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Biomedical subjects

M X Jiang

Publications and source records attributed to M X Jiang.

At least 19 recordsLinked to original sources
PubMed2001

Effect of sea anemone toxin anthopleurin-Q on sodium current in guinea pig ventricular myocytes.

AIM: To investigate the effects of a sea anemone toxin anthopleurin-Q (AP-Q) isolated from Anthopleura xanthogrammica on sodium current (INa) in isolated guinea pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. INa was recorded using whole-cell patch-clamp technique. RESULTS: AP-Q (3 - 300 nmol/L) increased INa in a concentration-dependent manner. The EC50 value for increasing INa was 104 nmol/L (95 % confidence range: 78 - 130 nmol/L). AP-Q 300 nmol/L shifted the I-V curve to the leftward, changed the membrane potential of half maximal activation to more negative potential from (-36.3 +/- 2.3) mV to (-43 +/- 3) mV (n = 6, P < 0.01) and changed the membrane potential of half maximal inactivation to more positive potential from (-75 +/- 6) mV to (-59 +/- 5) mV (n = 6, P < 0.01). AP-Q 300 nmol/L shortened the half-recovery time of INa from (114 +/- 36) ms to (17 +/- 2) ms (n = 6, P < 0.01). The fast inactivation time constant (tauf) of INa was markedly increased by AP-Q 300 nmol/L. CONCLUSION: AP-Q has a stimulating effect on I(Na) with slowing the inactivation course of INa.

Animals↗
PubMed2001

[Effects of 4-aminopyridine on calcium currents and sodium currents in guinea pig ventricular myocytes].

AIM: To investigate the effect of 4-aminopyridine (4-AP) on ion channels of myocytes. METHODS: L-type calcium channel and sodium channel currents were recorded in guinea pig single ventricular myocyte using whole-cell patch-clamp techniques. RESULTS: 4-AP, 0.1, 0.5 and 1.0 mmol.L-1 were shown to inhibit L-type calcium channel currents (ICa, L) and sodium channel currents (INa) concentration-dependently. The percentage of inhibition were (11.6 +/- 1.7)%, (37.5 +/- 8.3)% and (54.5 +/- 6.9)% (P < 0.01) respectively for ICa, L, and (22.1 +/- 14.3)% (P < 0.05), (39.4 +/- 8.8)% and (62.3 +/- 6.8)% (P < 0.01) respectively for INa. 4-AP 0.5 mmol.L-1 shifted the I-V curves of ICa, L and INa upwardly. CONCLUSION: 4-AP blocked L-type calcium channel and sodium channels in guinea-pig ventricular myocytes concentration-dependently.

4-Aminopyridine↗
PubMed2000

[Effects of amiloride on calcium current in thyroxine-induced hypertrophied rat heart].

AIM: The L-Type calcium currents were investigated in normal, hypertrophied and amiloride-treated rat ventricular myocytes so as to clarify the possible cause of the action potential lengthening that has been reported in thyroxine-induced hypertrophy. The interactions between agents such as thyroxine, Ang II and phenylephrine which induced hypertrophy with amiloride on the calcium current were analyzed. METHODS: Myocardial hypertrophy was induced by i.p. L-thyroxine in rats. The cell length, cell width and cell area were measured by image analysis technique. For recording ICaL, the whole cell patch clamp technique was used. Potassium currents were suppressed by replacing K+ ions with Cs+ ions in intracellular media, and sodium current was blocked by 50 mumol.L-1 tetrodotoxin. RESULTS: The Ca2+ current was found to be larger in hypertrophied cells (783pA) than in normal cells (433pA) and in amiloride-treated cells (429pA). However, no significant difference was observed in current density (6.54, 8.33, 5.74 pA/pF) in normal, hypertrophied and amiloride-treated cells. ICa displayed the same voltage dependence in three cell types. The potential giving 50% of activation (V1/2) moved towards more negative and the slope of activation curve was smaller in hypertrophied cells than in normal cells and amiloride cells. When expressed as percentages, the maximal increases in ICa were obtained with 1 mumol.L-1 Ang II and 100 mumol.L-1 phenylephrine in normal cells (+45.5% and +81.8%). Thyroxine 100 mumol.L-1 showed no effect on ICa. After giving amiloride, Ang II and phenylephrine did not increase the amplitude of ICa. CONCLUSION: At the dose of 0.5 mg.kg-1.d-1, amiloride (p.o.) was shown to prevent the amplitude of ICa from increasing and to be effective against increases of amplitude of ICa by Ang II and phenylephrine.

Amiloride↗
PubMed1997

[The synergistic effect of tetrandrine and rotundine on the action potential of rabbit sinus node dominant pacemaker cell and calcium currents of ventricular myocytes from guinea-pig].

