目的：探讨转化生长因子β1（ TGF-β1）及其受体对血管损伤后内膜增殖的作用及机制。方法培养 SD大鼠正常及损伤颈动脉血管平滑肌细胞，应用逆转录PCR（RT-PCR）及蛋白印迹（Western印迹）方法分别检测血管平滑肌细胞（VSMCs）生物学标记物 SM22α，Matrix Gla，Os-teopontin；TGF-β1，纤维连结蛋白（FN）及TGF-β1Ⅰ型和Ⅱ型受体（TGF-β1-RⅠ，TGF-β1-RⅡ）mRNA和蛋白质的表达。结果①TGF-β1呈浓度依赖性刺激损伤颈动脉VSMCs增殖；但在0.2％血清条件下，TGF-β1浓度依赖性抑制正常颈动脉VSMCs增殖；②正常组 VSMCs SM22αmRNA表达水平明显高于损伤组VSMCs；而Matrix Gla及Osteopontin损伤组VSMCs的表达水平则显著升高；③损伤组VSMCs TGF-β1 mRNA和蛋白质的表达水平显著高于正常组，且FN的合成也较正常组显著增高；④损伤组TGF-β1-RⅠ mRNA和蛋白质的表达与正常组并无明显差别；但TGF-β1-RⅡ的表达水平损伤组却显著高于正常组。结论血管损伤后，VSMCs表型发生改变，呈现异常增殖，合成和分泌TGF-β1及FN明显增多；TGF-β1对损伤后VSMCs有显著促增殖效应；同时血管损伤后VSMCs TGF-β1不同受体亚型的表达也发生了变化。

[ABSTRACT]AIM:ToevaluatetheeffectsofantisenseTGF-β1oligodeoxynucleotide(ASTGF-β1)ontheex-pression of TGF-β1 , deposition of extracellular matrix ( ECM) and the neointima formation in the arteries after balloon inju-ry.METHODS:The unmodified and phosphorothioate-modified AS TGF-β1 which containing 15 bases and surrounding the initiation codon region (ATG) of rat TGF-β1 complementary DNA (cDNA) were designed.At the same time, sense TGF-β1 oligodeoxynucleotide ( S TGF-β1 ) with the base sequence complement to AS TGF-β1 was synthesized as a control . The oligodeoxynucleotides were introduced into in vivo and in vitro experiments , respectively .RESULTS:The AS TGF-β1 significantly inhibited the protein expression of TGF-β1 in a concentration-dependent manner , and S TGF-β1 did not have the same effect.Furthermore, no effect of the AS TGF-β1 on the mRNA expression of TGF-β1 in injured VSMCs was ob-served.Moreover, for the injured VSMCs, AS TGF-β1 significantly and concentration-dependently inhibited the basal DNA synthesis.Both AS TGF-β1 and S TGF-β1 did not exhibit dose-dependent effects on DNA synthesis in uninjured VSMCs . Fibronectin ( FN) mRNA expression in injured VSMCs was significantly decreased by AS TGF-β1 in a concentration (0.01~1 μmol/L)-dependent manner .AS TGF-β1 significantly increased the mRNA expression of contractile marker SM 22α, and decreased the mRNA expression of synthetic markers osteopontin and matrix Gla , especially at the concentration of 0.01μmol/L and 0.1 μmol/L.After treatment with AS TGF-β1 (90 μg· kg-1 · d-1 ) for 28 d, the neointima formation was significantly inhibited , and the area ratio of intima/media was markedly decreased by 68% compared with untreated group , but S TGF-β1 had no effect on neointimal formation .CONCLUSION:The AS TGF-β1 specifically inhibits the pro-tein expression of TGF-β1 in the VSMCs derived from injured arteries .Moreover , it significantly inhibits DNA synthesis and cell proliferation, and decreases the expression of FN .Therefore, AS TGF-β1 dramatically attenuates neointima formation after balloon njury .The effects of AS TGF-β1 on the injured VSMCs may be associated with its reverse effects on the altera-tion of VSMC phenotype after balloon injury .

