离子通道蛋白GIRK1及CaV1.3在青壮年猝死综合征窦房结中的表达及意义  

Expressions of GIRK1 and CaV1.3 in SAN pacemaker cells of the sudden manhood death syndrome

作　　者：陈飞[1] 郑雷[2] 王超群[3] 

机构地区：[1]徐州市公安局,江苏徐州221000 [2]丰县公安局,江苏徐州221700 [3]徐州医学院,江苏徐州221000

出　　处：《现代医学》2015年第12期1523-1526,共4页Modern Medical Journal

摘　　要：目的:研究青壮年猝死综合征(sudden manhood death syndrome,SMDS)心脏窦房结组织中G蛋白耦合的内向整流钾(G-coupled inward rectifying K,GIRK1)及L-型钙离子通道蛋白Ca V1.3表达的变化。方法:实验组为2006至2014年徐州医学院病理学教研室尸体解剖中诊断SMDS者14例,对照组为交通事故颅脑损伤死亡者20例,应用免疫组化方法检测GIRK1及Ca V1.3在窦房结组织中的表达。结果:SMDS组窦房结组织中GIRK1的阳性表达率为(20.89±3.17)%,Ca V1.3的阳性表达率为(18.33±1.54)%,均明显低于对照组(P<0.05)。结论:SMDS者中窦房结离子通道GIRK1及Ca V1.3的蛋白表达量显著下调,提示其可能反馈影响迷走神经的心脏调节作用,从而引起呼吸功能的抑制,导致SMDS患者死亡。Objective： To investigate the expression of G-coupled inward rectifying K（ GIRK） and L-type calcium channel Ca V1. 3 in sinus nodes in patients with the sudden manhood death syndrome. Methods： 14 cases of sudden manhood death syndrome,chosen as experimental group were collected from pathology department of Xuzhou Medical College from 2006 to 2014. 20 cases died of severe craniocerebral injury in traffic accident were selected as the control group. Immunohistochemical staining was employed to examine GIRK1 and Ca V1. 3expression in sinoatrial node. Result： Expressions of GIRK1 [（ 20. 89 ± 3. 17） %] and Ca V1. 3 [（ 18. 33 ±1. 54） %] in sinoatrial node of the sudden manhood death syndrome were significantly lower than those of the control group（ P 0. 05）. Conclusion： The descending expression of GIRK1 and Ca V1. 3 in SAN pacemaker cells might be related to the death cause of the sudden manhood death syndrome. Its mechanism may be the inhibition of vagus nerve activity and the induction of the abnormalities of sinoatrial node electrophysiology.

关 键 词：法医病理学 青壮年猝死综合征 窦房结 G蛋白耦合的内向整流钾 CaV1.3 

分 类 号：R33[医药卫生—人体生理学] R36[医药卫生—基础医学]