Biomedical subjects

Congxin Huang

Publications and source records attributed to Congxin Huang.

9 recordsLinked to original sources

PubMed2006

Abnormal intracellular calcium handling underlying T-wave alternans and its hysteresis.

AIMS: To investigate the mechanism underlying T-wave alternans (TWA) and its hysteresis under ischemia conditions. METHODS: Transmembrane action potential (AP) from endocardial, M, and epicardial cells and monophasic AP (MAP) from four epicardial sites were recorded in ventricular wedge preparation and in isolated intact rabbit heart, respectively. The AP/MAP duration (APD/ MAPD), effective refractory period (ERP), activation time, and APD/MAPD restitution were determined under control and ischemia conditions. The effects of ryanodine (0.01 and 1 micromol x l(-1)) on TWA, and the effects of low extracellular Ca2+ and 4-aminopyridine on its hysteresis were studied. RESULTS: Ischemia shortened the APD/MAPD and effective refractory period of all recording sites symmetrically, except the APD of M cells, which shortened markedly. In the ischemia group, TWA was induced within a cycle length (CL) range from 160 to 250 ms, which corresponded to a diastolic interval region of 0-70 ms. In this diastolic interval region, the repolarization restitution curve was the steepest (slope > 1.0). All TWA were accompanied by repolarization alternations. Low concentration ryanodine (0.01 micromol x l(-1)) facilitated TWA, high concentration (1 micromol x l(-1)) abolished it. Alternans of calcium transient were observed in myocytes purfused with ischemia solution during rapid stimulation. Ryanodine (0.1 micromol x l(-1)) abolished alternans of calcium transient, and ryanodine (0.01 micromol x l(-1)) facilitated them. After 60 min pacing at a CL of 200 ms, TWA persisted until the initial several beats at a CL of 300 ms at which a TWA was exceptional. The suppression of hysteresis by low extracellular Ca2+ and 4-aminopyridine indicated an underlying role of the intracellular Ca2+ overload and transient outward current (I(to)). CONCLUSION: TWA is principally due to repolarization alternans, which is secondary to steep APD/MAPD restitution, and relates to intracellular calcium cycling. Hysteresis relates to intracellular Ca2+ overload and I(to).

4-Aminopyridine↗

PubMed2006

Effects of metoprolol on sympathetic remodeling and electrical remodeling at infarcted border zone after myocardial infarction in rabbits.

BACKGROUND: The findings of sympathetic remodeling and its electrophysiological implications force us to rerecognize the drugs presently used. The aim of this study was to investigate the effects of metoprolol on sympathetic remodeling and electrical remodeling at the infarcted border zone (IBZ) after myocardial infarction (MI). METHODS: Forty rabbits were randomly assigned into two groups: MI group (n = 20), ligation of the anterior descending coronary; Metoprolol group (n = 20), ligation of the anterior descending coronary and administration of oral metoprolol 5 mg/kg/day. Eight weeks after surgery, transmural dispersion of repolarization (TDR) at baseline, TDR and difference of TDR (deltaTDR) during sympathetic nerve stimulation were measured at the IBZ. The distribution and densities of growth associated protein 43 and tyrosine hydroxylase positive nerves at the IBZ were detected with immunohistochemical techniques. RESULTS: The study was completed in the 36 surviving animals (18 rabbits in each group). The densities of growth associated protein 43 and tyrosine hydroxylase positive nerves in the Metoprolol group (2,550 +/- 554 and 1,779 +/- 458 microm2/mm2, respectively) were lower than in the MI group (3,217 +/- 589 and 2,616 +/- 528 microm2/mm2, respectively; both p < 0.01). TDR at baseline, TDR and deltaTDR during sympathetic nerve stimulation were shorter in the Metoprolol group than in the MI group (p < 0.01 for all). CONCLUSION: Metoprolol can inhibit sympathetic remodeling and electrical remodeling at the IBZ after MI. The association of metoprolol with improved electrical remodeling may be partly related to the inhibition of sympathetic remodeling.

Action Potentials↗

PubMed2006

Predictors of early recurrence and delayed cure after segmental pulmonary vein isolation for paroxysmal atrial fibrillation without structural heart disease.

