N Zhong

Shanghai Institute of Technology, Shanghai, Shanghai Shi, China

Are you N Zhong?

Claim your profile

Publications (9)14.35 Total impact

  • Yi Zhang · Ning Zhong · Z N Zhou
    [Show abstract] [Hide abstract]
    ABSTRACT: Although it has been reported that intermittent hypoxia had the anti-arrhythmia effect, little is known about the effects on the action potential (AP) and contraction of papillary muscle, as well as the mechanism of anti-arrhythmia. The purpose of present study is to observe the effects of intermittent hypoxia on action potential and contraction of papillary muscle in rat left ventricle simultaneously using conventional intracellular microelectrode and contraction recording. The effects of intermittent hypoxia on AP and contraction during ischemic solution perfusion were also investigated. After exposed to intermittent hypoxia (six hours daily) for 42 days (IH42), duration (APD20) of 20%, 50% (APD50) and 90% (APD90) repolarization of AP prolonged significantly compared with animals in control (Con). Effective refractory period (ERP) in IH42 also prolonged significantly. Perfused with mimic ischemic solution, the changes of electric and mechanical activities in IH42 and in 28 days exposure to intermittent hypoxia (IH28) were much smaller than that in Con and IH14. The result of the study suggested that intermittent hypoxia prolonged the APD and ERP, offered the resistance against the ischemic damage on myocardium, which may be the electrophysiological basis of the anti-arrhythmia of intermittent hypoxia.
    Life Sciences 11/2000; 67(20):2465-71. DOI:10.1016/S0024-3205(00)00832-8 · 2.70 Impact Factor
  • N Zhong · Y Zhang · H F Zhu · Z N Zhou
    [Show abstract] [Hide abstract]
    ABSTRACT: In the present study, polymerase chain reaction (PCR) was conducted to determine mtDNA(4834) deletion, and myocardial ultrastructure was visualized by electron microscope to see whether intermittent hypoxia (high altitude) adaptation exerts some action on mitochondria against ischemia/reperfusion injury. Myocardial ischemia/reperfusion in isolated perfused rat hearts induced severe damage to the ultrastructure of myocardial mitochondria and mtDNA4834 deletion down to 87.5% of normoxia rats. After the rats were exposed to intermittent hypoxia (5000 m; 6 h/d for 28 d), the myocardial structure was well reserved and mtDNA(4834) deletion dropped to 28.57%of control (P<0.05). It is suggested that intermittent hypoxia adaptation prevents mtDNA deletion, and preserves normal structure of mitochondria, which would be beneficial to the maintenance of normal mitochondrial function, and increases tolerance of myocardium against ischemia/reperfusion injury.
    Sheng li xue bao: [Acta physiologica Sinica] 10/2000; 52(5):375-80.
  • Source
    Y Zhang · N Zhong · Z N Zhou
    [Show abstract] [Hide abstract]
    ABSTRACT: To study the effects of estradiol (Est) on antiarrhythmic and antioxidative effects of intermittent hypoxia in rat heart. Ligating and loosening the coronary artery of rat to induce ischemic and reperfusion arrhythmias, using arrhythmia score (AS) to evaluate the arrhythmias, measuring the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in myocardium. AS of arrhythmia induced by ischemia and reperfusion in intermittent hypoxia 28-d group (IH28) and in intermittent hypoxia with Est group (IH14-Est) are lower than that in control group (CON), respectively. AS of ischemic arrhythmia but not reperfusion arrhythmia in Est treated group (ESTG) was lower than that in CON. No significant difference in AS of ischemia and reperfusion existed among CON, vehicle group (VEH), and intermittent hypoxia 14-d group (IH14). The activity of SOD was higher and the content of MDA was lower in IH28 and in IH14-Est compared with that in CON. No significant difference of the activity of SOD and the content of MDA existed among CON, VEH, IH14, and ESTG. Est potentiated the antiarrhythmic and antioxidative effects of intermittent hypoxia on rat heart.
    Acta Pharmacologica Sinica 08/2000; 21(7):609-12. · 2.91 Impact Factor
  • Y Zhang · J Xu · N Zhong
    [Show abstract] [Hide abstract]
