Lin Wang

Chinese PLA General Hospital (301 Hospital), Peping, Beijing, China

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Publications (36)52.04 Total impact

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    ABSTRACT: Background Deceleration capacity (DC) is a newly found predictor of mortality after myocardial infarction. Age-, gender-, and circadian rhythm–related differences in DC may limit its predictive value, which should be considered in clinical settings.MethodsDC, average heart rate, and HRV parameters, including 24 hours, awaking state (15:00–20:00) and sleeping mode (00:00–05:00) strips from 24 hours Holter recordings in 636 subjects without heart diseases were examined. Heart rate variability was analyzed in time domains (standard deviation of all normal-to-normal intervals [SDNN], normal-to-normal RR intervals in all 5-minute segments [SDANN], and root mean square successive difference [RMSSD]).ResultsThe DC, SDNN, SDANN, RMSSD, and heart rate decreased with age. Deceleration capacity was significantly lower in patients greater than 50 years of age. The largest decrease of SDNN, SDANN, and RMSSD occurred in patients 30–39 years of age. The values of SDNN, SDANN, and DC of women were lower than that of men in the young and middle-aged groups, but age-related decrease of DC in men was greater than that in women. Heart rate of women was significantly higher than that of men in younger subjects, especially in a sleeping mode. There were higher values of DC and RMSSD during sleeping than that during a waking state.Conclusions The age, gender, and circadian rhythm may be useful when evaluating cardiac autonomic function and need to be considered when evaluating DC and HRV in clinical and scientific researches.
    Annals of Noninvasive Electrocardiology 08/2014; 20(2). DOI:10.1111/anec.12189 · 1.08 Impact Factor
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    ABSTRACT: The major structure elements of the AMP-activated protein kinase (AMPK) are α, β, and γ sunbunits. Mutations in γ2 subunit (PRKAG2) have been associated with a cardiac syndrome including inherited ventricular preexcitation, conduction disorder and hypertrophy mimicking hypertrophic cardiomyopathy. The aim of the present study was to identify PRKAG2 syndrome among patients presenting with left ventricular hypertrophy (LVH). Nineteen unrelated subjects with unexplained LVH were clinically and genetically evaluated. Among 4 patients with bradycardia, manifestations of preexcitation were only found in a 19 year old male who also developed congestive heart failure 3 years later. Electrophysiological study of this case identified the coexistence of an AV accessory pathway and AV conduction defect. Histological analysis of his ventricular tissue isolated by biopsy confirmed excessive glycogen accumulation, prominent myofibrillar disarray and interstitial fibrosis. Direct sequencing of his DNA revealed a heterozygous mutation in PRKAG2 consisting of an A-to-G transition at nucleotide 1453 (c.1453A>G), predicting a substitution of a glutamic acid for lysine at highly-conserved residue 485 (p.Lys485Glu, K485E), which was absent in his unaffected family members and in 215 healthy controls. To assess the role of K485 in the structure and function of the protein, computational modeling calculations and conservation analyses were performed. Electrostatic calculations indicate that K485 forms a salt bridge with the conserved D248 residue in the AMPK β subunit, which is critical for proper regulation of the enzyme, and the K485E mutant disrupts the connection. Our study identifies a novel de novo PRKAG2 mutation in a young, in which progression of the disease warrants close medical attention. It also underlines the importance of molecular screening of PRKAG2 gene in patients with unexplained LVH, ventricular preexcitation, conduction defect, and/or early onset of heart failure.