BACKGROUND: Early recurrence of atrial fibrillation (ERAF) and delayed cure are commonly observed after atrial fibrillation (AF) ablation. The purpose of this study was to determine the predictors of ERAF and delayed cure after a single pulmonary vein isolation (PVI) performed in paroxysmal AF patients without structural heart disease. METHODS AND RESULTS: In 108 consecutive patients (93 men, 15 women; mean age 51 +/- 8 years) with paroxysmal AF and no structural heart disease, segmental PVI guided by a Lasso catheter was performed. Forty-one percent (44/108) AF patients had ERAF after a single PVI. Univariate analysis revealed that left atrial diameter (p = 0.004), age (p = 0.024) and P-wave dispersion (p = 0.045) were significantly related to ERAF. Logistic regression analysis revealed that left atrial enlargement was the only independent predictor of ERAF (odds ratio [OR] 1.17; 95% confidence interval [CI] 1.04-1.30, p = 0.006). Delayed cure occurred in 32% (14/44) patients with ERAF. P-wave dispersion (p = 0.001), left atrial diameter (p = 0.008) were significantly related to delayed cure. P-wave dispersion was the only independent predictive factor of delayed cure (OR 0.91; 95% CI 0.85-0.97, p = 0.004). CONCLUSIONS: Elderly patients with left atrial enlargement and a high dispersion of P wave are susceptible to ERAF after a single PVI. Left atrial enlargement is the only independent predictor of ERAF. Among patients with ERAF, those with less P-wave dispersion and less left atrial diameter have a higher probability of delayed cure. P-wave dispersion can independently predict delayed cure.

Adult↗

PubMed2006

Differences in the aging-associated trends of the monophasic action potential duration and effective refractory period of the right and left atria of the rat.

BACKGROUND: The incidence of atrial fibrillation (AF) increases with aging, but the aging-associated electrophysiological changes of atrial myocardium are poorly understood. METHODS AND RESULTS: Based on the hypothesis that aging of the atrium enhances AF susceptibility, 30 Wistar rats were divided into 3 age groups: adult, middle-aged, and aged (n=20 per group). Their hearts were isolated and perfused by Langendorff apparatus. Monophasic action potential duration at 90% repolarization (MAPD(90)) and effective refractory period (ERP) at the basic stimulation cycle length (BCL: 400 ms), and MAPD(90) at other different stimulation cycle lengths in each age group were measured. At the BCL, the MAPD (90) of the right atrial myocardium was prolonged from the adult to the aged group, that of the left atrial myocardium was prolonged from the adult to middle-aged group, and the MAPD(90) of the left atrial myocardium in the aged group were shorter than that in the adult and middle-aged groups. The ERP of the atrial myocardium showed the same age-associated trend as MAPD(90). As the stimulation frequency increased, the MAPD(90) of both the left and right atrial myocardium shortened correspondingly in the adult and middle-aged groups, but in the aged group the MAPD(90) of the right atrial myocardium shortened markedly more than that of the left atrial myocardium. CONCLUSIONS: There are different aging-associated electrophysiological changes in the right and left atrium, and the older heart is more vulnerable to developing the substrate for AF.

Action Potentials↗

PubMed2004

Differences in the changing trends of monophasic action potential duration and effective refractory period of the ventricular myocardium after myocardial infarction in vivo.

BACKGROUND: The relationship between monophasic action potential duration (MAPD) and effective refractory period (ERP) is poorly understood after myocardial infarction (MI) in vivo. METHODS AND RESULTS: Forty rabbits were randomized into either a sham operation (SO) group (n=10) or MI group (n=30), both of which underwent thoracotomy, but the left anterior descending coronary artery was occluded in the MI group only. The MAPD and ERP of the endocardial, midmyocardial and epicardial cells of the infarction zone were observed at baseline, 2 days after thoracotomy and then 5 min, 15 min, 30 min, 2 days, 14 days and 60 days after coronary occlusion (CO). At baseline, ERP correlated strongly with MAPD90. During the 5-30 min after CO, both MAPD90 and ERP of the 3 layers of the myocardium shortened markedly (eg, MAPD90 Mid) was approximately 50% of the baseline value at 5 min after CO). MAPD90 and ERP recovered gradually over the 2-60 days after MI. ERPMid exceeded MAPD90 Mid and the post repolarization refractoriness phenomenon appeared during the 5-30 min after CO. CONCLUSIONS: The different changing trends of the MAPD and ERP of the mid-myocardial cells may underlie the arrhythmias that occur after MI.

