Aim To study the effects of cyclovirobuxine D on inward rectifier K^- current(I_(k1) ) > transient outward K^+ current (I_(to)), L-type Ca^(2+) current (I_(Ca-L)), and actionpotential duration (APD) in isolated rat...Aim To study the effects of cyclovirobuxine D on inward rectifier K^- current(I_(k1) ) > transient outward K^+ current (I_(to)), L-type Ca^(2+) current (I_(Ca-L)), and actionpotential duration (APD) in isolated rat ventricular myocytes. Methods The whole cell patch-clamptechniques were used to study the changes of I_(k1), I_(to), I_(Ca-L) and APD in rat ventricularmyocytes. Results Cyclovirobuxine D (1-10 μmol·L^(-1)) significantly prolonged APD_(50) andAPD_(90) in isolated rat ventricular myocytes. Resting potential (RP) was decreased by 10μmol·L^(-1) of cyclovirobuxine D. Cyclovirobuxine D significantly decreased both inward andoutward components of I_(k1) . At - 100 mV, 1 and 10 μmol·L^(-1) of cyclovirobuxine D decreasedI_(k1), density from (-8.0+- 1.1) pA/pF to ( - 4.1 +- 0.7) pA/pF and ( - 3.4 +- 0.8) pA/pF,respectively, whereas at - 30 mV, I-(k1) density was decreased from (1.10 +-0.24) pA/pF to (0.61+-0.18) pA/pF and (0.36+- 0.11) pA/pF, respectively. 1_(to) was markedly inhibited bycyclovirobuxine D from the test potential of 0 mV to + 60 mV. At + 40 mV, 1 and 10μmol·L^(-1) ofcyclovirobuxine D decreased I_(to) density from (8.9+- 2.0) pA/pF to (5.5 +- 1.2) pA/pF and (4.9+-0.9) pA/pF, respectively. Cyclovirobuxine D inhibited I_(Ca-L) in a concentration-dependentmanner. At 10 mV, 1 and 10μmol·L^(-1) of cyclovirobuxine D decreased I_(Ca-L) density from ( - 9.9+- 1.8) pA/pF to ( - 6.4 +- 1.4) pA/pF and (-4.2+-0.6) pA/pF, respectively. ConclusionCyclovirobuxine D significantly prolonged APD and inhibited I_(k1), I_(to), and I_(Ca-L) in ratventricular myocytes. The inhibitory effects of cyclovirobuxine D on _(k1) and I_(to) are majormolecular mechanisms of APD prolongation in rat.展开更多
The improved current-doubler-rectifier zero-voltage-switching PWM full-bridge converter (CDR ZVS PWM FB converter) achieves ZVS for the switches in a wide load range with the use of the energy stored in the output fil...The improved current-doubler-rectifier zero-voltage-switching PWM full-bridge converter (CDR ZVS PWM FB converter) achieves ZVS for the switches in a wide load range with the use of the energy stored in the output filter inductances, and the rectifier diodes commute naturally, therefore no oscillation and voltage spike occurs. The transformer needs no special manufacture method to limit the leakage inductance. The ZVS achievement and the design considerations for the output filter inductances and the blocking capacitor are discussed for the improved CDR ZVS PWM FB converter. A 540 W prototype converter is built in the lab to verify the operational principle and design considerations for the improved converter, the experimental results are also included.展开更多
On the basis of detailed analysis of a novel harmonic counteracting method which can be used to effectively compensate the supply line harmonic currents of a passive single phase diode bridge rectifier, this paper pr...On the basis of detailed analysis of a novel harmonic counteracting method which can be used to effectively compensate the supply line harmonic currents of a passive single phase diode bridge rectifier, this paper presents two simpler single phase diode bridge rectifier configurations and their alternatives which can achieve low supply line current THD(total harmonic distortion) too. Moreover, this paper also proposes a few passive hamonic counteracting networks for multi single phase rectifiers which are connected in parallel.展开更多
Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea p...Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ_23 at 10, 30and 100 μmol ·L_-1 slowed the repolarization in AP dose-dependently. The APD_90 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca^2+. In voltageclamp mode, IQ_23 effectively blocked both the components of the delayed rectifier potassium current(I_k), i.e., I_ks and I_kr. At concentrations of 30 and 100 μmol· L^-1, IQ_23 suppressed I_ks by 21% and 26%and suppressed I_kr by 67% and 86% respectively. But even at 100 μmol·L^-1, IQ_23 had little effect onthe inward rectifier potassium current (I_k1). It is concluded: 1. IQ_23 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca^2+; 2.IQ_23 blocks both I_ks and Ikr in the ventricular myocytes without obvious specificities between them.展开更多
