostic criterior of coronary heart disease (CHD) and the results of CAG, 84 cases of CHD and 20 cases of non-CHD (NCHD) were included in this study. 84 cases of CHD were divided into three groups: 30 cases in acute myocardial infarction (AMI) group, 30 cases in unstable angina (UA), 24 cases in stable angina (SA). The sera levels of sCD40L in four groups were detected by the enzyme-linked immunosorbent assay (ELISA) and the results were expressed with μg/L. CAG were all conducted in four cases and the results were further evaluated by Jenkins score. ESR and CRP were detected at the same time. RESULTS: The sera levels of sCD40L in four groups were significantly different (P<0.01). The level of sCD40L in AMI group (8.48±4.13) μg/L was higher than that in SA group (4.36±2.68) μg/L, P<0.01 and NCHD group (4.12±1.96) μg/L, P<0.01. The level of sCD40L in UA group (8.72±4.26) μg/L was higher than that in SA group and NCHD group (P<0.01). The level of sCD40L in UA group was slightly higher than that in AMI group, but the difference of two group is not significant (P>0.05). The level of sCD40L in SA group was slightly higher than that in NCHD group, but the difference of two group is not significant (P>0.05). The sera levels of sCD40L in CHD were significantly and positively correlated with Jenkins score (r=0.524, P<0.01). The sera level of sCD40L was positively correlated with the levels of CRP and ESR. CONCLUSION: The sera levels of sCD40L in the patients with various types of CHD are significantly different. The level of sCD40L in the patients with AMI and UA are significantly higher than those in SA and NCHD groups, which may reflect the vulnerability of coronary atherosclerotic plaque. The sera levels of sCD40L is increased with the increasing number of diseased coronary branches and Jenkins score, suggesting that sCD40L promotes atherosclerosis and also can be used as a parameter to predict pathological severity of coronary atherosclerosis. The level of sCD40L is obviously correlated with the levels of CRP and ESR.     

Effects of splenectomy on CD4+ , CD8+ and spleen function in cirrhotic rats with portal hypertension

AIM:To investigate the effect of subtotal splenectomy on the expression of CD4+、CD8+ and tuftsin in cirrhosic rats with portal hypertension (PHT) . METHODS:Rats liver cirrhosis was induced by subcutaneous injection of 40% CCl4. Fifty rats were randomly divided into five groups (n=10). Group A:control rats;group B:PHT rats;group C:normal rats with total splenectomy;group D:PHT with total splenectomy and group E:PHT with subtotal splenectimy. The hepatic function, the expression of CD4+, CD8+, the ratio of CD4+ to CD8+ and tuftsin were analyzed at the fourth week after treatment. RESULTS:The expression of tuftsin ,the ratio of CD4+ to CD8+ was significantly decreased in PHT rats with total splenectomy compared with PHT rats ［（171±21） ng/L vs （433±44）ng/L,P<0.01;(2.01±0.22 vs 1.12±0.12),P<0.01］. In the group of PHT rats with subtotal splenectomy, the expression of tuftsin, the ratio of CD4+ to CD8+ was higher than those in the PHT rats with total splenectomy ［（434±42） ng/L vs （171±21） ng/L,P<0.01;（1.97±0.18 vs 1.12±0.12,P<0.01］, however, the hepatic function was not show difference（P>0.05）. CONCLUSION:Spleen and immune function is significantly improved in PHT rats after subtotal splenectomy, but the hepatic function is not changed significantly.     

Effects of ERK1/2 on pressure overload-induced cardiomyopathy and heart failure in mice