Standard microelectrode technique and the whole-cell clamp technique were used to investigate the effects of tetrandrine and rotundine on the action potential of rabbit sinus node dominant pacemaker cell and calcium currents of ventricular myocytes from guinea-pig. The results indicate that: tetrandrine 1-200 mumol.L-1 and rotundine 3-300 mumol.L-1 decreased the action potential amplitude(APA), the maximal upstroke velocity (Vmax), spontaneous depolarizing velocity of phase 4(SP4) and prolonged the sinus circle length(SCL) in a dose-dependent manner. Tetrandrine 0.1 mumol.L-1 in combination with rotundine 0.3 mumol.L-1 was shown to effectively reduce the ICa of ventricular myotytes from guinea-pig, the rate of inhibition is 19.6%. The results suggest that the two drugs have a good synergistic effect on inhibiting calcium current. These results might also put forward a valuable theoretic base for using the two drugs together in treating patients.

Action Potentials↗
PubMed1996

Effects of 7-bromoethoxybenzene-tetrahydropalmatine on voltage-dependent currents in guinea pig ventricular myocytes.

AIM: To study the anti-arrhythmic mechanism of 7-bromoethoxybenzene-tetrahydropalmatine (EBP). METHODS: Whole-cell current and voltage clamp on isolated guinea pig ventricular cells. RESULTS: EBP 30 mumol.L-1 prolonged APD90 from 430 +/- 47 ms to 514 +/- 61 ms (n = 5, P < 0.05) without effects on the action potential amplitude and resting potential. Delayed outward K+ current and its tail current were blocked by EBP in a concentration-dependent fashion, while EBP did not change the amplitudes of the sodium current, the L type calcium current, and the inwardly rectifying potassium current. CONCLUSION: The mechanism of anti-arrhythmic action of EBP was to prolong the APD through inhibiting the delayed rectified potassium current.

Action Potentials↗
PubMed1996

[Blocking effects of benzyltetrahydropalmatine on delayed rectified K+ currents expressed in Xenopus oocytes and in toad oocytes].

The effects of benzyltetrahydropalmatine (BTHP) on delayed rectified K+ currents (Ik) expressed in Xenopus oocytes and Ik of toad (Bufo bufo gargarizans) oocytes were studied. The Ik expressed in Xenopus oocytes was measured after microinjection of mRNA isolated from carp fish (C anratus L.) brains with double -microelectrode voltage clamp technique. The maximum and mean value of Ik expressed in Xenopus oocytes were 600 nA and 360 +/- 104 nA, respectively. BTHP reduced the current amplitude of Ik expressed in Xenopus oocytes in 10-1000 mumol.L-1 dose-dependently, EC50 was 29 mumol.L-1. Also, the reduction of Ik of toad oocytes was 9.1%, 29.1%, 54.7% and 68.6% by BTHP 10, 30, 100 and 1000 mumol.L-1, respectively, EC50 was 33 mumol.L-1. The results showed that BTHP possesses an inhibitory effect on Ik, the main ion mechanism of antiarrhythmic action of BTHP.

Animals↗
PubMed1995

[Protective effects of tetrandrine on ischemic myocardia in anesthetized dogs].

The present study indicates that iv tetrandrine may transiently decrease blood pressure, while other hemodynamic parameters such as LVP, +/- dp/dtmax, LVEDP, HR and CO may not be significantly altered. During coronary occlusion three of five dogs developed ventricular fibrillation (VF) and died in the control group, i.e. incidences of VF and mortality were 60%. While tetrandrine (Tet) appeared to reduce the severity of ischemic injury. It may alleviate arrhythmia and prevent VF and death in four of the five dogs. Tet also attenuated Ca2+ accumulation in myocardial cell, reduced melondialdehyde (MDA) production in ischemic myocardial and decreased CPK release in comparison with the control. It appears that Tet may have significant protective effects against ischemia induced cardiac damage in anesthetized dogs.

Alkaloids↗
PubMed1993

[Effects of linesinine on slow action potentials in myocardium and slow inward current in canine cardiac Purkinje fibers].

