Effects of Fluvastatin on Characteristics of Stellate Ganglion Neurons in a Rabbit Model of Myocardial Ischemia  

作　　者：Li-Jun Cheng Guang-Ping Li Jian Li Yan Chen Xing-Hua Wang 

机构地区：[1]Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, China

出　　处：《Chinese Medical Journal》2016年第5期549-556,共8页中华医学杂志（英文版）

摘　　要：Background：Stellate ganglion （SG） plays an important role in cardiovascular diseases.The electrical activity of SG neurons is involved in the regulation of the autonomic nervous system.The aim of this research was to evaluate the effects offluvastatin on the electrophysiological characteristics of SG neurons in a rabbit model of myocardial ischemia （MI）.Methods：The MI model was induced by abdominal subcutaneous injections of isoproterenol in rabbits.Using whole-cell patch clamp technique,we studied the characteristic changes of ion channels and action potentials （APs） in isolated SG neurons in control group （n =20）,MI group （n =20） and fluvastatin pretreated group （fluvastatin group,n =20）,respectively.The protein expression of sodium channel in SG was determined by immunohistochemical analysis.Results：MI and the intervention of fluvastatin did not have significantly influence on the characteristics of delayed rectifier potassium channel currents.The maximal peak current density of sodium channel currents in SG neurons along with the characteristics of activation curves,inactivation curves,and recovery curves after inactivation were changed in the MI group.The peak current densities of control group,MI group,and fluvastatin group （n =10 in each group） were-71.77 ± 23.22 pA/pF,-126.75 ± 18.90 pA/pF,and-86.42 ± 28.30 pA/pF,respectively （F=4.862,P =0.008）.Fluvastatin can decrease the current amplitude which has been increased by MI.Moreover,fluvastatin induced the inactivation curves and post-inactive recovery curves moving to the position of the control group.But the expression of sodium channel-associated protein （Nav 1.7） had no significantly statistical difference among the three groups.The percentages of Nav 1.7 protein in control group,MI group,and fluvastatin group （n =5 in each group） were 21.49 ± 7.33%,28.53 ± 8.26%,and 21.64 ± 2.78%,respectively （F =1.495,P =0.275）.Moreover,MI reduced the electrical activity of AP and increased amplitude of AP,fluvastBackground：Stellate ganglion （SG） plays an important role in cardiovascular diseases.The electrical activity of SG neurons is involved in the regulation of the autonomic nervous system.The aim of this research was to evaluate the effects offluvastatin on the electrophysiological characteristics of SG neurons in a rabbit model of myocardial ischemia （MI）.Methods：The MI model was induced by abdominal subcutaneous injections of isoproterenol in rabbits.Using whole-cell patch clamp technique,we studied the characteristic changes of ion channels and action potentials （APs） in isolated SG neurons in control group （n =20）,MI group （n =20） and fluvastatin pretreated group （fluvastatin group,n =20）,respectively.The protein expression of sodium channel in SG was determined by immunohistochemical analysis.Results：MI and the intervention of fluvastatin did not have significantly influence on the characteristics of delayed rectifier potassium channel currents.The maximal peak current density of sodium channel currents in SG neurons along with the characteristics of activation curves,inactivation curves,and recovery curves after inactivation were changed in the MI group.The peak current densities of control group,MI group,and fluvastatin group （n =10 in each group） were-71.77 ± 23.22 pA/pF,-126.75 ± 18.90 pA/pF,and-86.42 ± 28.30 pA/pF,respectively （F=4.862,P =0.008）.Fluvastatin can decrease the current amplitude which has been increased by MI.Moreover,fluvastatin induced the inactivation curves and post-inactive recovery curves moving to the position of the control group.But the expression of sodium channel-associated protein （Nav 1.7） had no significantly statistical difference among the three groups.The percentages of Nav 1.7 protein in control group,MI group,and fluvastatin group （n =5 in each group） were 21.49 ± 7.33%,28.53 ± 8.26%,and 21.64 ± 2.78%,respectively （F =1.495,P =0.275）.Moreover,MI reduced the electrical activity of AP and increased amplitude of AP,fluvast

关 键 词：Action Potential Delayed Rectifier Potassium Channel Fluvastatin： Myocardial Ischemia Sodium Channel Stellate Ganglion 

分 类 号：R4[医药卫生—临床医学]