Objective:To observe the effects of Notch signaling pathway on the differentiation of embryonic stem cells to myocardial cells.Methods:The experiments were divided into two parts:regulating the switch of Notch signaling pathway to study the effects on differentiation rates of embryonic stem cells to cardiomyocytes,and determining the expression of myocardium differentiation related proteins.Mouse embryonic stem cells were labeled with DAPI fluorescence(200 μg/ml).Then Jagged protein(5 mg/L),an activator of notch signal,or MW167(100 μmol/L),an inhibitor of notch signal,was added to culture embryonic stem cells for 14 days.The appearance of spontaneously contractive cells was observed under phase contrast microscope.The expression of myocardial specific contractive protein was identified by cell immunofluorescence assay,and the differentiation ratio of embryonic stem cells to cardiomyocytes was calculated.The expression of myocardial differentiation related proteins were identified by Western blot.Results:At the 14th day,there were about 15% embryonic stem cells differentiated into spontaneously contractive cardiomyocytes,and the differentiation ratio was significantly reduced with Jagged treatment,whereas dramatically increased with MW167 treatment.Western blot results suggested that the expression of early myocardial differentiation related proteins were significantly reduced when cells were treated with Jagged,whereas dramatically increased when the cells were treated with MW167.Conclusion:Jagged protein inhibits the differentiation of embryonic stem cells to cardiomyocytes through activating notch signaling pathway,however,MW167 can promote the differentiation of embryonic stem cells to cardiomyocytes through inhibiting notch signaling pathway.

Objective:To investigate the relationship of electrophysiological remodeling and arrhythmias via observing the alterations of QT interval and action potential duration(APD)in ventricular of diabetic rabbits in vivo.Method:Diabetes was induced by a single injection of alloxan(145mg/kg,i.v.)in rabbits.After the devel- opment of diabetes(10weeks),the main electrophysiological parameters and ventricular effective refractory period (ERP)as well as arrhythmias induced by program and burst-pacing electrical stimulation protocols were perfo- romed using ECG measurements and monophasic action potential recording in healthy and diabetic rabbits.Result: Compared with control group,heart rate was significantly retarded and QT interval was lengthened(all P0.05) in diabetic group.Moreover,ST segment was remarkedly altered upward and T amplitude was increased(all P 0.05)in diabetic group.The phases of AP of ventricular myocytes in diabetic rats were obviously wider than that in control rats.Compared with control group,the duration of AP at 10%,20%,and 50%level of repolarization (APD10,APD20and APD50)were significantly elongated in diabetic group(all P0.05).ERP was also obviously prolongated from (105.21±9.78)ms in control group to(168.95±10.03)ms in diabetic group(P0.05).Ven- tricular arrhythmias and/or fibrillation evens were markedly induced with occurrence of 87.5% by burst-pacing. Conclusion:The diabetic cardiomyopathys are significant vulnerabilities to ventricular arrhythmias,which is attrib- uted to severely electrophysiological remodeling in diabetic nullitus.