Standard microelectrode and two-microelectrodes voltage clamp techniques were used to study the effects of linesinine (Lien), an alkaloid extracted from the green seed embryo of Nelumbo nucifera Gaertn, on slow action potentials (AP) and slow inward current (Isi). Lien 10-100 mumol/L was shown to concentration-dependently decrease the action potential amplitude (APA), the maximal velocity of phase 0 depolarization (Vmax) and prolong the sinus cycle length (SCL) of slow AP in isolated sinoatrial node (SAN) pacemaker cells of rabbits. On both slow APs of rabbit SAN cells and guinea pig papillary muscles partly depolarized by high K+, Bay K 8644 0.03 mumol/L markedly increased the APA and Vmax, which were obviously antagonized by Lien 10 mumol/L. Moreover, Lien 1-100 mumol/L was found to inhibit the Isi of canine cardiac Purkinje fiber in concentration-dependent manner. Lien 3 and 100 mumol/L reduced the peak value of Isi by 14% and 88% respectively. The results suggest that Lien possesses calcium antagonistic effects.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

Comparison of effects of tetrandrine on ionic channels of isolated rat neurohypophysial terminals and Y1 mouse adrenocortical tumor cells.

UNLABELLED: The effects of tetrandrine on the voltage-gated Ca2+, K+, and Na+ channels of the isolated rat neurohypophysial nerve terminals and Y1 mouse adrenocortical tumor cells were studied using standard and perforated patch-clamp techniques. Among the inward ionic currents, the T-type Ca2+ channel current (I(Ca)) in the Y1 cell line was strongly inhibited (by 52.9%) by a low concentration (13 mumol.L-1) of externally applied tetrandrine. The L-type I(Ca) in the isolated nerve terminals was also strongly inhibited (by 54.2%) by externally applied tetrandrine 33 mumol.L-1, whereas the N-type I(Ca) and Na+ current were not significantly affected by the same dose of the alkaloid. While it had no effect on the fast, transient K+ channels, external application of tetrandrine 1 mumol.L-1 blocked a slowly-gating, maxi Ca(2+)-activated K+ (K+(Ca)) channel in the nerve terminals, decreasing its P(o) by 84.4%. CONCLUSIONS: (1) The order of the sensitivities of ionic channels to tetrandrine is K+(Ca) > T- > L- > N-type Ca2+ > Na+; (2) tetrandrine serves as a specific blocker of the slowly-gating K+(Ca) channel.

Adenoma↗
PubMed1992

[Effects of benzyltetrahydropalmatine on rat portal vein and guinea pig myocardium].

In isolated rat portal vein, benzyltetrahydrophalmatine (BTHP) 0.3-100 mumol.L-1 dose-dependently increased the spontaneous mechanical activity. However, BTHP 300 mumol.L-1 showed an inhibitory effect on the spontaneous contraction. BTHP 200 mumol.L-1 reversed positive staircase phenomenon to negative ones in left atrium of guinea pig and inhibited the amplitude and Vmax and shortened the action potential duration (APD50) of the slow action potentials induced by high K+ (24 mmol.L-1) in guinea pig papillary muscles. BTHP reduced also the contractile force in papillary muscles of guinea pig. These results suggest that BTHP possesses calcium antagonistic effect in high concentration.

Action Potentials↗
PubMed1991

Effects of benzyltetrahydropalmatine on delayed after depolarization and triggered activity and on His-bundle electrogram and ECG in animal experiment.

Standard microelectrode techniques were used to study the effects of benzyltetrahydropalmatine (BTHP) on ouabain-induced delayed after depolarization (DAD) and triggered activity in isolated guinea papillary muscles. The results indicate that ouabain-induced DAD and triggered activity were abolished by BTHP 100 mumol/L. In anesthetized rabbit ECG heart rate was reduced in a dose-dependent manner from control value of 288 +/- 14 to 261 +/- 14 (BTHP 5 mg/kg) and 226 +/- 36 bpm (BTHP 10 mg/kg). P-R interval was prolonged. In His-bundle electrogram, H-V interval and V duration were not affected, but A-H interval was prolonged from 41 +/- 3 to 45 +/- 5 ms.

Alkaloids↗
PubMed1990

A new kalium channel blocker of Chinese medicinal origin--benzyltetrahydropalmatine hydrochloride.

Benzyltetrahydropalmatine hydrochloride (BTHP) exhibited antiarrhythmic action in animal models. I. Electrophysiological effects of BTHP were investigated in various heart preparations. 1) BTHP markedly prolonged functional refractory period and inhibited adrenaline-induced automaticity. It decreased spontaneously beating rate of right atrium and abolished ouabain-induced delayed afterdepolarization and triggered activity of papillary muscle. 2) In standard microelectrode and contractility experiments BTHP concentration-dependently prolonged the action potential duration (APD) and effective refractory period (FRP) between 1-100 mumol/L; the force of contraction remained unchanged. 3) In voltage clamp experiments BTHP 1-100 mumol/L inhibited in dose-dependent manner the Ik with IC50 of 13 mumol/L and inhibited also Is at high concentration. 4) In monophasic action potential (MAP) of feline ventricle MAPD50 and MAPD90 were prolonged by BTHP in normal myocardium, and shortened APD induced by ischemia and reperfusion was restored to normal level. 5) In ECG and His-bundle electrogram heart rate was reduced; P-R and A-H interval were prolonged, but H-V interval and V duration were unaffected. II. BTHP showed a competitive alpha 1-adrenoceptor-blocking effect with pA2 value of 5.8 and 5.86 in rat anococcygeus muscle and rabbit aortic strips respectively. Radioligand binding assays showed that BTHP had affinity for both alpha 1 and alpha 2-adrenoceptor. The results from these experiments show that BTHP is a new K+ channel blocker of Chinese medicinal origin with alpha 1-adrenoceptor-blocking action.