    PLoS ONE 05/2013; 8(5):e64603. DOI:10.1371/journal.pone.0064603 · 3.53 Impact Factor
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    ABSTRACT: To investigate the effects of pioglitazone on transforming growth factor beta1 (TGFbeta1) expression in ischemia/reperfusion injury myocardium of rats. Thirty SD rats were randomly divided into five groups (n = 6): ischemia/reperfusion group, pioglitazone 5 mg/(kg x d) group, pioglitazone 10 mg/(kg x d) group, pioglitazone 20 mg/(kg x d) group and pioglitazone 20 mg/(kg x d) + peroxisome proliferator-activated receptor gamma (PPARgamma) specific antagonist GW9662 group. Left anterior descending coronary artery of rats were ligated for 30 min and reperfused for 120 min to establish the model of ischemia/reperfusion in vivo. RT-PCR was performed to detect the expression of TGFbeta1 mRNA. Western blot was performed to detect the expression of TGFbeta1 protein. Myocardial apoptosis was significantly suppressed by pioglitazone. Pioglitazone upregulated TGFPbeta1 expression both in mRNA and protein level. GW9662 reversed the inhibition of myocardial apoptosis and the upregulation of TGFbeta1 expression by pioglitazone. Pioglitazone can inhibit the myocardial apoptosis induced by ischemia/reperfusion. Pioglitazone may protect the myocardium from ischemia/reperfusion via upregulation of TGFbeta1. This protection may be mediated by PPARgamma.
    Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 01/2013; 29(1):1-4.
  • Hereditas (Beijing) 06/2011; 33(6):601-606. DOI:10.3724/SP.J.1005.2011.00601
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    ABSTRACT: The objective of the present study was to explore the relationship between mitochondrial tRNAMet mutation and development of essential hypertension in Chinese Han individuals. A total of 990 patients with essential hypertension were involved. The general data (sex, age, body mass index, onset age, and family history) and information on routine blood test, blood biochemical examination, and color Doppler echocardiography of these patients were collected. All subjects under-went venous blood drawing for seperating white blood cells and DNA extraction. Then, mitochondrial tRNAMet was amplified and sequenced after purification. The patients who carried the tRNAMet mutation were taken as the indicative cases and the controls were the patients with essential hypertension who did not carry the mutation. We performed a comparative analysis on the routine blood test, blood biochemical examination, color Doppler echocardiography, and other data between the indicative cases and control cases. Among the 990 essential hypertensive patients, there were 8 who carried the tRNAMet mutation, and 6 mutation sites were confirmed, including A4401G, C4410A, U4418C, A4435G, U4454C, and C4456U. Compared with the control cases, the indicative cases developed essential hypertension at earlier ages. The average levels of high density of lipoprotein cholesterol, left ventricular end diastolic diameter, stroke volume, and cardiac index were higher in the indicative cases than in the controls. While the average levels of hemoglobin and left ventricular ejection fraction were lower in the indicative cases than in the control cases. Among the 8 indicative cases, 5 had maternally inherited hyper-tension; one had paternally inherited hypertension; and two denied any family history of hypertension. These results indicated that the mitochondrial tRNAMet mutations might induce the changes in structure and function, which was involved in the progress of the essential hypertension by disturbing the blood metabolism, the steady-state of the blood cells, and the cardiac structure and function.
    Hereditas (Beijing) 06/2011; 33(6):601-6.
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    ABSTRACT: The role of ATP-sensitive potassium (K(ATP)) channels in cerebral ischemia-reperfusion has been well documented. K(ATP) channel openers protect neuron by mimicking ischemic preconditioning. However, the different protection between the mitochondrial and sarcolemma K(ATP) openers has been seldom studied. In the experiment, we investigated the effects of K(ATP) channel openers diazoxide and pinacidil on the hypoxia-ischemia-reperfusion in cultured hippocampal neurons and gerbil brain. The cultured hippocampal neurons and gerbil brain were pretreated with diazoxide or pinacidil before oxygen-glucose deprivation (OGD) and cerebral ischemia-reperfusion, respectively. Survival rate, apoptosis rate and lactate dehydrogenase (LDH) releasing after the reperfusion were subsequently detected. Then the subunits mRNA was detected by RT-PCR. The survival rate and LDH content in diazoxide group increased more than that in pinacidil group (86.21±2.73% vs. 78.59±1.94%, P<0.05; 133.29±15.00 U/L vs. 193.47±3.39 U/L, P<0.01). The apoptosis rate in diazoxide group decreased significantly more than that in pinacidil group (23.82±0.14% vs. 37.05±0.67%, P<0.01). Diazoxide pretreatment increased the expression of Kir6.1 mRNA obviously. The results suggested that mitoK(ATP) channels opener diazoxide played a major protective role on cerebral ischemia-reperfusion. Furthermore, diazoxide might become a new treatment for cerebral ischemia diseases through increasing the expression of Kir6.1 mRNA.