AIM: To explore the changes in extracellular regulated protein kinase (ERK1/2) in the hypertrophic myocardium induced by pressure overload at the different time courses and to determine the molecular mechanism in the myocardium from hypertrophy to heart failure. METHODS: C57/BL mice, aged 12 week old, were subjected to sham-operation (SH) or transversing aortic constriction (TAC) to establish left ventricular hypertrophy. Echocardiographic assessments, hemodynamic determination, organ weight measurement, morphological and histological examination were performed at 1, 4, 8, 12 and 16 weeks after surgery. Meanwhile mRNA levels of atrial natriuretic peptide (ANP), α-myosin heavy chain (α-MHC), bcl-2 and bax were measured by RT-PCR, and ERK1/2 levels were detected by Western blotting. The animals in SH group were performed the same tests then sacrificed at 16 weeks. RESULTS: (1) Compared to SH group, LVESd, LVEDd, Awsth, Awdth, Pwsth and Pwdth progressively increased after TAC. Meanwhile, ejection fraction (EF%) significantly decreased at 16th week (P<0.05). LVSP, dp/dtmax and dp/dtmin in TAC group were progressively increased after 4 weeks. From 8-12 weeks these parameters maintained stable and then sharply decreased at 16th week (all P<0.05). However, LVEDP was statistically increased at 8th week. These echocardiographic and hemodynamic changes indicated a development of LVH and eventually progressing towards to heart failure. (2) Histologically, cardiac collagen measured by percentage of Sirius red positive stained area and apoptosis index showed progressive increases from 4 to 16 weeks. (3) Compared to SH group, mRNA levels of ANP was time-dependently increased while α-MHC and Bcl-2 were time-dependently decreased. The ratio of Bcl-2 /Bax was decreased. Phosphorylation of ERK1/2 was increased at 4th week, then decreased with age of TAC (all P<0.05). CONCLUSION: Pressure-overload induced by TAC results in a development of LVH from early concentric hypertrophy to late eccentric hypertrophy, and eventually toward cardiac dysfunction or heart failure. Those changes are associated with increase in cell size and cardiac fibrosis. ERK1/2 signaling pathway may involve in the regulation of myocardial cell apoptosis in hypertrophic and failure heart.     

Changes of coronary flow reserve and myocardial blood flow after coronary microembolization

AIM:To investigate the changes of coronary flow reserve (CFR) and myocardial blood flow (MBF) after coronary microembolization (CME).METHODS:The left anterior descending coronary artery of 12 pigs was embolized by injection of 42 μm microspheres with a total of 120 000.Study was divided as acute study (base, 2 h and 6 h) and chronic study (base and 1 week).CFR was measured using Doppler wire.Regional myocardial blood flow (MBF) was detected using colored microspheres.Serum endothelin-1(ET-1) was determined by ELISA.RESULTS:CFR decreased significantly after CME at acute phase (2.10±0.60 at baseline, 1.40±0.10 at 2 h and 1.10±0.10 at 6 h, 2 h and 6 h compared with base, P<0.01, respectively).At chronic phase, CFR was 2.03±0.43 at base and 1.58±0.22 at 1 week after CME.No changes were found for MBF at acute and chronic study.Serum ET-1 only elevated at 6 h after CME.CONCLUSION:CFR decreases with time at acute phase after CME and resumes 1 week later.Changes of CFR correlate with changes of endothelial function.Changes of CFR and MBF are mismatched after CME.     

Role of free hemoglobin and its receptor CD163 in the rat atherosclerosis formation

AIM: To investigate the influence of free hemoglobin on the initiation and progression of atherosclerosis and the role of CD163 in this process.METHODS: Thirty male SD rats were randomly divided into three groups: control group (group C),atherosclerosis group (group A),atherosclerosis and hemolysis group (group P).The hemolysis and atherosclerosis animal model was established.The free hemoglobin（FHb） and MDA levels in plasma,(RAAPIs) and intima area/midmembrane area (I/M) of each group were measured.The expressions of CD163 and heme oxygenase-1 (HO-1) in atherosclerosis plaques in group A and P were detected and measured by means of immunohistochemistry and Western blotting.RESULTS: Compared with group C,the FHb,MDA,CD163 and HO-1 in group A and group P increased significantly (P<0.05).Compared with group A,the RAAPIs,FHb,MDA,CD163 and HO-1 in group P increased significantly (P<0.01),while the I/M had no significant difference (P>0.05).The FHb level in plasma and the expressions of CD163 and HO-1 in atherosclerotic plaques correlated with each other (r=0.526，r=0.498，r=0.653；P<0.01).CONCLUSION: Free hemoglobin promoted the initiation and progression of atherosclerosis through facilitating lipid peroxidation,and upregulating the expressions of CD163 and HO-1.     