Alkaloids↗
PubMed1990

[The mechanism of antiarrhythmic action of 7-bromoethoxybenzene-tetrahydropalmatine].

The mechanism of antiarrhythmic action and the electrophysiologic effects of 7-bromoethoxybenzene-tetrahydroptamine (EBP) have been studied using conventional microelectrode technique. The effect of EBP on the membrane ISi and I(X) currents were investigated in the canine cardiac purkinje fibres using the double microelectrode voltage clamp methods. EBP was shown to increase the duration of action potential at 20 and 90% of repolarization of isolated guinea pig papillary muscles. However, the amplitude of action potential, the resting potential and the overshoot and maximum rate of 0 phase depolarization (Vmax) remained unchanged. The membrane potential was held at 40 mV and command potential at -15 mV, 0.3 Hz 500 ms. After 10 min of perfusion of EBP 30 mumol/L, the slow inward current (ISi) was reduced markedly. When the holding potential was held at -20 mV, and the command potential at +10 mV, EBP (10-100 mumol/L) exerted a depressed effect on the delayed (outward) rectifier current (I(X)) in a dose-dependent manner. It may be concluded that the antiarrhythmic effects of EBP is mainly related to decrease the automaticity and prolong the duration of action potential at 20-90% of repolarization of isolated guinea pig papillary muscles.

Action Potentials↗
PubMed1990

[Effects of dauricine on slow action potentials in myocardium].

The effects of dauricine were examined on the slow action potentials induced by both high K+ (24 mmol/L) or TTX (40 mumol/L) in guinea pig papillary muscles and in sinoatrial node cells of rabbit. Dauricine 40 mumol/L decreased the maximal upstroke velocity (Vmax) of slow action potentials and prolonged the action potential duration at 50% repolarization (APD50). Bay K 8644 (50 nmol/L) increased the amplitude and Vmax of slow action potentials, which were antagonized by dauricine (40 mumol/L). An inhibitory influence of dauricine on the action potential amplitude was observed in papillary muscles superfused with Tyrode's solution containing high K+ and in rabbit sinoatrial node cells, but it was not with TTX. The resting potentials of the 3 slow action potentials were not affected by dauricine. The results suggest that dauricine possesses calcium-antagonistic effect.

Action Potentials↗
PubMed1990

[Effects of benzyltetrahydropalmatine on action potentials of myocardium and transmembrane K+ and Ca2+ currents in Purkinje fibers].

Standard microelectrode and two-microelectrode voltage clamp techniques were used to study the effects of benzyltetrahydropalmatine (BTHP) on action potentials of isolated myocardium and transmembrane K+ and Ca2+ currents in Purkinje fibers. The effect of BTHP 3-100 mumol/L consisted of prolongation of the action potential duration and reduction of delayed rectifier current (Ik) in concentration-dependent manner. At concentration above 200 mumol/L, the contractile force of the isolated myocardium was depressed and in voltage clamp experiments the slow inward current (Isi) was reduced. These results suggest that the inhibition of Ik induced by BTHP was in relation to its anti-arrhythmic action.

Action Potentials↗
PubMed1990

[Effects of benzyltetrahydropalmatine on delayed after depolarization and triggered activity and rabbit His-bundle electrogram].

Standard microelectrode techniques were used to study the effects of benzyltetrahydropalmatine (BTHP) on ouabain-induced delayed after depolarization (DAD) and triggered activity in isolated guinea pig papillary muscles. The results indicate that ouabain-induced DAD and triggered activity were abolished by BTHP 100 mumols/L. In anesthetized rabbit ECG heart rates were reduced in a dose-dependent manner from its control value of 288 +/- 14 to 261 +/- 14 (5 mg/kg) and 226 +/- 36 bpm (BTHP 10 mg/kg). P-R interval was prolonged. In His-bundle electrogram, H-V interval and V duration were not affected, but A-H interval was prolonged from 41 +/- 3 to 45 +/- 5 ms.

Action Potentials↗