    Neuroscience Letters 03/2011; 491(1):63-7. DOI:10.1016/j.neulet.2010.12.065 · 2.06 Impact Factor
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    ABSTRACT: In this study, we investigated the effects of the voltage-dependent anion channel (VDAC) on the mitochondrial calcium cycle in cell lines carrying the mitochondrial DNA A4263G mutation. We established lymphoblastoid cell lines from three symptomatic individuals and one asymptomatic individual from the large Chinese Han family carrying the A4263G mutation; these were compared with three control cell lines. The mitochondrial Ca(2+) concentration and membrane potential were detected by loading cells with Rhod-2 and JC-1, respectively. Confocal images showed the average Rhod-2 and JC-1 fluorescence levels of individuals carrying the tRNA(Ile) A4263G mutation were lower than those of the control group (P<0.05). The baseline Rhod-2 fluorescence in the control group increased after exposure to atractyloside (an opener of the adenine nucleotide translocator, P<0.05), but no significant change was detected in the cell line harboring the A4263G mutation (P>0.05). The baseline JC-1 fluorescence in both the mutated and control cell lines decreased after subsequent exposure to atractyloside (P<0.05), whereas this effect of atractyloside was inhibited by Cyclosporin A (CsA, a VDAC blocker). We conclude that the mitochondrial VDAC is involved in both the increase of mitochondrial permeability to Ca(2+) and the decrease of mitochondrial membrane potential in cell lines carrying the mtDNA A4263G mutation.
    Biochemical and Biophysical Research Communications 01/2011; 404(1):364-9. DOI:10.1016/j.bbrc.2010.11.124 · 2.28 Impact Factor
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    ABSTRACT: Of multiple factors contributing to essential hypertension, mitochondrial variants exhibited the trends for serving as molecular and genetic markers for the disease in last five years. However, previous studies focused on African-American or Caucasian pedigrees, knowledge of mitochondrial tRNA genes and population-based Chinese hypertensives were limited. We performed sequence analysis in tRNA genes, hot spots for cardiovascular diseases, in 270 Chinese Han essential hypertensives and 270 controls. Lymphoblastoid cell lines were immortalized by transformation with the Epstein-Barr virus. Rates of oxygen consumption in intact cells were determined with a YSI 5300 oxygraph (Yellow Springs Instruments) on samples, harboring variants in tRNA genes. There were 26 variants in tRNA genes that were found in hypertensives and these variants were not in controls. Functional analysis found that these variants may lead to deficiencies in tRNA 3' end metabolism and/or impairment of critical subunits of the respiratory chain. Most importantly, the oxygen consumption rate in cells harboring variants T4454C (P=0.0010) and A4263G (P=0.0001) decreased as compared to the average level of control cell lines. Variants located in mitochondrial tRNA genes may have biologic plausibility to implicate in the pathogenesis of Chinese essential hypertension.