The effects of BTHP on Ca 2+ independent action potential and the two components of delayed rectifier potassium currents were studied in guinea pig single ventricular myocytes by using whole cell patch clamp tec...The effects of BTHP on Ca 2+ independent action potential and the two components of delayed rectifier potassium currents were studied in guinea pig single ventricular myocytes by using whole cell patch clamp technique. BTHP 30 μmol·L -1 significantly prolonged APD 90 from 143±16 ms to 184±21 ms ( P 【0.01, n=5) without affecting either the RP or APA, and the APD prolonging effects of BTHP were independent of extracellular Ca 2+ . BTHP inhibited both I kr (IC 50 =7 9 μmol·L -1 ) and I ks (IC 50 =22 4 μmol·L -1 ) in a concentration dependent fashion. The results demon strated that BTHP had no obvious selectivity for I kr and I ks .展开更多
文摘Aim To study the effects of cyclovirobuxine D on inward rectifier K^- current(I_(k1) ) > transient outward K^+ current (I_(to)), L-type Ca^(2+) current (I_(Ca-L)), and actionpotential duration (APD) in isolated rat ventricular myocytes. Methods The whole cell patch-clamptechniques were used to study the changes of I_(k1), I_(to), I_(Ca-L) and APD in rat ventricularmyocytes. Results Cyclovirobuxine D (1-10 μmol·L^(-1)) significantly prolonged APD_(50) andAPD_(90) in isolated rat ventricular myocytes. Resting potential (RP) was decreased by 10μmol·L^(-1) of cyclovirobuxine D. Cyclovirobuxine D significantly decreased both inward andoutward components of I_(k1) . At - 100 mV, 1 and 10 μmol·L^(-1) of cyclovirobuxine D decreasedI_(k1), density from (-8.0+- 1.1) pA/pF to ( - 4.1 +- 0.7) pA/pF and ( - 3.4 +- 0.8) pA/pF,respectively, whereas at - 30 mV, I-(k1) density was decreased from (1.10 +-0.24) pA/pF to (0.61+-0.18) pA/pF and (0.36+- 0.11) pA/pF, respectively. 1_(to) was markedly inhibited bycyclovirobuxine D from the test potential of 0 mV to + 60 mV. At + 40 mV, 1 and 10μmol·L^(-1) ofcyclovirobuxine D decreased I_(to) density from (8.9+- 2.0) pA/pF to (5.5 +- 1.2) pA/pF and (4.9+-0.9) pA/pF, respectively. Cyclovirobuxine D inhibited I_(Ca-L) in a concentration-dependentmanner. At 10 mV, 1 and 10μmol·L^(-1) of cyclovirobuxine D decreased I_(Ca-L) density from ( - 9.9+- 1.8) pA/pF to ( - 6.4 +- 1.4) pA/pF and (-4.2+-0.6) pA/pF, respectively. ConclusionCyclovirobuxine D significantly prolonged APD and inhibited I_(k1), I_(to), and I_(Ca-L) in ratventricular myocytes. The inhibitory effects of cyclovirobuxine D on _(k1) and I_(to) are majormolecular mechanisms of APD prolongation in rat.
文摘The improved current-doubler-rectifier zero-voltage-switching PWM full-bridge converter (CDR ZVS PWM FB converter) achieves ZVS for the switches in a wide load range with the use of the energy stored in the output filter inductances, and the rectifier diodes commute naturally, therefore no oscillation and voltage spike occurs. The transformer needs no special manufacture method to limit the leakage inductance. The ZVS achievement and the design considerations for the output filter inductances and the blocking capacitor are discussed for the improved CDR ZVS PWM FB converter. A 540 W prototype converter is built in the lab to verify the operational principle and design considerations for the improved converter, the experimental results are also included.
文摘On the basis of detailed analysis of a novel harmonic counteracting method which can be used to effectively compensate the supply line harmonic currents of a passive single phase diode bridge rectifier, this paper presents two simpler single phase diode bridge rectifier configurations and their alternatives which can achieve low supply line current THD(total harmonic distortion) too. Moreover, this paper also proposes a few passive hamonic counteracting networks for multi single phase rectifiers which are connected in parallel.
文摘Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ_23 at 10, 30and 100 μmol ·L_-1 slowed the repolarization in AP dose-dependently. The APD_90 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca^2+. In voltageclamp mode, IQ_23 effectively blocked both the components of the delayed rectifier potassium current(I_k), i.e., I_ks and I_kr. At concentrations of 30 and 100 μmol· L^-1, IQ_23 suppressed I_ks by 21% and 26%and suppressed I_kr by 67% and 86% respectively. But even at 100 μmol·L^-1, IQ_23 had little effect onthe inward rectifier potassium current (I_k1). It is concluded: 1. IQ_23 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca^2+; 2.IQ_23 blocks both I_ks and Ikr in the ventricular myocytes without obvious specificities between them.
文摘The effects of BTHP on Ca 2+ independent action potential and the two components of delayed rectifier potassium currents were studied in guinea pig single ventricular myocytes by using whole cell patch clamp technique. BTHP 30 μmol·L -1 significantly prolonged APD 90 from 143±16 ms to 184±21 ms ( P 【0.01, n=5) without affecting either the RP or APA, and the APD prolonging effects of BTHP were independent of extracellular Ca 2+ . BTHP inhibited both I kr (IC 50 =7 9 μmol·L -1 ) and I ks (IC 50 =22 4 μmol·L -1 ) in a concentration dependent fashion. The results demon strated that BTHP had no obvious selectivity for I kr and I ks .