Effect of rosiglitazone on myocardial energy substrate utilization in type 2 diabetic rats

AIM: To study the effect of rosiglitazone (RSG) to improve insulin sensitivity on myocardial energy substrate utilization as well as the cardiac function in a rat model of type 2 diabetes mellitus. METHODS: Sprague-Dawley rats were conducted into three groups: chow-fed rats were fed with normal chow (12% of calories as fat); fat-fed/STZ rats were fed with high-fat diet (40% of calories as fat) for 4 weeks and then injected with streptozotocin 35 mg/kg intraperitoneal; fat-fed/STZ/RSG rats were fat-fed/STZ rats treated with rosiglitazone (3 mg·kg-1·d-1) for 2 weeks. A cannula connected to a passive transducer was inserted the heart for the measurement of the cardiac function including heart rate (HR), left ventricular end-diastolic pressure (EDP) and ±dp/dtmax. Then the isolated hearts were mounted onto a Langendorff perfusion apparatus to perfuse with Krebs-Henseleit buffer in the presence of 5 mmol/L glucose and 0.4 mmol/L ［3H］ labelled palmitate. Glucose uptake and ［3H2O］ collection were measured to evaluate the rate of carbohydrate and fatty acid oxidation. RESULTS: Compared with the chow-fed rats, fat-fed/STZ rats had a significantly depression of glucose uptake in the hearts ［(54.7±6.2 vs 69.0±5.7) μmol·g-1 dry weight, P<0.01］ after 30 min perfusion. The oxidation of glucose and palmitate were 18% and 82%, respectively. Paralleling the reduction was a change of EDP ［(14.3±1.8 vs 10.5±1.1) mmHg, P<0.05］ and -dp/dt ［(550±57 vs 650±42) mmHg/s, P<0.01］, indicating a impaired left ventricular diastolic function. In the hearts subjected to fat-fed/STZ group, rosiglitazone treated for 2 weeks resulted in a elevated level of glucose uptake ［(63.5±6.4 vs 54.7±6.2) μmol·g-1 dry weight, P<0.05］. A protective role of the ventricular function ［EDP decreased from （14.8±1.9） to （11.0±0.8） mmHg/s and -dp/dtmax increased from （558±60） to （629±51） mmHg/s, P<0.05］ were observed. CONCLUSIONS: Our study indicates that there is a depression of glucose oxidation and at increase in fatty acid oxidation in type 2 diabetic hearts. Elevation of insulin sensitivity using rosiglitazone increases the myocardial glucose metabolism and shows a benefitial result to heart functions.     

Comparison between mobilization and transplantation of bone marrow stem cells for the therapy of myocardial infarction in rabbits

AIM: To compare bone marrow stem cell mobilization with bone marrow-derived mononuclear cells (BMCs) transplantation for the therapy of myocardial infarction (MI) in rabbits, and to explore more effective and practical stem cell therapeutic strategy for MI. METHODS: In mobilization group (M, n=10), granulocyte-colony stimulating factor (G-CSF) (30 μg·kg-1·d-1) was injected subcutaneously 3 hours after MI and every 24 hours for 5 days. On the 5th day, the BMCs from 10 mL peripheral blood were labeled with bromodeoxyuridine (BrdU) for 24-48 hours, then reinjected intravenously. In transplantation group (T, n=10), BMCs transplantation was performed 5-7 days after MI. After being obtained from bone marrow (3-5 mL) of iliac crest and labeled with BrdU for 24-48 hours, BMCs were transplanted into infracted myocardium through intramyocardial injection. Control animals (C, n=10) did not receive any treatment after MI. Echocardiography were performed for the evaluation of cardiac function 1 week and 5 weeks after MI. Hemodynamic studies and histological study were performed 5 weeks after MI. RESULTS: LV ejection fraction increased significantly in group M, had no change in group T, and decreased 1 week and 5 weeks after MI in group C. Group M and group T had higher LV max +dp/dt and max -dp/dt, lower LV end-diastolic pressure compared with group C 5 weeks after MI. Histological studies revealed that there were BrdU positive cells in the infarcted area in group M and group T. The vascular density of group M and group T in the infarcted area was significantly greater in comparison with group C. No regeneration of smooth muscle cells and cardiomyocytes were found in the infarcted area. CONCLUSION: Bone marrow stem cell mobilization with G-CSF and transplantation of BMCs both significantly improve the cardiac function for the therapy of MI through vascular genesis in the infarcted area. Bone marrow stem cell mobilization may offer a new and non-invasive therapeutic strategy for MI.     