    Clinica chimica acta; international journal of clinical chemistry 09/2009; 410(1-2):64-9. DOI:10.1016/j.cca.2009.09.023 · 2.76 Impact Factor
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    ABSTRACT: Earlier genetic studies of essential hypertension have focused on nuclear genes or family-based mitochondrial screening in Caucasian and African-American pedigrees. The role of mitochondria in sporadic Chinese hypertensives is unknown. We sequenced mitochondrial genomes in 306 age- and gender-balanced Chinese Han hypertensives and controls. In 153 hypertensives, putative functional changes included 4 changes in rRNA genes, 11 changes in tRNA genes and 25 amino-acid substitutions. The remaining variants were synonymous changes or non-coding regions. In the 153 controls, 2 base changes in the tRNA genes and 13 amino-acid substitutions were found. A8701G in ATP6 gene (belongs to haplogroup M; P=0.0001) and C8414T in ATP8 gene (belongs to haplogroup D; P=0.01) were detected significantly different in the cases and controls. Interestingly, the cases were more likely to have two or more amino-acid changes and RNA variants compared with the controls (57.43 versus 23.81%, P=0.0001). In addition, several variants we found were highly conserved and/or specifically located at the 3' end adjacent to the anticodon, which may contribute to the stabilization of structure, and thus lead to the decrease of tRNA metabolism. In conclusion, mitochondrial SNPs (mtSNPs) may affect the course of hypertension in sporadic Chinese hypertensives. Some specific mtSNP within mitochondria may have potential role in the Chinese hypertensives due to their function. Synergetic interaction between mitochondrial mtSNPs and/or haplogroups is needed to be investigated in the future.
    European journal of human genetics: EJHG 05/2009; 17(11):1501-6. DOI:10.1038/ejhg.2009.63 · 4.23 Impact Factor
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    ABSTRACT: The left ventricular hypertrophy (LVH) is one of the most important organ damage targets in hypertension. Despite the involvement of multiple factors, the genetic factors have been shown to have an important function in the pathogenesis of LVH. The aim of our study was to evaluate the role of mitochondria in LVH for Chinese hypertensives. A systematic and extended mutational screening for the mitochondrial genome has been initiated in a large cohort of Chinese population by the Geriatric Cardiology Clinic at the Chinese PLA General Hospital, Beijing, China. Specific mutations within the mitochondria were further evaluated. Changes of total RNAs (tRNAs) were measured by northern blotting using nonradioactive digoxigenin (DIG)-labeled oligodeoxynucleotides specific for each RNA. Rates of oxygen consumption in intact cells were determined with av YSI 5300 oxygraph. Sequence analysis of mitochondrial DNA in one Chinese pedigree identified a novel A-G transition at position 4401 (A4401G) at the junction of tRNA(Met) and tRNA(Gln). The noncoding region mutation appeared to affect the processing of precursors in these mitochondrial tRNAs. The reduction in the rate of respiration and marked decreases in the steady-state levels of tRNA(Met) and tRNA(Gln) were detected in the cells carrying this mutation. The novel mutation was absent in 270 Chinese control patients. In conclusion, the noncoding mitochondrial sequence alteration (A4401G) alters mitochondrial function, implicating this mutation in the pathogenesis of LVH in Chinese hypertensives.