    ABSTRACT: To observe the expression of NF-kappa B activation and the effect of dexamethasone on the NF-kappa B activity in the human airway epithelial cell line 16HBE after TNF-alpha stimulation. After 16HBE was treated with different concentration of TNF-alpha(10 U/ml, 100 U/ml, 1,000 U/ml) and dexamethasone (100 nmol/L), total RNA and cellular, nuclear protein were extracted at 1 hour, 2 hour, 4 hour, respectively. RT-PCR and electrophoresis mobility shift assay(EMSA) were used to detect the expression of IL-8 mRNA and NF-kappa B activation. The activity of NF-kappa B activation became stronger at 1 hour in the TNF-alpha stimulated group than the control, peaked at 2 hours and then decreased at 4 hours. Supershift assay confirmed that both p50 and p65 were components of active NF-kappa B. At the same time, IL-8 mRNA expression was elevated at 4 hours. After dexamethasone treatment, the expression of NF-kappa B activation and IL-8 mRNA became lower. It is suggested that activated NF-kappa B played a key role in the inflammatory process of respiratory diseases through regulating the expression of some important factors (cytokines). Glucocorticoid inhibited the activation of NF-kappa B and showed antiinflammatory effect.
    Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 06/2000; 23(5):296-9.
  • N Zhong · Y Zhang · Q Z Fang · Z N Zhou
    [Show abstract] [Hide abstract]
    ABSTRACT: To quantify the levels of HSP70 induced by different durations of intermittent (high altitude) hypoxia and to correlate them with the degree of protection of the rat heart from ischemic injury. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the level of HSP70 mRNA expression in rat myocardium. Ischemia/reperfusion injury was presented as severity of arrhythmias induced by occlusion and reperfusion of the left anterior descending coronary artery of rat heart. The level of HSP70 mRNA expression increased progressively along with the duration of intermittent hypoxia training. It was 2.6, 3.6, and 3.8 folds after 14-, 28-, and 42-d exposures compared to that of normoxia. The tolerance of rat heart to ischemia/reperfusion injury increased with hypoxia pretreatment. Such an effect was significant after rat were exposed to a 28-d intermittent hypoxia (IH). The scores for ischemia and reperfusion inducing arrhythmia for 28- and 42-d IH were 1.2 +/- 0.5, 1.0 +/- 0.5 and 1.0 +/- 0.5, 0.9 +/- 0.5 (P < 0.01 compared with 4.0 +/- 0.7, 3.3 +/- 0.6 in normoxia rats). The overexpression of HSP70 and the increased tolerance to subsequent acute ischemia/reperfusion injury could last for 2 wk after the rats (subjected to 28 d IH) returned to normoxia. Furthermore, there was a reverse correlation between the amount of HSP70 induced and the arrhythmia occurrence (r = -0.98, -0.92 for ischemia and reperfusion induced arrhythmia, P < 0.01). These results suggest that increased resistance of rat heart to ischemia/reperfusion injury after intermittent hypoxia exposure may be related to the amount of HSP70 induced.
    Acta Pharmacologica Sinica 06/2000; 21(5):467-72. · 2.91 Impact Factor
  • Source
    Y Zhang · N Zhong · H F Zhu · Z N Zhou
    [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of the study was to observe the effects of intermittent hypoxia exposure (IH) on the arrhythmia and antioxidation with ligation of coronary artery of rat heart together with measuring SOD (superoxide dismutase) and MDA (malondialdehyde) in myocardium. Comparison with continued hypoxia exposure was also made. The results obtained are as follows. (1) Arrhythmia scores of ischemic arrhythmia and reperfusion arrhythmia observed in the rats treated with IH 28-day (IH28) and 42-day (IH42), one week (IH28-1W) and two weeks (IH28-2W) after 28-day IH, as well as in those with continued hypoxia 28-day (CH28) and 42-day (CH42), were significantly lower than controls. (2) SOD in IH28, IH42, CH28, CH42, IH28-1W, IH28-2W and three weeks after 28-day IH were significantly higher than controls; MDA in IH14, IH28, IH42, CH28, CH42, IH28-1W and IH28-2W were significantly lower than controls. It is suggested that IH for 28 or 42 days has some definite antiarrhythmic effect against ischemia and reperfusion, which was related to the strength of antioxidation in myocardium. The antiarrhythmic effects occurred gradually after 14 days IH and persisted for about two weeks after 28 days IH.
    Sheng li xue bao: [Acta physiologica Sinica] 05/2000; 52(2):89-92.
  • N Zhong · Q.Z. Fang · Y Zhang · J.Q. Qian · Z.N. Zhou
    [Show abstract] [Hide abstract]