Action Potentials↗

PubMed2003

Predictors of left atrial appendage stunning after electrical cardioversion of non-valvular atrial fibrillation.

OBJECTIVE: To identify predictors of left atrial appendage stunning after the use of electrical cardioversion to restore sinus rhythm in patients with non-valvular atrial fibrillation. METHODS: A total of 68 consecutive patients (45 men, 23 women, 60.5 +/- 8.7 years of age) with non-valvular atrial fibrillation undergoing electrical cardioversion were enlisted in this study. Clinical and echocardiographic variables were analyzed by univariate regression and multivariate logistic regression to investigate the relationship between occurrences of left atrial appendage stunning and these factors. RESULTS: Univariate analysis revealed that, in comparing patients without and with left atrial appendage stunning, there were significant differences in the duration of atrial fibrillation > 8 weeks (32.3% vs 75.5%, P < 0.001), left atrial diameter > 50 mm (29.0% vs 54.1%, P < 0.05), left atrial emptying fraction (31.5% +/- 7.8% vs 27.1% +/- 8.5%, P < 0.05), left ventricular ejection fraction < 50% (38.7% vs 67.6%, P < 0.05), maximum electrical energy (96.8 J +/- 65.8 J vs 156.8 J +/- 100.8 J, P < 0.01), cumulative electrical energy 146.8 J +/- 142.6 J vs 290.5 J +/- 242.1 J, P < 0.01) and number of electrical cardioversion shocks (1.7 +/- 0.9 vs 2.43 +/- 1.20, P < 0.05). However, backward stepwise multivariate logistic regression analysis identified as significant and independent predictors of left atrial appendage stunning only duration of atrial fibrillation > 8 weeks (OR = 7.249, 95% CI = 1.998 - 26.304, P < 0.01), left atrial diameter > 50 mm (OR = 3.896, 95% CI = 1.105 - 13.734, P < 0.05), left ventricular ejection fraction < 50% (OR = 4.465, 95% CI = 1.51713.140, P < 0.01) and cumulative energy of electrical cardioversion (OR = 1.004, 95% CI = 1.000 - 1.008, P < 0.05). CONCLUSIONS: Duration of atrial fibrillation > 8 weeks, left atrial diameter > 50 mm, left ventricular ejection fraction < 50%, and cumulative energy of electrical cardioversion are independent predictors of left atrial appendage stunning. Anticoagulation treatment should be individualized for patients undergoing electrical cardioversion to reduce the risk of both cardioversion-related thromboembolic events and hemorrhagic complications caused by warfarin treatment.

Aged↗

PubMed2003

Effects of BmkTXK beta on electrophysiological properties of rabbit atrial myocytes.

OBJECTIVE: To investigate the effects of BmkTXK(beta), a newly purified 'long chain' peptide inhibitor of K(+) channels from the Chinese scorpion Buthus martensi Karsch (BmK), on the electrophysiological properties of isolated rabbit atrial myocytes. METHODS: The standard whole-cell patch-clamp technique was used to study the effects of multiple concentrations of BmkTXK(beta) on potassium currents and action potentials. RESULTS: BmkTXK(beta) produced concentration-dependent prolongation of action potential duration at 20%, 50%, and 90% repolarization (APD(20,50,90)) without any use-dependence. Meanwhile, it had no significant effect on RMP, APA, or V(max) (n = 9). At a dose of 1 micro mol/L, BmkTXK(beta) decreased I(to) by 41.4% (n = 10, P < 0.01) at a membrane potential of +50 mV [from (13.63 +/- 0.87) pA/pF to (7.98 +/- 0.78) pA/pF]. I(to) was reduced significantly with an IC(50) value of 1.82 micromol/L (95% confidence interval: 1.47 - 2.17 micro mol/L), in a clear concentration-dependent manner. BmkTXK(beta) blocked I(Ks) and I(Ks),tail with an IC(50) of 20.15 micromol/L and a 95% confidence interval of 16.93 - 23.37 micromol/L. At a concentration of 10 micromol/L, BmkTXK(beta) blocked both I(Ks) (mean reduction 37.3% +/- 4.2%, P < 0.01, n = 7) and I(Ks), tail (mean reduction 35.8% +/- 4.1%, P < 0.01, n = 7). At 0 mV, 10 micromol/L BmkTXK(beta) inhibited both I(Kr) (mean reduction 40.5% +/- 2.6%, P < 0.01, n = 6) and I(Kr), tail (mean reduction 42.3% +/- 2.9%, P < 0.01, n = 6). Blocking of I(Kr) by BmkTXK(beta) occurred in a concentration-dependent manner, with an IC(50) of 17.21 micromol/L (95% confidence interval: 14.76-19.66 micromol/L). An absence of effects on I(K1) was observed for BmkTXK(beta), with no change in reversal-potential (n = 6, P > 0.05). CONCLUSIONS: BmkTXK(beta) exerts direct blocking effects on several potassium channels involved in cardiac repolarization, and has a strong effect on prolonging the repolarization of rabbit cardiomyocytes without reverse frequency dependence. This finding suggests that BmkTXK(beta) could be a promising class III drug for anti-arrhythmic therapy without the risk of proarrhythmia.