    European journal of human genetics: EJHG 09/2008; 17(2):172-8. DOI:10.1038/ejhg.2008.151 · 4.23 Impact Factor
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    ABSTRACT: To observe the effects of aspirin on nuclear factor kappaB (NF-kappaB)-DNA binding activity and on the expression of cyclooxygenase-2 (COX-2) in atherosclerotic plaque so as to explore its antiatherosclerotic mechanism. Thirty-six New Zealand male rabbits were randomly divided into 3 equal groups: high-cholesterol (HC) group, fed with food high in cholesterol and perfused into the empty stomach daily with distilled water for 12 weeks, high-cholesterol and aspirin (HC + A) group, fed with food high in cholesterol and perfused into the empty stomach daily with aspirin solution, and normal control (NC) group, fed with normal food and perfused into the empty stomach daily with distilled water, before the experiment, and 4, 8, and 12 weeks after the beginning of experiment peripheral blood samples were collected. The serum lipids were detected with enzymatic assays; and enzyme-linked immunosorbent assay was used to detect the level of high sensitive C-reactive protein (hs-CRP). By the end of experiment the rabbits were killed to take out the specimens of aorta to observe the neointima thickness and plaque area of aorta. Electrophoretic mobility shift assay was used to detect the NF-kappaB-DNA binding activity, and immunohistochemistry and morphometry were performed to observe the expression of COX-2 protein, the neointima thickness and plaque area of aorta respectively in all three groups. The levels of serum lipids, hs-CRP, NF-kappaB-DNA binding activity, expression of COX-2 protein, and neointima thickness and plaque area of aorta in the HC and HC + A groups were all significantly higher than those in the NC group (P < 0.05 -0.01). There was no significant differences in the serum lipids between the HC and HC + A groups (all P > 0.05), however, the levels of hs-CRP, NF-kappaB-DNA binding activity, expression of COX-2 protein, and neointima thickness and plaque area of aorta of the HC + A group were (5.14 +/- 0.32) microg/ml, (14.6 +/- 2.7) microg/ml, (0.342 +/- 0.02)A, (165 +/- 24) microm, and (24.3 +/- 7.6)% respectively, all significantly lower than those of the HC group [(9.39 +/- 0.79) microg/ml, (32.4 +/- 4.7) microg/ml, (0.572 +/- 0.061) A, (337 +/- 64) microm, and (49.5 +/- 21.3)%, all P < 0.05). By reducing the expression of COX-2.
    Zhonghua yi xue za zhi 12/2007; 87(46):3298-301.
  • Mitochondrion 12/2007; 7(6):429-429. DOI:10.1016/j.mito.2007.08.090 · 3.52 Impact Factor
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    ABSTRACT: In order to confirm the hypothesis that during acute hypoxia, the antiarrhythmic peptide (AAP10) could improve conductance by changing the phosphorylation state of connexin43 (Cx43), isolated perfused rat hearts were randomly divided into three groups: control, hypoxia and AAP10 (n=9 in each group). The change in Cx43 phosphorylation was tested by Western-blot; the distribution of Cx43 was observed by confocal immunofluorescence microscopy. Western-blot analysis revealed that the expression of total Cx43 protein was significantly decreased during acute hypoxia, while nonphosphorylated Cx43 (NP-Cx43) was unchanged. AAP10 could increase the expression of total Cx43 protein, but had no effects on the NP-Cx43 protein. Immunofluorescence study showed that during acute hypoxia, both total Cx43 and NP-Cx43 proteins were greatly decreased, while AAP10 only increased the expression of total Cx43 protein, but had no effect of the NP-Cx43 protein expression. These findings suggested that the decrease of intercellular communication may be associated with the reduction of phosphorylated Cx43 (p-Cx43) and translocation of NP-Cx43 from the surface of gap junction into intracellular pools during acute hypoxia. AAP10 can improve intercellular communication by enhancing phosphorylation of Cx43.