Objective To investigate the effects of diabetes on action potential(AP) and transient outward potassium current(Ito) in ventricular myocytes in rats.Methods Diabetes was induced by a single injection of streptozotocin(STZ,65 mg/kg,i.v.) in rats.At 14 weeks after STZ-treatment,AP and Ito were recorded via whole-cell patch clamp technique in enzymatically dissociated single rat ventricular myocytes coming from control and diabetic group.The dynamic curves of Ito were fitted by Boltzmann equations or biexponential function according to relationship between current densities and clamp voltage of Ito in contral and diabetic group.Results The phases of AP of ventricular myocytes in diabetic group were obviously wider than that in control group.Compared with control group,the AP duration(APD) at 20,50 and 90% level of repolarization(APD20,APD50 and APD90) were significantly elongated in diabetic group(64.3±7.5 ms vs 29.7±9.2 ms;174.3±6.8 ms vs 98.9±4.2 ms;276.7±8.3 ms vs 173.7±7.2 ms,all P0.01,n=12).With the +50 mV clamp potential,the current densities of Ito were significantly decreased from 17.43±1.98 pA/pF in control group to 11.51±1.37 pA/pF in diabetic group(P0.05,n=12).Compared with control group,The I-V curve of Ito was vitally suppressed downward,and the steady-state inactivation curve of Ito was significantly shifted to left(P0.01,n=12),as well as the recovery time of inactivation of Ito was markedly retarded in diabetic group.Conclusion APD of ventricular myocytes in diabetic rats is significantly prolongated,which is attributed to decrease of current densities of Ito,and acceleration of inactivation of Ito,as well as inhibition of recovery of inactivation of Ito in ventricular myocytes of diabetic rats.

Objective:To observe the effects of Jagged protein on the differentiation of embryonic stem cells to myocardial cells.Methods:Mouse embryonic stem cells were labelled by fluorescent dye DAPI(200 mg/L).Then Jagged protein(5 mg/L),the activator of notch signal,was added to embryonic stem cells in vitro for 14 days.The spontaneously contractive cells were observed under phase contrast microscope,ultra microstructure of spontaneously contractive cells were observed under transmission electron microscope.The expression of myocardial specific contactive protein was identified by cell immunofluorescent assay,and the differentiation ratio of embryonic stem cells to cardiomyocytes was calculatd.Results:The spontaneous differentiation of embryonic stem cells is strong.On the 14th day,there were about 15% embryonic stem cells differentiated into spontaneously contractive cardiomyocytes.When Jagged protein was added,the differentiation ratio was significantly reduced.Conclusion:Jagged protein added to embryonic stem cells activates the notch signal,which would inhibit the differentiation of embryonic stem cells to cardiomyocytes.

Objective To investigate properties of electrophysiology and effects of ouabain on transient outward potassium current (Ito) and L-type calcium current (ICa-L) of left atrium posterior wall (LAPW) and left atrium appendage tissue (LAA) of rabbit, it could provide the scientific explanations that LAPW and ouabain could enhance atrial fibrillation (AF) vulnerability via increasing electrophysiological heterogeneity and electrical remodelling of different region of left atrium in rabbits. Methods Atrial myocytes coming from LAPWs and LAAs of rabbits perfused via vitro heart perfusion system were obtained by enzymatic dissociation. The whole-cell patch-clamp technique was used to assess effects of ouabain on Ito and ICa-L. The current-voltage (I-V) curves of Ito and ICa-L on LAPW and LAA myocytes were fitted before and after of ouabain administration. Results (1) With holding potential −50 mV and commanding potential +50mV, the current densities of LAPW Ito were decreased slightly less than that of LAA Ito in control groups in control groups (p>0.05). After administration of ouabain. the current densities of LAPW Ito were significantly larger than that of LAA Ito ((10.97±0.58) pA/pF vs (9.39±0.83) pA/pF, p<0.05, respectively). The I∼V curve of LAPW Ito was gently lowered to I∼V curve of LAA Ito in control groups. But with perfusion of ouabain, the I∼V curve of LAPW Ito opposed to I∼V curve of LAA Ito was significantly changed from the bottom to the top with same upward direction. (2) At voltage clamp protocol of ICa-L, the current densities of LAPW ICa-L were markedly decreased compared with that of LAA ICa-L in control groups (p<0.05). With the addition to ouabain, the peak of amplitude of LAPW ICa-L at +20 mV was obviously increased to that of LAA ICa-L ((−11.13±0.99) pA/pF vs (−8.86±0.51) pA/pF, p<0.01, respectively). At the control groups, the I∼V curve of LAPW ICa-L was arranged the bottom of all I∼V curves of ICa-L. The I∼V curve of LAPW ICa-L, but through effects of ouabain, was completely upgraded to the top of other I∼V curves of ICa-L. However, all shapes and directions of current peak of I∼V curves of ICa-L were not changed between the control group and ouabain groups. Conclusion The distribution properties of ICa-L have significant difference on LAPW of rabbit. Ouabain could accentuate the electrophysiological heterogeneity and electrical remodelling of Ito and ICa-L in LAPW of rabbits. It might contribute trigger and persistence factors to AF vulnerability.

