CAJ | 학술논문

目的探讨超极化激活的环核苷酸门控离子通道亚型4 (HCN4)蛋白在室性心动过速(室速)中的作用.方法数字随机选择新西兰大白兔10只,应用HE染色及免疫组织化学检测中间神经纤维丝(NF-M),观察心室流出道组织是否存在浦肯野纤维.另选择新西兰大白兔40只平均分4组即对照组(SO)、室速组(ⅤT)、室速+艾司洛尔干预组(ⅤT+ ESM)、室速+伊伐布雷定干预组(ⅤT+ⅣA).采用免疫组化方法检测心室流出道HCN4蛋白的表达,观察并记录各组诱发室速时所需电压的输出幅值、停止刺激后自发性室速发生的次数及持续时间.结果 (1)兔心室流出道存在浦肯野纤维.(2)左、右心室流出道HCN4蛋白的表达ⅤT组与SO组比较明显增多(左室:97.6±16.7与29.0±8.0,P＜0.01;右室:92.7±12.3与26.0±10.8,P＜0.01);ⅤT+ ⅣA组与ⅤT组比较明显减少(左室:32.0±9.4与97.6±16.7,P＜0.01;右室:30.8±12.4与92.7±12.3,P＜0.01).(3)ⅤT +ESM组和ⅤT+ ⅣA组与YT组相比,在同等高频刺激的条件下诱发流出道室速所需的输出电压幅值增加(P＜0.01),停止刺激后自发性室速的发生次数减少(P＜0.01),自发性室速持续时间缩短(P＜0.01).结论 (1)心室流出道存在浦肯野纤维,且室速发生时HCN4蛋白表达上调;(2)艾司洛尔及伊伐布雷定可以预防及减少室速的发生,伊伐布雷定作为HCN通道的特异性通道抑制剂效果更强.
목적 탐토초겁화격활적배핵감산문공리자통도아형4 (HCN4)단백재실성심동과속(실속)중적작용.방법 수자수궤선택신서란대백토10지,응용HE염색급면역조직화학검측중간신경섬유사(NF-M),관찰심실류출도조직시부존재포긍야섬유.령선택신서란대백토40지평균분4조즉대조조(SO)、실속조(ⅤT)、실속+애사락이간예조(ⅤT+ ESM)、실속+이벌포뢰정간예조(ⅤT+ⅣA).채용면역조화방법검측심실류출도HCN4단백적표체,관찰병기록각조유발실속시소수전압적수출폭치、정지자격후자발성실속발생적차수급지속시간.결과 (1)토심실류출도존재포긍야섬유.(2)좌、우심실류출도HCN4단백적표체ⅤT조여SO조비교명현증다(좌실:97.6±16.7여29.0±8.0,P＜0.01;우실:92.7±12.3여26.0±10.8,P＜0.01);ⅤT+ ⅣA조여ⅤT조비교명현감소(좌실:32.0±9.4여97.6±16.7,P＜0.01;우실:30.8±12.4여92.7±12.3,P＜0.01).(3)ⅤT +ESM조화ⅤT+ ⅣA조여YT조상비,재동등고빈자격적조건하유발류출도실속소수적수출전압폭치증가(P＜0.01),정지자격후자발성실속적발생차수감소(P＜0.01),자발성실속지속시간축단(P＜0.01).결론 (1)심실류출도존재포긍야섬유,차실속발생시HCN4단백표체상조;(2)애사락이급이벌포뢰정가이예방급감소실속적발생,이벌포뢰정작위HCN통도적특이성통도억제제효과경강.
Objective To confirm the existence of purkinje fibers in rabbit outflow tract tissue and explore the role of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 4 (HCN4) protein in idiopathic ventricular tachycardia.Methods A total of ten New Zealand white rabbits were randomly selected to observe whether there were pukinje fibers in outflow tract by the methods of HE staining and immunohistochemical detection of midsize neurofilament (NF-M).Forty rabbits were randomly divided into four groups : normal control group (SO), ventricular tachycardia group (ⅤT), ventricular tachycardia + esmolol intervention group (ⅤT + ESM) and ventricular tachycardia + ivabradine intervention group (ⅤT + ⅣA).Immunohistochemistry was used to detect the expression of HCN4 protein in ventricular outflow tract;the required output voltage amplitude was recorded when ventricular tachycardia was induced;the times and duration of spontaneous ventricular tachycardia when stimulation stopped were also recorded for each group.Results (1)Purkinje fibers existed in the myocardial tissue of rabbit outflow tract.(2)HCN4 protein expression significantly increased in ⅤT group compared with SO group (left ventricular: 97.6 ± 16.7 vs 29.0 ± 8.0, P ＜ 0.01;right ventricular: 92.7 ± 12.3 vs 26.0 ± 10.8, P ＜ 0.01), the expression of HCN4 protein obviously reduced in ⅤT + ⅣA group compared with ⅤT group (left ventricular: 32.0 ± 9.4 vs 97.6 ± 16.7, P ＜ 0.01;right ventricular: 30.8 ± 12.4 vs 92.7 ± 12.3, P ＜ 0.01).(3) The output voltage amplitude required to induce the desired ventricular tachycardia in ⅤT + ESM group and ⅤT + ⅣA group were higher than the ⅤT group, under the same high frequency stimulation (P ＜ 0.01);the times and duration of spontaneous ventricular tachycardia in ⅤT + ESM group and ⅤT + ⅣA group significantly reduced when the stimulation stopped, compared with the ⅤT group (both P ＜ 0.01).Conclusions (1) Purkinje fibers exist in ventricular outflow tract, which may be the histological origin of the ventricular tachycardia.(2) HCN4 protein is up-regulated in ventricular outflow tract when ventricular tachycardia occurs.(3) Esmolol and ivabradine can prevent and reduce the occurrence of ventricular tachycardia, and as the specific inhibitor of the HCN channel, the effect of ivabradine is more obvious.