    ABSTRACT: To study the effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenyl-ethylamino) propane hydrochloride (DDPH) on action potential (AP), inward rectifier K+ current (IK1), and delayed rectifier K+ current (IK) in isolated guinea pig ventricular myocytes. Whole cell patch-clamp recording techniques. DDPH 0.1-100 mumol.L-1 decreased 50% duration of action potential (APD50) concentration-dependently. APD50 was shortened from (493 +/- 58) to (262 +/- 38) ms (n = 7 cells from 5 guinea pigs, P < 0.01) by DDPH 10 mumol.L-1. However, 90% duration of action potential (APD90) was increased by DDPH (> 1 mumol.L-1). At high concentration (> 10 mumol.L-1) DDPH decreased resting membrane potential (RP) and amplitude of action potential (APA). DDPH inhibited tail current of IK (IK.tail) concentration-dependently, 46% at 10 mumol.L-1 and 78% at 100 mumol.L-1. EC50 for DDPH inhibiting IK was 13.3 (11.6-16.7) mumol.L-1. DDPH also blocked IK1. DDPH at high concentration (> 10 mumol.L-1) shifted the reverse potential of IK1 positively. All the effects of DDPH were reversible after washout. DDPH blocked both IK1 and IK current in guinea pig ventricular myocytes.
    Acta Pharmacologica Sinica 05/2000; 21(4):301-5. · 2.91 Impact Factor
  • Source
    N Zhong · Q Z Fang · Y Zhang · Z N Zhou
    [Show abstract] [Hide abstract]
    ABSTRACT: To characterize the properties of chloride currents and its modulation in human umbilical vein endothelial cells (HUVEC). Using whole-cell patch-clamp recording techniques. Exposure of HUVEC to 13.5% and 27% hypotonic solution (HTS) induced a current ICl, vol. This current was correlated with the changes in cell volume and showed a modest outward rectification. It was slowly inactivated at positive potential (> 50 mV), and it was time- and voltage-independent in kinetics. The current densities (pA/pF) were 20 +/- 3 (13.5% HTS) and 58 +/- 4 (27% HTS, n = 7), respectively at +100 mV test potential. Applying GTP gamma s (300 mumol.L-1) elicited a current similar to ICl, vol, while cAMP (0.5 mmol.L-1) had no effect on the current. Increase in [Ca2+]i, either by directly loading cells with high concentration of Ca2+ (CaCl2), or by perfusing vasoactive agonist ATP (10 mumol.L-1), activated ICl, Ca. The current density was only (23 +/- 5) pA/pF (n = 8 cells). Such current was slowly activated at positive potential, inactivated quickly at negative potential, and showed strong outward rectification. Both currents were inhibited by DIDS and verapamil. Challenging a cell with elevated [Ca2+]i and HTS activated ICl, vol on the top of ICl, Ca in the same cell, suggested co-existence of these two currents and that they were modulated by different ways. cAMP-regulated chloride channel and ClC (chloride channel family) channel were absent. HUVEC express two kinds of chloride channels, ICl, vol activated by change in cell volume and ICl, Ca by elevation of [Ca2+]i, respectively.
    Acta Pharmacologica Sinica 03/2000; 21(3):215-20. · 2.91 Impact Factor
  • N Zhong · J Q Qian
    [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the influence of selective antagonist for muscarinic (M) receptor subtype on tetrandrine (Tet) reducing heart rate, inhibiting sinoatrial node (SAN) function, and its ionic mechanism. Effects of reducing heart rate of Tet were maintained in isolated right atrium and pithed rats. Modification on action potentials (AP) of SAN cells and L-type calcium current (ICa-L) by Tet were recorded by means of standard microelectrode and patch-clamp whole cell recording techniques. Tet inhibited spontaneous beating rate of isolated right atrium (EC50, 23.7 mumol.L-1) and reduced heart rates in pithed rats in a concentration-dependent manner (EC50, 18.6 mg.kg-1). Automaticity of SAN was inhibited by Tet. AP upstroke velocity (Vmax), spontaneous depolarization rates in phase 4 (SP4) were decreased and sinus cycle length (SCL) was prolonged when treated with Tet. Tet (30 mumol.L-1) caused a reduction in peak value of ICa-L from (1275 +/- 190) pA to (498 +/- 94) pA in isolated single cardiomyocyte. Atropine and AF-DX 116 (M2 subtype selective antagonist) could attenuate such effects of Tet in a competitive mode. Negative chronotropic effects of Tet are due to its inhibition of ICa-L. Modification on ICa-L is the major mechanism of M receptor modulating Tet effects.
    Zhongguo yao li xue bao = Acta pharmacologica Sinica 01/2000; 20(12):1068-72.

Publication Stats

93 Citations
14.35 Total Impact Points


  • 2000
    • Shanghai Institute of Technology
      Shanghai, Shanghai Shi, China
    • Chinese Academy of Sciences
      • Institute of Plant Physiology and Ecology
      Peping, Beijing, China
    • Guangzhou Institute of Respiratory Disease
      Shengcheng, Guangdong, China