BACKGROUND:Atrial fibrillation (AF) is a common complication of myocardial infarction (MI). Angiotensin II receptor antagonists prevent the promotion and propagation of AF. However, the activation of the acetylcholine-regulated K(+) current (I(K,ACh)) in the atrium after MI and the effect of valsartan on I(K,ACh) are less understood.METHODS:Twenty-four adult rabbits were randomly divided into three groups: sham-operated, MI and MI plus valsartan administration (MI+valsartan). The sham-operated group received a median sternotomy without left ventricular coronary artery ligation. Both the MI group and the MI+valsartan group received a median sternotomy followed by ligation of the midpoint of the left ventricular coronary artery. The MI+valsartan group was administered oral valsartan for 12 weeks. After 12 weeks, the initiation of AF was measured by vagal stimulation followed by quick excision of the heart. I(K,ACh) in the left atrial myocardium was measured by the patch clamp technique.RESULTS:AF was induced in four animals in the MI group, two in the sham-operated and two in the MI+valsartan groups, with the total AF duration expectedly longer in the MI group than in the sham-operated and MI+valsartan groups (38 s versus 9 s and 9 s, respectively). Furthermore, the mean (+/- SEM) density of I(K,ACh) increased significantly more in the left atrial myocardia of the MI group than in the sham-operated and the MI+valsartan groups (-13+/-0.42 pA/pF versus -9+/-0.38 pA/pF and -10+/-0.37 pA/pF, respectively at -100 mV; and 4.1+/-0.28 pA/pF versus 3.1+/-0.27 pA/pF and 3.3+/-0.27 pA/pF, respectively at 20 mV; P<0.05). However, there was no statistically significant difference in I(K,ACh) between the sham-operated group and the MI+valsartan group.CONCLUSIONS:AF is associated with increased I(K,ACh) after MI. Inhibition of increased IK,ACh may be the mechanism by which valsartan prevents AF following MI.

OBJECTIVE:To investigate the effects of recombinant BmKIM (poly-peptide derived from Asian Scorpion Buthus martensi Karsch) on the sodium current (I(Na)) of isolated ventricular myocytes, transmembrane action potential and aconitine induced arrhythmia in vivo in rabbits.METHODS:Ventricular myocytes were enzymatically dissociated from adult rabbits. Whole-cell patch-clamp technique was used to record voltage-dependent I(Na). Standard transmembrane action potentials in rabbit hearts in vivo were recorded by using floating glass microelectrodes. Incidence of arrhythmias, the early after depolarization (EAD) and/or delay after depolarization (DAD) were measured in vivo in rabbits post aconitine (100 microg/kg, iv) in the absence or presence of BmKIM (50 microg/kg iv).RESULTS:(1) BmKIM significantly inhibited I(Na) in a voltage-dependent manner and significantly shifted the I-V curves of I(Na) upward. BmKIM left shifted the inactivation curve of I(Na) and voltages at 50% inactivation of I(Na) were changed from (-70.8 +/- 2.6) mV to (-84.8 +/- 3.5) mV (P < 0.05). BmKIM prolonged the recovery of inactivation of I(Na). In the presence of BmKIM, the time constants of recovery (both tau(f) and tau(s)) of I(Na) were significantly prolonged from (28.9 +/- 6.1) ms and (107 +/- 21.6) ms in control group to (54.2 +/- 7.9) ms (P < 0.05) and (211.1 +/- 34.6) ms (P < 0.01), respectively. (2) BmKIM significantly shortened 50% and 90% of action potential duration (APD(50) and APD(90)), and reduced action potential amplitude (APA), declined maximum up stroke velocity of action potential (V(max)) in vivo. The Q-T duration was shortened and heart rate significantly increased post BmKIM injection. (3) Incidence of aconitine induced ventricular arrhythmias (77.8%) was significantly reduced by BmKIM (22.2%, P < 0.01).CONCLUSIONS:BmKIM significantly blocked I(Na) through affecting the inactivated state of I(Na) in rabbit ventricular myocytes. BmKIM could attenuate the influx of I(Na), therefore shorten action potential duration and reduce action potential amplitude and reduce the incidence of aconitine induced arrhythmias.