    Journal of Huazhong University of Science and Technology 07/2007; 27(3):241-4. DOI:10.1007/s11596-007-0306-8 · 0.78 Impact Factor
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    ABSTRACT: Malignant ventricular arrhythmias can arise in a subset of congestive heart failure (CHF) patients after they undergo cardiac resynchronization therapy (CRT), thus counteracting the haemodynamic benefits typically associated with biventricular pacing. This study seeks to assess whether alteration of the ventricular transmural repolarization and conduction due to reversal of the depolarization sequence during epicardial or biventricular pacing facilitate the development of ventricular arrhythmias. ECGs and monophasic action potential (MAP) were recorded during programmed stimulation from right ventricle (RV) endocardium (RV-Endo), left ventricle (LV) epicardium (LV-Epi), or both (biventricular, Bi-V) in 15 individuals without structural heart diseases. In patients with severe CHF and CRT (n=21), ECGs were collected during RV-Endo, LV-Epi, and Bi-V pacing. MAP duration on intracardiac electrogram, the QT, JT, and T(peak)-T(end) intervals on ECGs at different pacing sites were measured and compared. In subjects with or without structural heart disease, compared with RV-Endo pacing, LV-Epi and Bi-V pacing resulted in a longer JT (341.78+/-61.97 ms with LV-Epi, 325.86+/-59.69 ms with Bi-V vs. 286.14+/-38.68 ms with RV-Endo in CHF individuals, P<0.0001) or T(peak)-T(end) interval (121.55+/-19.88 ms with LV-Epi, 117.71+/-42.63 ms with Bi-V vs. 102.28+/-12.62 ms with RV-Endo in normal-heart subjects, P<0.0001; 199.70+/-62.44 ms with LV-Epi, 184.89+/-74.08 ms with Bi-V vs. 146.41+/-31.06 ms with RV-Endo in CHF patients, P<0.0001), in addition to prolonged myocardial repolarization time and delayed endocardial activation. During follow-up, sudden death and arrhythmia storm occurred in two CHF patients after CRT. Epicardial and biventricular pacing prolong the time and increase the dispersion of myocardial repolarization and delay the transmural conduction. All of these should be considered as potential arrhythmogenic factors in CHF patients who receive CRT.
    Europace 12/2006; 8(11):1002-10. DOI:10.1093/europace/eul110 · 3.05 Impact Factor
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    ABSTRACT: To evaluate the effects of antiarrhythmic peptide (AAP10) on ventricular arrhythmias in rabbits with healed myocardial infarction (OMI). Thirty rabbits were randomly divided into three groups (n = 10 each): Sham group, left thoracotomy was performed without coronary ligation; OMI group and OMI + AAP10 group, the circumflex coronaries were ligated. Three months post operation, the electrophysiological and antiarrhythmic effects of AAP10 were assessed in the arterially perfused rabbit left ventricular wedge preparation. Sham and OMI group were perfused with Tyrode's solution and OMI + AAP10 group was perfused with Tyrode's solution + AAP10 (80 nmol/L). Transmembrane action potentials were recorded simultaneously from endocardium and epicardium together with a transmural ECG by use of 2 separate intracellular floating microelectrodes. The stimulus-response-interval (SRI) of the epicardium and the incidence of ventricular tachycardia (VT) were observed. Whole heart and left ventricular weights, the left ventricular thickness at infarct border zone were measured. Whole heart and left ventricular weights as well as the left ventricular thickness at the infarct border zone significantly increased post infarction. VT was induced in 8 out of 10 rabbits in OMI group and in 2 out of 10 rabbits in OMI + AAP10 group (P < 0.05). SRI was also significantly shortened in OMI + AAP10 group compared to OMI group [SRI-1: (20.59 +/- 0.79) ms vs. (28.71 +/- 0.55) ms; SRI-2: (30.42 +/- 0.74) ms vs. (38.67 +/- 0.49) ms, all P < 0.01]. However, the action potential morphology and duration were similar between OMI and OMI + AAP10 groups. The antiarrhythmic peptide (AAP10) can increase gap junctional intercellular conductance without affecting the action potential morphology and duration and decrease the incidence of inducible ventricular tachycardia.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 09/2006; 34(9):825-8.