Inhibitory effect of high-dose Xuezhikang on inflammatory response induced by percutaneous coronary intervention in patients with unstable angina

AIM: To study the inhibitory effect of high-dose Xuezhikang,administered before percutaneous coronary intervention (PCI) on inflammatory response induced by PCI in patients with unstable angina (UA).METHODS: All patients with UA in class Ⅲ and ⅡB according to Braunwald classification were considered for inclusion in the present study.Finally,196 patients received Xuezhikang treatment 72 h before coronary angiography and successfully performed PCI with elevated C-reactive protein (CRP) level (>3 mg/L) were randomised to 2 groups: 1.2 g/d of Xuezhikang as group A,or 2.4 g/d of Xuezhikang as group B.The levels of CRP were measured at baseline,after 3 days of therapy (before procedure) and 48 hours after PCI.The patients were followed-up for 6 months for major adverse coronary events and left ventricular ejection fraction.RESULTS: There was no significant difference in the mean CRP level among the two randomized groups (P>0.05),however,after three days of pharmacological treatment,there was significantly reduced CRP content in group A ［(5.44±1.57） mg/L vs （4.04±1.54） mg/L,P<0.05］ and in group B ［(5.42±1.36） mg/L vs （3.60±1.14） mg/L,P<0.05］ compared with admission.Measurements performed 48 hours after the procedure revealed a marked CRP level increase in group A (up to 9.22 mg/L±5.03 mg/L) and an obvious increase in groups B (up to 4.97 mg/L±1.75 mg/L,P<0.05) compared with pre-procedure.The serum level of CRP in B group was distinctly lower than that in A group before (P<0.05) and after the procedure (P<0.05),respectively.Major adverse coronary events during the 6-month clinical follow-up occurred less in group A than that in group B ［21/104 (20.2%) vs 9/92 (9.8%); patients,P<0.05］.Follow-up echocardiography revealed lower left ventricular ejection fraction in group A than that in group B (55.41%±10.93% vs 59.30%±9.99%,P<0.05).CONCLUSION: High-dose Xuezhikang therapy,administered before PCI,has better inhibition effect than low-dose on inflammatory response induced by PCI in patients with UA.Attenuation of inflammatory response may be crucial for the reduction of coronary events following invasive coronary interventions.     

Inhibitory effect of hypoxia preconditioning on hypoxia/reoxygenation-induced apoptosis in cardiomyocytes

AIM: To study the role of hypoxia preconditioning (HP) in hypoxia-reoxygenation (HR)-induced apoptosis in neonatal rat cardiomyocytes and the possible mechanisms. METHODS: Cultured neonatal rat cardiomyocytes were divided into three groups: normal group, HP+H/R group and H/R group. Acridine orange (AO) staining was performed to detect morphological changes of apoptotic cells. Apoptosis rates of cardiomyocytes were detected by flow cytometry. Colorimetric assay was used to detect caspase-3 activity. Expression of Bcl-2 protein was detected by immunohistochemistry combined with computer image analysis. RESULTS: Apoptotic cells were detected by AO staining after hypoxia of 6 h followed by 3 h-reoxygenation. The hypodiploid apoptotic peak was detected by flow cytometry with the apoptotic rates of (29.7±5.4)%. A significantly reduced apoptotic rates of (7.8±1.3)% was detected in HP group（P＜0.01）. The caspase-3 relative activity of cardiomyocytes induced by H/R was 5.9±0.8, significantly higher than that of control group. HP markedly reduced caspase-3 relative activity to 2.6±0.5 in contrast with H/R group （P＜0.01）. Bcl-2 protein was positive in normal cardiomyocytes with an A value of 119.4±7.1. The A value of H/R group was 99.6±5.0, significantly lower than that in normal group （P＜0.01）. The A value of HP+H/R group was 126.5±6.2, significantly higher than that in H/R group（P＜0.01）. CONCLUSION: HP inhibits H/R-induced apoptosis of cardiomyocytes by improving the expression of Bcl-2 and reducing caspase-3 activity.     

Electrophysiological characters in a noble model of atrial fibrillation induced by left atrium pacing after right atrial infarction

AIM: To explore a noble chronic atrial fibrillation model induced by left atrium pacing after right atrial infarction and to investigate the atrial electrophysiological characters of the model. METHODS: 24 rabbits were randomly divided into 3 groups: control group (C group, n=8), pacing group (P group, n=8), artial infarction+pacing group (I group, n=8). C group: a pacing pole was fixed under adventitia of the left atrium without pacing; P group: a pacing pole was fixed under adventitia of the left atrium with 1 000 beats/min of pacing; I group: the animals were placed under 1 000 beats/min of left atrial pacing after ligating the atrial branch of right coronary artery. The technique of programmed stimulating was used to measure electrophysiological indexes of atrial in the groups. RESULTS: (1) After 3 weeks pacing AF was induced with a higher rates, and reached to 100% in I group. (2) At driving cycle length of 200 ms, ERPA was (115.0±7.6) ms in C group, (81.3±12.5) ms in P group and (87.5±12.8) ms in I group, which were statistically shorter in the later two groups compared to control group (both P<0.01). (3) I group and P group showed a significantly poor performance of frequency adaptability compared to control group after 3 week stimulation (P<0.01, P<0.05, respectively). (4) 3 weeks after pacing, the interval of P-wave in I group was significantly prolonged compared to P group and C group (P<0.05, P<0.01, respectively). (5) ERPA was obviously shortened and RRPA was prolonged significantly in I group compared to control group (P<0.01, respectively). Inter-atrial conduction defect (IACD) was significantly prolonged in I group compared to C group and P group after 1 h to 3 week stimulation (P<0.01, respectively). CONCLUSION: Compared to the traditional AF model induced by pacing only, a noble model of left atrium pacing after right atrial infarction has a higher AF incidence. The apparent electrophysiological changes of the AF model include: shortening of ERPA, the frequency inadaptability, extension of P-wave interval and prolonged RRPA as well as IACD.     