Objective:To study the clinical value of head-up tilt table test in elderly patients with unexplained syncope.Methods:A total of 140 elderly patients with unexplained syncope underwent in quiet circumstance.Heart rate and blood pressure were monitored simultaneously.Results:Eighty(malefemale,4337) of 140 elderly patients with unexplained syncope were positive by head-up tilt table test.In which the patients with hemodynamic pattern of vasodepressor was 39(malefemale,2118) cases,the cardioinhibitore pattern 9(malefemale:45) cases,mixed pattern 32(malefemale:1814) cases.In the subjects with vasodepressor response,systolic blood pressure(SBP) and diastolic blood pressure(DBP) abruptly decreased at syncope,it decreased from(122±1469±15)mmHg to(82±1545±10)mmHg(P0.01).In the subjects with cardioinhibitory response,heart rate before immediate syncope was(95±17) bpm and abruptly decreased by(51±8) bpm(P0.01) when syncope occurred.For the subjects with mixed response,heart rate abruptly decreased from(110±21) bpm to(63±21) bpm(P0.01) at syncope;meanwhile SBP and DBP abruptly decreased,it decreased from(115±1865±18)mmHg to(83±1946±10)mmHg(P0.01).Conclusion:Head-up tilt table test is an effectively diagnostic method in elderly patients with unexp1ained syncope,and the most common type is vasodepressor response.There is no difference in different gender groups at the positive rate and the distribution of the model of hemodynamic response in elderly.

Aims:The aim of this study is to evaluate the effect of carvedilol-induced heart rate changes on left ventricular function and physical capacity in heart failure (HF) patients.Material and methods: A total of 96 patients, with systolic HF, ejection fraction , 40%, and NYHA class II/III not receiving b-blockers.Depending on changes in heart rate at rest (HRr) from baseline to 3 months after carvedilol treatment, two groups were identified: Group I-with an early response to b-blocker (62 patients) and reduction in HR and Group II-with a late response to b-blocker (34 patients) and unchanged or increased HR at 3 months.We analysed functional capacity according to NYHA, HRr, echocardiographic parameters, physical capacity during a cardiopulmonary exercise (CPX) test, heart rate variability in 24 h ECG recording, and plasma brain natriuretic peptide levels.Results: At baseline, Group I showed higher HRs (P ¼ 0.04).At 3 months, HRr was reduced in both groups, however, HRr remained higher in Group II (P ¼ 0.04).In Group II, fNYHA class was not improved, left ventricular ejection fraction was reduced (P ¼ 0.04), and E/A was increased (P ¼ 0.003).The duration of CPX was increased in both groups as compared with baseline values, but VO 2 peak increased in Group I only and remained unchanged in Group II.In Group II but not in Group I, VE/VC02 was increased.Conclusion: Changes in heart rate at 3 months after treatment may be a valuable measure of response to b-blocker therapy.No changes in heart rate at 3 months after treatment may reflect poorer potential for improvement in echocardiographic parameters and physical capacity in patients with chronic HF treated with b-blockers.

