岩滩水电站1号机调速器电气部分改造浅析

笔者结合岩滩水电站1号机调速器电气部分改造实例,分析了设备升级改造原因,从“失电动作”规则实现、三选二逻辑功能选择、B码对时应用等8个方面介绍改造情况,详细阐述改造过程中遇到的问题和解决措施以及后续待优化的问题和解决措施。试验证明,改造后的各项指标和功能均满足要求,改造取得了良好的效果。此次改造,为岩滩水电站其他机组调速器改造以及同类型水电站调速器改造提供借鉴和参考。

关于调速器系统主配压阀的改进分析

某电厂原有调速器主配压阀为掉电自复中式,断电后导叶保持不动,同时调速器系统还存在一些需要进一步改进和优化的问题:事故配压阀和紧急停机电磁阀同时动作时关机速度加快,导致蜗壳水压异常上升;主配压阀内漏情况较严重;主配动作时,管道振动较大等。为提高机组运行的安全性和可靠性,对现有调速器系统进行了升级改造。文章主要针对改造后调速器系统主配压阀的“失电动作”进行详细的介绍。

Effects of IQ_23 on the Repolarization and Both Components of the Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytcs

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.

Effects of IQ23 on the Repolarization and Both Components of the Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytcs

Using patch clamp whole cell recording techiques, we examined the effects ofIQ23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential （AP） andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ23 at 10, 30and 100 μmol ·L-1 slowed the repolarization in AP dose-dependently. The APD90 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca2+. In voltageclamp mode, IQ23 effectively blocked both the components of the delayed rectifier potassium current（Ik）, i.e., Iks and Ikr. At concentrations of 30 and 100 μmol· L-1, IQ23 suppressed Iks by 21% and 26%and suppressed Ikr by 67% and 86% respectively. But even at 100 μmol·L-1, IQ23 had little effect onthe inward rectifier potassium current （Ik1）. It is concluded: 1. IQ23 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca2+; 2.IQ23 blocks both Iks and Ikr in the ventricular myocytes without obvious specificities between them.

Characterization of a Chinese KCNQ1 mutation （R259H） that shortens repolarization and causes short QT syndrome 2

Objectives To evaluate the association between a KCNQ 1 mutation, R259H, and short QT syndrome （SQTS） and to explore the elec- trophysiological mechanisms underlying their association. Methods We performed genetic screening of SQTS genes in 25 probands and their family members （63 patients）. We used direct sequencing to screen the exons and intron-exon boundaries of candidate genes that en- code ion channels which contribute to the repolarization of the ventricular action potential, including KCNQI, KCNH2, KCNE1, KCNE2, KCNJ2, CACNAlc, CACNB2b and CACNA2D1. In one of the 25 SQTS probands screened, we discovered a KCNQ1 mutation, R259H. We cloned R259H and transiently expressed it in HEK-293 cells; then, currents were recorded using whole cell patch clamp techniques. Results R259H-KCNQ 1 showed significantly increased current density, which was approximately 3-fold larger than that of wild type （WT） after a depolarizing pulse at 1 s. The steady state voltage dependence of the activation and inactivation did not show significant differences between the WT and R259H mutation （P 〉 0.05）, whereas the time constant of deactivation was markedly prolonged in the mutant compared with the WT in terms of the test potentials, which indicated that the deactivation of R259H was markedly slower than that of the WT. These results suggested that the R259H mutation can effectively increase the slowly activated delayed rectifier potassium current （Irs） in phase 3 of the cardiac action potential, which may be an infrequent cause of QT interval shortening. Conclusions R259H is a gain-of-function muta- tion of the KCNQ1 channel that is responsible for SQTS2. This is the first time that the R259H mutation was detected in Chinese people.

Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardium

Objective Allocryptopine （ALL） is an effective alkaloid of Corydalis decumbens （Thunb.） Pers. Papaveraceae and has proved to be an- ti-arrhythmic. The purpose of our study is to investigate the effects of ALL on transmural repolarizing ionic ingredients of outward potassium current （Ito） and slow delayed rectifier potassium current （IKs）. Methods The monophasic action potential （MAP） technique was used to record the MAP duration of the epicardium （Epi）, myocardium （M） and endocardium （Endo） of the rabbit heart and the whole cell patch clamp was used to record/to and IKs in cardiomyocytes of Epi, M and Endo layers that were isolated from rabbit ventricles. Results The effects of ALL on MAP of Epi, M and Endo layers were disequilibrium. ALL could effectively reduce the transmural dispersion of repolarization （TDR） in rabbit transmural ventricular wall. ALL decreased the current densities of/to and IKs in a voltage and concentration dependent way and narrowed the repolarizing differences among three layers. The analysis of gating kinetics showed ALL accelerated the channel activation ofIto in M layers and partly inhibit the channel openings of/to in Epi, M and Endo cells. On the other hand, ALL mainly slowed channel deactivation of IKs channel in Epi and Endo layers without affecting its activation. Conclusions Our study gives partially explanation about the mechanisms of tmnsmural inhibition of/to and IKs channels by ALL in rabbit myocardium. These findings provide novel perspective regarding the anti-arrhythmogenesis application of ALL in clinical settings.

有关法国水电厂自动化的几个问题

介绍了法国水电厂为实现无人值班而采用的失电动作原理,无人值班电厂按容量不同所做的分类,以及不同无人值班电厂管理及待命值班人员职责的差异等。

Increased intracellular calcium concentration causes electrical turbulence in guinea pig ventricular myocytes

Dysregulation of intracellular Ca2+ homeostasis is associated with various pathological conditions and arrhythmogenesis of the heart.The objective of this study was to investigate the effects of an acute increase in intracellular Ca2+ concentration ([Ca2+] i) on the electrophysiology of ventricular myocytes by mimicking intracellular Ca 2+ overload.The [Ca2+] i was clamped to either a controlled (65-100 nmol L-1) or increased (1 μmol L-1) level.The transmembrane action potentials and ionic currents were recorded using whole-cell patch clamp techniques.We found that the acute increase in [Ca2+] i shortened the action potential duration,reduced the action potential amplitude,maximum depolarization velocity and resting membrane potential,caused delayed after-depolarizations (DADs),and triggered activity--compared with these parameters in the control.The increased [Ca2+] i augmented late I Na in a time-dependent manner,reduced ICaL and IK1,and increased IKr but not IKs.The results of this study can be used to explain calcium overload-induced ventricular arrhythmias.

Streptomycin inhibits electrophysiological changes induced by stretching of chronically infarcted rat hearts

Objective： To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin （SM） on these changes in vivo. Methods： Sixty Wistar rats were divided randomly into four groups： a control group （n=15）, an SM group （n=15）, a myocardial infarction （MI） group （n=15）, and an MI＋SM group （n=15）. Chronic MI was obtained by ligating the left anterior descending branch （LAD） of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels （SACs） was achieved by intramuscular injection of SM （180 mg/（kg·d）） for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential （MAP）. The effect of stretching was examined by assessing the 90% monophasic action potential duration （MAPD90）, premature ventricular beats （PVBs）, and ventricular tachycardia （VT）. Results： The MAPD90 decreased during stretching in both the control （from （50.27±5.61） ms to （46.27±4.51） ms, P〈0.05） and MI groups （from （65.47±6.38） ms to （57.47±5.76 ms）, P〈0.01 ）. SM inhibited the decrease in MAPD90 during inflation （（46.27±4.51） ms vs. （49.53±3.52） ms, P〈0.05 in normal hearts; （57.47±5.76） ms vs. （61.87±5.33） ms, P〈0.05 in MI hearts）. The occurrence of PVBs and VT in the MI group increased compared with that in the control group （PVB： 7.93±1.66 vs. 1.80±0.86, P〈0.01; VT： 7 vs. 1, P〈0.05）. SM decreased the occurrence of PVBs in both normal and MI hearts （0.93±0.59 vs. 1.80±0.86 in normal hearts, P〈0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P〈0.01）. Conclusions： Stretch-induced MAPD90 changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback （MEF）, but that there might be other mechanisms involved in causing VT in chronic MI.