sodiumionchannel：鈉離子通道-資料下載頁
2025-01-12 08:36本頁面
【正文】 xtensively ? “Please Shock Shock Shock, Everybody Shock, And Lets Make Patients Better” The purpose of defibrillation of ventricular arrhythmias is to apply a controlled electrical shock to the heart, which leads to depolarization of the entire electrical conduction system of the heart. When the heart repolarizes, the normal electrical conduction may restore itself Depolarization theoretically inactivates all voltagegated Na+ channels, and allows Voltagegated potassium channels to activate, and help hyperpolarize the membrane +40 mv 70 mv After Administration Of Procainamide V FIB/V TACH After phosphorylation/ phosphate cleavage ? Usedependent block of sodium channels. ? Blocks potassium channels. ? Blocks alphaadrenergic receptors. ? Blocks muscarinic receptors. ? Used to attempt to terminate persistent reentrant arrhythmias ? Reduces automaticity of ALL pacemakers (both the SA node and ANY tissue capable of generating a pacemaker potential) ? Slows Down Conduction of depolarization in ALL tissues of the heart and decreases cardiac excitability ? This is your last resort. Giving this drug may stop the arrhythmia, but make it almost impossible for the heart to spread impulses after Summary For the Lecture ? Na+ channels are prised subunits, the Alpha of 4 repeating motifs, each motif with 6 transmembrane domains ? There are voltage, ligand, and mechanicallygated Na + channels ? Na+ channels are involved in the depolarization of excitable membranes ? Na+ channels have multiple modalities of modulation, which can alter neuronal/membrane excitability ? Na+ channels are the target of a multitude of pharmacological agents Summary ? Na+ channels Are involved in the remissionrelapse of MS ? Na+ channel gating can be significantly affected by modulation (phosphorylation, mutation, proteolytic cleavage) ? Mutation in Nav is implicated in Long QT syndrome, generating persistent and slow inactivating sodium current
教學(xué)課件相關(guān)推薦
鄂ICP備17016276號-1