59例平板运动试验阳性或可疑阳性并且行选择性冠状动脉造影(SCA)的患者,根据SCA结果分组,无冠心病组,80%ST段变化发生在运动峰值之前以及运动峰值,单支病变组45%在运动停止后或者运动峰值和运动后;多支病变组90%在运动早期或运动峰值。三组ST段下移持续时间无差异。结论:平板运动试验ST段变化特点受冠状动脉病变程度的影响。

Objective: We investigated the electrophysiological effect of vagal stimulation (VS) on atrial myocardium in vivo and differential densities of M-2 receptor and acetylcholine-induced inward rectifier K+ current (I-K,I-ACh) to discuss the mechanisms of atrial fibrillation (AF).Methods: With the monophasic action potential (MAP) recording technique, data from twenty-four sites, i.e. right atrial appendage (RAA), left atrial appendage (LAA), right atrium (RA) and left atrium (LA) were recorded by electrode probes, which were applied to the epicardial atrial surface of each dog. After cervical vagosympathetic cut, VS1 (20 Hz, 0.2 ms pulse duration and at a voltage 10 V), VS2 (20 Hz, 0.2 ms pulse duration and at a voltage 30 V) and sinus node (SN) damage were administrated respectively. MAP, dispersion of action potential duration (dAPD) and AF was recorded. Then, RAA, LAA, RA and LA were dissected. Finally, distribution of M-2 receptors and I-K,I-ACh in atrial myocardium were measured by western blot and patch clamp respectively.Results: During VS1 and VS2, AF could be induced at first in right atrial appendage (RAA) and right atrium (RA) without left atrial appendage (LAA) and left atrium (LA). Compared to the parameters in control group and VS2 group, dAPD was increased significantly by VS1 and SN damage, but there was no significant difference between control group and VS2 group. However, AF was not evoked after SN damage. Densities of M-2 receptor and IK, ACh were higher in RAA, LAA than those in LA and RA (M-2 receptor: 1 and 1.01 over 0.83 and 0.51, P<0.05; I-K,I- ACh: 20 +/- 0.89, 19 +/- 0.82, 14 +/- 0.64, 9 +/- 0.45 pA/pF, P<0.05). Furthermore, densities of M-2 receptor and I-K,I-ACh were higher in LA than those in RA (P<0.05).Conclusions: Decreased APD is the base in initiation of cholinergic AF by VS and increased dAPD alone can not induce AF. A greater abundance of M-2 receptor and I-K,I-ACh in RAA and LAA imply atrial appendage plays an important role in initiation of cholinergic AF. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

Objective To investigate effects of propofol on action potential(AP) and L-type calcium channel curent(ICa-L) of subepicardial myocytes of both left and right ventricular walls of rabbits.Methods The subepicardial myocytes were obtained by enzymatic dissociation in left and right ventricular walls of rabbits.AP and ICa-L were recorded via whole-cell patch-clamp technique.Results According to current clamp protocol,APs which were recorded in subepicardial myocytes of both left and right ventricular walls consisted of five phases from upstroke to phase four,and were attached to a dome in the second plateau of the APs before propofol adminstration.Nonetheless,Propofol(250μmol/L) deleted the dome of the second plateau of the APs of subepicardial myocytes of left and right ventricular walls,which had not the second plateau and was shaped an acute triangle in APs of right subepicardial myocytes.Propofol significantly shortend the APD50 and APD90 in right and left subepicardium,and right subepicardium were more obvious during the voltage clamp protocol.Propofol(250μmol/L) significantly attenuated the peak amplitude of ICa-L and right subepicardium were more obvious those of that in left subepicardium(P0.01).Propofol shifted upward the I-V curve of ICa-L of both left and right subepicardial myocytes,but lifted outstandingly the I-V curve of ICa-L of right subepicardial myocytes on the top of all I-V curves. Conclusion Propofol attenuated more significantly on the APs and ICa-L of subepicardial myocytes of right ventricular wall than those of the same layer of left ventricular wall,so that induces cardiac electrical heterogeneity of subepicardial myocytes of both left and right ventricular walls.

