有波动性电生理改变的Lambert-Eaton肌无力综合征一例

Lambert-Eaton肌无力综合征(LEMS)系P/Q型电压门控钙通道(P/Q type voltage-gated calcium channel, VGCC)抗体导致神经-肌肉接头突触前膜乙酰胆碱释放量减少的免疫性疾病,其电生理特征改变为低频重复电刺激(LRS)波幅递减,高频刺激(HRS)波幅递增超过60%(Oh)等的标准),或超过100%.

西比灵防治蛛网膜下腔出血后脑血管痉挛的分析

Background:Cerebrovascular disease(CVS)is one of the major complications of subarachnoid hemorrhage(SAH) and the major cause of disability and death in SAH patients.Xibiling is a blocking agent of calcium channel and can prevent the occurrence of CVS.We analyzed the effect of Xibiling in prevention of CVS after SAH in patients from April 1995 to April 2001 in our hospital in this paper.

AIM:Increasing evidence indicates that inflammation contributes to the initiation and perpetuation of atrial fibrillation ( AF) .Al-though tumor necrosis factor ( TNF)-αlevels are increased in patients with AF , the role of TNF-αin the pathogenesis of AF remains unclear.Recent research has revealed that T-type Ca2+currents ( ICa,T ) play an important role in the pathogenesis of AF .METH-ODS:In this study , we used the whole-cell voltage-clamp technique and biochemical assays to explore the role of TNF-αin the regula-tion of ICa,T in atrial myocytes.RESULTS:We found that compared with sinus rhythm (SR) controls, T-type calcium channel (TCC) subunit mRNA levels were decreased , while TNF-αexpression levels were increased , in human atrial tissue from patients with AF .In murine atrial myocyte HL-1 cells, after cultured for 24 h, 12.5, 25 and 50 μg/L TNF-αsignificantly reduced the protein expression levels of the TCC α1G subunit in a concentration-dependent manner .The peak current was reduced by the application of 12.5 or 25μg/L TNF-αin a concentration-dependent manner [from ( -15.08 ±1.11) pA/pF in controls to ( -11.89 ±0.83) pA/pF and (-8.54 ±1.55) pA/pF in 12.5 and 25 μg/L TNF-αgroups, respectively].TNF-αapplication also inhibited voltage-dependent inactivation of ICa,T shifted the inactivation curve to the left .CONCLUSION:These results suggest that TNF-αis involved in the path-ogenesis of AF, probably via decreasing ICa,T function in atrium-derived myocytes through impaired channel function and down -regula-tion of channel protein expression .This pathway thus represents a potential pathogenic mechanism in AF .

TRP离子通道

钙离子作为一种第二信使,在许多细胞功能中发挥着重要作用.短期的,如递质、腺体分泌,肌肉收缩;长期的,如细胞分化、程序死亡等[1].正常细胞都有一套完善的体系来维持钙的内稳定平衡.内质网/肌浆网的钙释放和来自质膜上钙通道的钙流入升高胞浆钙,而同时位于这两个部位的Ca2+-泵也不断地将胞浆钙储存回钙库或泵出胞外.质膜上钙通道的种类常因组织部位的不同而不同.在兴奋性细胞中,伴随着动作电位的产生,电压门控钙通道(voltage-gatedcalcium channel,VGCC)开放带进大量的钙离子,以维持神经递质分泌或肌细胞收缩.NMDA受体和N型乙酰胆碱受体等的激活是神经细胞内另一个重要的钙来源,但该类受体本身就是非选择性阳离子通道,配体和胞外受体部位的结合引起通道的开放.因此,这类钙通透性离子通道受体又可称为配体门控钙通道(ligand-gated calcium channel,LGCC).