Action Potentials↗

PubMed2002

Comparative study of catheter-mediated gene transfer into heart.

OBJECTIVE: To investigate the feasibility and features of 3 catheter-mediated approaches of gene transfer into heart, including direct myocardial injection (DMI), coronary artery perfusion (CAP), and intrapericardial cavity injection (ICI). METHODS: Fifteen dogs were used, and 0.3 ml (1 x 10(9) pfu) of an adenovirus (Adex1SR LacZ) was injected into the heart by 3 methods. The dogs were killed 5 days following injection, and gene expressions in heart and liver were evaluated by histochemical analysis. RESULTS: The results showed that (1) the CAP method was relatively less damaging and induced sparse LacZ expression in the myocardium, and the gene expression was also found in both vessels within the myocardium and liver; (2) gene transfer by DMI resulted in intense LacZ expression around the injection accompanied by a local inflammatory response; (3) LacZ expression elicited by ICI was detected in either the inner surface of the parietal pericardium or epicardial surface of the heart, and also in the myocardium underlying the visceral pericardium. CONCLUSION: Three catheter-mediated methods of gene transfer into the heart may be used and a reasonable approach should be chosen according to purpose.

Adenoviridae↗

PubMed2002

Effect of arsenic trioxide on inhibition of restenosis after rabbit vascular injury and its mechanism.

OBJECTIVE: To investigate the effect and mechanism of arsenic trioxide (As(2)O(3)) on the prevention of restenosis after vascular injury. METHODS: Apoptosis induction of As(2)O(3) on cultured rabbit vascular smooth muscle cells (VSMCs) in vitro was observed. Thirty-two New Zealand white rabbits were randomly divided into 2- and 4-wk study groups, and their controls. 10% As(2)O(3) at 2.5 mg x Kg(-1) x d(-1) or 0.9% sodium chloride was intraperitoneally infused for 3 days before left common carotid arteries were denudated with a balloon. After denudation 2- and 4-wk animals were sacrificed for morphometry and immunohistochemical studies on carotid arteries, and for histopathology on liver and kidney. RESULTS: It was shown via cellular morphology and DNA fragments in electrophoresis that promotion of As(2)O(3) on cultured vascular smooth muscle cell apoptosis was dependent upon its concentration and duration. Compared with the control animals, the mean vascular intimal proliferation areas were reduced in 2-wk study animals (P < 0.05) and no difference was shown in 4-wk (P > 0.05), while the mean vascular luminal areas were all enlarged in both study groups (all P < 0.05). The downregulated bcl-2 expression (all P < 0.05 in 2- and 4-wk) and the upregulated bax expression (P < 0.01 in 2-wk; P < 0.05 in 4-wk) were detected by immunohistochemistry, in comparison with control groups. Gene bcl-2 and bax protein expression were consistent with the suppression of intimal proliferation and the enlargement of luminal areas in corresponding sections. CONCLUSION: As(2)O(3) induces apoptosis of VSMCs and inhibits experimental restenosis effectively after artery injury, via downregulation of bcl-2 and upregulation of bax expression.

Animals↗