Short-term administration of losartan reduced the aortic surface lesion area and mean intimal thickness. The mechanisms for reducing atherosclerotic progression by losartan may be related to decreased macrophage proliferation and accumulation in the arterial wall, decreased activation of nuclear factor-kappa B and expression of its target gene ICAM-1. Objective — Recent studies suggest that angiotensin II (Ang II) may contribute to the vascular inflammatory response and atherosclerosis. Losartan is a specific AT| receptor antagonist which can effectively inhibit the effects of Ang II. However, the effects of losartan on atherogenesis have been rarely demonstrated. We designed this study to investigate the effects of short-term administration of losartan on atherosclerotic lesions in the aorta from rabbits fed a cholesterol-enriched diet and the possible mechanisms of its anti-atherogenic effects. Methods and results — The rabbits were randomly divided into three groups: (a) cholesterol group;(b) losartan-treated group;(c) normal control group. We observed that mean serum lipid levels in the cholesterol group were significantly higher than those in normal control rabbits, while blood pressure between two groups did not change significantly.Treatment with losartan did not affect serum lipid levels or systolic blood pressure but did reduce the aortic surface lesion area and mean intimal thickness.The number of macrophages markedly decreased after administration of losartan. Losartan also attenuated the activation of nuclear factor-kappa B and the expression of its target gene ICAM-1. Conclusions — In summary, losartan inhibited atherosclerotic progression by decreasing macrophage proliferation and accumulation in the arterial wall.The mechanisms for reducing atherosclerotic progression by losartan may be related to decreased activation of nuclear factor-kappa B.

[Objective] To study the influences of endogenous and exogenous androgen on the expression of vascular cell adhesion molecule-1 (VCAM-1) and neointimal proliferation of injuried vascular tissue. [Methods] Thirty male rabbits were randomly divided into three groups: replacement group, only castrated group and control group. The two former groups were castrated and the control group were sham operated. All animals were performed deendothelializing balloon injury in right iliac artery. Replacement group was received testosterone undecanonate replacement therapy. After 2 weaks of endothelial denudation, all animals were killed, VCAM-1 expression were tested with immunohistochemistry and morphological changes were observed with hematoxylin and eosin (HE) staining. [Results] Compared with only castrated group and control group, VCAM-1 expression, the neointimal area and the ratio of intimal/medial area were increased in replacement group (P <0.001 or P <0.01).There were no siginificantly differences between only castrated group and control group(P >0.05). [Conclusion] When male rabbits were castrated, exogenous testosterone replacement treatment could promote the expression of VCAM-1 and neointimal formation of injuried vascular tissue, while the declining endogenous testosterone didn′t effect them in a short term.

Background: The reentrant mechanism of vagally mediated AF is not clearly elucidated.Methods and results: After vagal stimulation, thirty dogs were divided AF group (AF could be induced) and control group (AF could not be induced). Western blot and patch clamp were used to determine M-2 receptor and I-K,I-ACh in left atrial appendage (LAA), right atrial appendage (RAA), left atrium (LA), right atrium (RA), pulmonary veins (PVs) and superior vena cava (SVC). In control group, the densities of M-2 receptor and I-K,I-ACh in LAA, RAA and LA were higher than that in RA, PVs and SVC. However, there was no significant difference in LAA, RAA and LA. In AF group, the densities of M-2 receptor and I-K,I-ACh in LAA, RAA and LA were higher than that in RA, PVs and SVC. Furthermore, the densities of the M-2 and I-K,I-ACh in LAA and RAA were higher than that in LA.Conclusions: Atrial appendage perhaps play an important role in initiation of cholinergic AF. However, PVs and SVC less often play an important role in vagotonic paroxysmal AF. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

Objective To observe effects of bone marrow stem cell implantation on ventricular arrhythmia after acute myocardial infarction in rat. Methods Thirty rats were randomly divided into two groups. Cell implantation group was treated with bone marrow stem cell injection, and control group was treated with the same quantity of serum-free medium injection. Then Holter was used to observe arrhythmia on the first and twenty-eighth day after injection. Results On the first day after injection, there wasn′t difference in the incidence rate of ventricular arrhythmia between the two groups. While on the twenty-eighth day after injection, the incidence rate of ventricular arrhythmia was decreased significantly in cell implantation group(P0.05). Conclusions Bone marrow stem cell implantation can effectively reduce the occurrence of ventricular arrhythmia after acute myocardial infarction.

