CAJ | 학술논문

目的探讨氟伐他汀对心肌缺血情况下支配心脏的颈上交感神经节(SCG)神经元电生理特性的影响.方法利用异丙肾上腺素皮下注射(85 mg·kg-1 ·d-1,共2d)制作兔急性心肌缺血模型,通过全细胞膜片钳技术研究对照组、心肌缺血组及氟伐他汀(10 mg· kg-1·d-1,共7d)干预组的SCG神经元延迟整流钾通道特性的改变.结果对照组、缺血组和氟伐他汀干预组的兔SCG神经元的延迟整流钾通道最大峰值电流幅值分别为(80.80±22.80) pA/pF、(154.93±31.56) pA/pF、(119.82±24.82)pA/pF,3者的半数激活电压分别为(9.86±0.57)mV、(12.36±1.09) mV和(9.52±0.49) mV,斜率因子分别为(19.66±0.75)mV、(27.33±1.64) mV和(17.76±0.61) mV.急性心肌缺血使SCG神经元延迟整流钾通道电流(IK)幅度增大,氟伐他汀的干预可一定程度上使这种增大的电流有所减小.同时,氟伐他汀干预可使心肌缺血组移动的激活曲线向对照组方向移动.结论心肌缺血情况下SCG神经元延迟整流钾通道特性产生的变化可一定程度上通过氟伐他汀的干预得到修复,这可能是氟伐他汀治疗心脏疾病的机制之一.
목적 탐토불벌타정대심기결혈정황하지배심장적경상교감신경절(SCG)신경원전생리특성적영향.방법 이용이병신상선소피하주사(85 mg·kg-1 ·d-1,공2d)제작토급성심기결혈모형,통과전세포막편겸기술연구대조조、심기결혈조급불벌타정(10 mg· kg-1·d-1,공7d)간예조적SCG신경원연지정류갑통도특성적개변.결과 대조조、결혈조화불벌타정간예조적토SCG신경원적연지정류갑통도최대봉치전류폭치분별위(80.80±22.80) pA/pF、(154.93±31.56) pA/pF、(119.82±24.82)pA/pF,3자적반수격활전압분별위(9.86±0.57)mV、(12.36±1.09) mV화(9.52±0.49) mV,사솔인자분별위(19.66±0.75)mV、(27.33±1.64) mV화(17.76±0.61) mV.급성심기결혈사SCG신경원연지정류갑통도전류(IK)폭도증대,불벌타정적간예가일정정도상사저충증대적전류유소감소.동시,불벌타정간예가사심기결혈조이동적격활곡선향대조조방향이동.결론 심기결혈정황하SCG신경원연지정류갑통도특성산생적변화가일정정도상통과불벌타정적간예득도수복,저가능시불벌타정치료심장질병적궤제지일.
Objective To determine the effects of flurastatin on electrophysiological characteristics of superior cervical ganglion (SCG) neurons during myocardial ischemia (MI).Methods The rabbit model of MI was induced by subcutaneous injection of isoproterenol [85 mg · kg 1 · d-1 for 2 days].The electrophysiological characteristics of delayed rectifier potassium channels of SCG neurons were evaluated using whole-cell patch-clamp in control group,MI group and fluvastatin [10 mg· kg 1· d-1,for 7 days]intervention group respectively.Results The maximal peak current density of delayed rectifier potassium channels of rabbit SCG neurons was (80.80±22.80) pA/pF in control group,(154.93±31.56) pA/pF in MI group and (119.82±24.82) pA/pF in fluvastatin intervention group.The voltages of half-activation were (9.86±0.57) mV,(12.36±1.09) mV and (9.52±0.49) mV,respectively,and the slope factors were (19.66± 0.75) mV,(27.33±1.64) mV and (17.76±0.61) mV,respectively in three groups.There was an increase in delayed rectifier potassium channel current (IK) of SCG neurons caused by MI,which was partially reduced by fluvastatin intervention.Furthermore,the activation curve of MI group was shifted by fluvastatin towards the control group.Conclusion To some extent,the characteristic change in delayed rectifier potassium channel of SCG neurons during MI can be ameliorated by fluvastatin intervention,which may be one of mechanisms underlying the fluvastatin-treated cardioprotection.