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    ABSTRACT: The present study retrospectively evaluated the reliability of detecting atrial tachyarrhythmias (ATA), the efficacy of automatic atrial antitachycardia pacing (ATP) and the performance of atrial preventive pacing (APP) algorithms in an implanted antitachycardia DDDRP pacemaker for patients with sick sinus syndrome and paroxysmal ATA. In all 24 patients, a DDDRP pacemaker (Medtronic AT500/AT501) was implanted. APP algorithms were switched on at the implanting physician's discretion. During each pacemaker follow-up, information was saved to disk and the ATA burden between those patients with APP algorithms switched "ON" and "OFF" were compared. Reliability of ATA detection was determined by reviewing the stored electrograms and ATP efficacy was also reviewed. Both the pacemaker memory data and manual EGM retrieval were used for the analysis. Complication-free survival at (17.63 +/- 8.79) months was 100%. In 12 patients APP was not turned "ON" until the latest follow-up, in 6 patients APP was switched "ON" at their first visit after implantation, and in another 6 patients APP was switched "ON" after a median follow-up of 9.29 months. There were 97 367 episodes of ATA detected by the devices, of those with stored atrial electrograms the correct classification of ATA was (76.77 +/- 20.52)%. The percentage of atrial pacing with APP algorithms turned on was (87.95 +/- 20.93)%, which was significantly higher than that in patients with APP "OFF" (50.73 +/- 34.46)% (P < 0.01). ATP efficacy was (50.27 +/- 19.29)%. However, the ATA burden (14.73% vs 16.52%, or 7.52 hours vs 6.58 hours per week, P > 0.05) and the longest duration of single ATA episode (27.27 hours vs 20.75 hours, P > 0.05) were not significantly different between those patients with APP "ON" and "OFF". No proarrhythmic effect or major cardiovascular event was observed. The antitachycardia DDDRP pacemaker correctly detects and diagnoses about 75% of the ATA episodes, while the ATP therapy successfully terminates atrial tachycardia or flutter in about 50% of attacks. However, there is no difference in ATA burden with the APP algorithms and high incidence of atrial pacing. As a non-curative therapy strategy, this high-cost device may only be used in strictly selected indication patients in addition to other treatments of ATA.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 04/2006; 34(4):333-7.
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    ABSTRACT: To observe the effects of simvastatin on nuclear factor kappaB (NF-kappaB)-DNA binding activity and on the expression of monocyte chemoattractant protein-1 (MCP-1) in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects. Thirty-six New Zealand male rabbits were randomly divided into low-cholesterol group (LC), high-cholesterol group (HC), high-cholesterol+simvastatin group (HC+S) and then were fed for 12 weeks. At the end of the experiment, standard enzymatic assays, electrophoretic mobility shiftassay (EMSA), immunohistochemical staining, and morphometry were performed to observe serum lipids, NF-kappaB-DNA binding activity, MCP-1 protein expression, intima thickness and plaque area of aorta respectively in all three groups. Our results showed that the serum lipids, NF-kappaB-DNA binding activity, expression of MCP-1 protein, intima thickness, and plaque area of aorta in the LC and HC+S groups were significantly lower than those in the HC group (P<0.05). There was no significant difference in the serum lipids between the LC and HC+S groups (P>0.05), but the NF-kappaB-DNA binding activity, the expression of MCP-1 protein and the intima thickness and plaque area of aorta in the HC+S group were significantly decreased as compared to the LC group (P<0.05). This study demonstrated that simvastatin could decrease atherosclerosis by inhibiting the NF-kappaB-DNA binding activity and by reducing the expression of MCP-1 protein.
    Journal of Huazhong University of Science and Technology 03/2006; 26(2):194-8. DOI:10.1007/BF02895814 · 0.78 Impact Factor
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    ABSTRACT: The effects of amiodarone on transmural dispersion of ventricular effective refractory periods (ERPs) in the normal and hypertrophic canine heart were investigated in vivo. By using the programmed stimulation protocol, the ERPs of epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were measured by inserting specially-designed electrodes into the three myocardial layers before and after mainlining of amiodarone. No significant ERPs-dispersion was observed in the three layers before and after mainlining of amiodarone in the normal group. In contrast, ERPs of all the three layers were prolonged in the hypertrophic heart, while the ERPs-dispersion was reduced significantly after mainlining of amiodarone. The ERPs-dispersion was significantly increased in the hypertrophic heart but not in the normal heart using "long-short" and "short-long" interval stimulation technique. It was concluded that (1) the differences in ERPs-dispersion among the three layers were significant in hypertrophic heart, and differences were not significant in normal canine heart; (2) ERPs of each three-myocardial layers were significantly prolonged after using amiodarone, but the ERPs-dispersion decreased in hypertrophic heart and (3) the programmed extrastimulus technique of "long-short" and "short-long" intervals increased the transmural ERPs-dispersion in the hypertrophic heart.