Objective To explore the relationship of interleukin-6 (IL-6) gene polymorphisms and its serum level with essential hypertension (EH) in Chinese Hans population and investigate the effect of IL-6 gene polymorphisms on serum IL-6 level. Methods The polymorphisms of IL-6 gene, -597 G/A, - 572 C/G and 174 G/C, were checked in 191 EH patients and 197 control subjects by PCR-RELP. Meanwhile their serum IL-6 level was determined by ELISA. Results Only -597 GG genotype and -174 GG genotype of IL-6 gene was found in the test population. There was significant difference in frequencies of - 572 genotype and allele between 2 groups. -572 CG+GG genotype and G allele were more frequent in patients than in controls (P<0.05, P<0.01). Compared to CC genotype,relative risk for hypertension were 1.68 (95%CI:1.12~2.53,P<0.05) for -572 CG + GG genotype. EH group showed significantly higher serum level of IL-6 than control group [ (15.41±8.09) pg/ml vs (4.68±2.90) pg/ml,P<0.01]. Serum IL-6 level of patients with -572 CG +GG genotype was higher than that of -572 CC genotype (P<0.05), and so the systolic blood pressure level (P<0.05). Conclusion No IL-6 gene -597 G/A and -174 G/C polymorphisms is seen in our study. IL-6 gene -572 C/G polymorphism may be one of genetic risk factors for EH and it may increase the risk of EH by enhancing the IL-6 expression.

Objective: To investigate the effects of autologous bone marrow mononuclear cell (BM-MNC) implantation into infarcted myocardium with or without transfection of phVEGF165 on cardiac function after acute myocardial infarction (AMI) in rabbits. Methods: AMI was replicated by ligating the left anterior descending coronary artery. Rabbits were randomised into three groups: ① BM-MNC implantation with transfection of phVEGF165 (n=7); ② BM-MNC implantation alone (n=7); ③ AMI controls(n=7); 4 sham-operated (n=5) rabbits to serve as non-infarction controls. Animals for cell implantation were received intramyocardial injection of autologous BM-MNC in myocardium bordering the infarction, and echocardiography and hemodynamic studies were performed to evaluate cardiac function following 4 weeks of implantation. Results: Compared with the sham-operated group, the left ventricular (LV) end diastolic pressure (LVEDP) was significantly increased (P0.05) in all AMI procedure groups, and ΔD (Dd minus Ds) to Dd ratio (ΔD/Dd), wall thickness to chamber radius, ejection fraction (EF), the left ventricle systolic pressure (LVSP) and maximum LV pressure rising rates (dp/dtmax) were all significantly reduced (all P0.05). These changes indicated LV remodelling occurred and LV functions were impaired. Comparison among all AMI procedure groups showed that impaired LV functions were improved by autologous BM-MNC implantation, as revealed by decreased LVEDP (BM-MNC implantation versus AMI alone, P0.05) and increased ΔD/Dd, wall thickness to chamber radius, EF, LVSP, and dp/dtmax (BM-MNC implantation versus AMI alone, all P0.05). Furthermore, BM-MNC implantation with transfection of phVEGF165 conferred a further improvement of cardiac function with significant changes of all assessed parameters when compared with BM-MNC implantation alone (all P0.05). Conclusion: BM-MNC implantation into infarcted myocardium can improve impaired cardiac function associated with LV remodelling after AMI, and such improvement was promoted further by transfection of phVEGF165.