Changes of the expression of CD27 and CD28 on cytokine-induced killer cells and natural killer cells during four week cultivation

AIM:To investigate the changes of CD27 and CD28 expression on cytokine-induced killer(CIK) cells and natural killer(NK) cells during cultivation.METHODS:The mononuclear cells were treated with interleukin-12(IL-2),IL-7,IL-15,stem cell factor and FLT3 ligand for four weeks.The CD27 and CD28 expression on CD3+CD56+ CIK cells and CD3-CD56+ NK cells were examined by flow cytometric analysis every week during four-week cultivation.RESULTS:The expression of CD27 on CIK and NK cells two weeks after cultivation reached the peak value at（44.57±4.07）% and（51.02±5.20）%, respectively.Then, their expression declined gradually to about 30% in the fourth week.The expression of CD28 on CIK and NK cells reached the peak at the third and the second week, the values were （4.40±0.66）% and （45.14±3.58）%, respectively, decreased rapidly and then were almost completely lost at the fourth week.CONCLUSION:According to the changes of expressions of CD27 and CD28 on CIK/NK cells, optimal harvest time of cultured CIK/NK cells should be at the third week of cultivation.     

Effects of atorvastatin on nitric oxide,endothelin-1 and myocardial function in a rabbit model of acute myocardial infarction and reperfusion

AIM: To evaluate the effects of atorvastatin on nitric oxide(NO), endothelin-1(ET-1)and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion(AMI/R). METHODS: Twenty-four rabbits were randomized into 3 groups: 8 in AMI/R group, 8 in atorvastatin-treated group(5 mg·kg-1·d-1)and 8 in sham-operated group. Animals in the former two groups were subjected to 60 min of coronary occlusion followed by 120 min of reperfusion. Data on haemodynamics were collected. NO in blood sample, and in normal, and in infarcted reflow and no-reflow myocardium were evaluated respectively by nitrate reductase method. The levels of ET-1 in blood sample, and in normal, infarcted reflow and no-reflow myocardium were determined by radioimmunoassay. RESULTS: (1)Compared to the baselines, the heart rate(HR), systolic blood pressure(SBP), diastolic blood pressure(DBP), left ventricular systolic pressure(LVSP), maximal rate of increase and decline in left ventricular pressure(±dp/dtmax)and cardiac output(CO)in AMI/R and atorvastatin-treated groups were significantly declined, whereas left ventricular end-diastolic pressure(LVEDP)was increased after 60 min of coronary occlusion and 120 min of reperfusion(P<0.05 or P<0.01). However, in atorvastatin-treated group, LVSP, LVEDP, ±dp/dtmax and CO at the time point of 120 min of reperfusion recovered more significantly than those at the time point of 60 min of coronary occlusion(P<0.01), which was more significant than those in AMI/R group(P<0.05 or P<0.01). Compared to AMI/R group, the SBP and DBP were significantly heigher in atorvastatin-treated group(P<0.01).(2)In atorvastatin-treated group, the levels of ET-1 in blood sample were significantly lower than those in AMI/R group(P<0.01), and the levels of NO were significantly higher(P<0.01). Moreover, the levels of NO or ET-1 in infarcted reflow myocardium were significantly lower than that in AMI/R group(P<0.05 or P<0.01).(3)Atorvastatin could ameliorate myocardial function. CONCLUSION: Atorvastatin is effective in increasing NO and reducing ET-1 in blood plasma and local myocardium, and in protection of endothelial cells. Atorvastatin also has a beneficial effect on improving left ventricular function during acute myocardial infarction and reperfusion in rabbits.