    Journal of Huazhong University of Science and Technology 02/2006; 26(2):182-4. DOI:10.1007/BF02895810 · 0.78 Impact Factor
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    ABSTRACT: Benefits of cardiac resynchronization therapy (CRT) are well established. However, less is understood concerning its effects on myocardial repolarization and the potential proarrhythmic risk. Healthy dogs (n = 8) were compared to a long QT interval (LQT) model (n = 8, induced by cesium chloride, CsCl) and a dilated cardiomyopathy with congestive heart failure (DCM-CHF, induced by rapid ventricular pacing, n = 5). Monophasic action potential (MAP) recordings were obtained from the subendocardium, midmyocardium, subepicardium, and the transmural dispersion of repolarization (TDR) was calculated. The QT interval and the interval from the peak to the end of the T wave (T(p-e)) were measured. All these characteristics were compared during left ventricular epicardial (LV-Epi), right ventricular endocardial (RV-Endo), and biventricular (Bi-V) pacing. In healthy dogs, TDR prolonged to 37.54 ms for Bi-V pacing and to 47.16 ms for LV-Epi pacing as compared to 26.75 ms for RV-Endo pacing (P < 0.001), which was parallel to an augmentation in T(p-e) interval (Bi-V pacing, 64.29 ms; LV-Epi pacing, 57.89 ms; RV-Endo pacing, 50.29 ms; P < 0.01). During CsCl exposure, Bi-V and LV-Epi pacing prolonged MAPD, TDR, and T(p-e) interval as compared to RV-Endo pacing. The midmyocardial MAPD (276.30 ms vs 257.35 ms, P < 0.0001) and TDR (33.80 ms vs 27.58 ms, P=0.002) were significantly longer in DCM-CHF dogs than those in healthy dogs. LV-Epi and Bi-V pacing further prolonged the MAPD and TDR in this model. LV-Epi and Bi-V pacing result in prolongation of ventricular repolarization time, and increase of TDR accounted for a parallel augmentation of the T(p-e) interval, which provides evidence that T(p-e) interval accurately represents TDR. These effects are magnified in the LQT and DCM-CHF canine models in addition to their intrinsic transmural heterogeneity in the intact heart. This mechanism may contribute to the development of malignant ventricular arrhythmias, such as torsades de pointes (TdP) in congestive heart failure (CHF) patients treated with CRT.
    Pacing and Clinical Electrophysiology 10/2005; 28(10):1098-106. DOI:10.1111/j.1540-8159.2005.00218.x · 1.25 Impact Factor
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    ABSTRACT: The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly: acute ischemia (AI) group and sham operation (SO) group. By using the monophasic action potential (MAP) technique, MAP and effective refractory period (ERP) of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization (TDR) and transmural dispersion of ERP (TDE) were analyzed. The results showed that in the AI group, MAP duration (MAPD) was shortened from 201.67 +/- 21.42 ms to 169.50 +/- 13.81 ms (P < 0.05), but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.
    Journal of Huazhong University of Science and Technology 09/2005; 25(5):497-500. DOI:10.1007/BF02895998 · 0.78 Impact Factor

Publication Stats

108 Citations
52.04 Total Impact Points

Institutions

  • 2008–2013
    • Chinese PLA General Hospital (301 Hospital)
      Peping, Beijing, China
  • 2002–2007
    • Tongji Hospital
      Wu-han-shih, Hubei, China
  • 2005–2006
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China