中华心律失常学杂志
中華心律失常學雜誌
중화심률실상학잡지
CHINESE JOURNAL OF CARDIAC ARRHYTHMIAS
2015年
3期
222-227
,共6页
于君%唐闽%陈柯萍%谷靖丽%曹济民%张澍
于君%唐閩%陳柯萍%穀靖麗%曹濟民%張澍
우군%당민%진가평%곡정려%조제민%장주
正中神经刺激%室性心律失常%去甲肾上腺素
正中神經刺激%室性心律失常%去甲腎上腺素
정중신경자격%실성심률실상%거갑신상선소
Median nerve stimulation%Ventricular arrhythmias%Norepinephrine
目的：本研究假设正中神经刺激( MNS)通过调节交感神经的活性来影响室性心律失常的发作。方法阜外医院动物实验中心提供新西兰大白兔32只随机分为4组(对照组、β受体阻滞剂组、MNS组及阿片受体阻滞剂组,n=8)。采用下丘脑刺激(HPS)诱发室性心律失常模型,比较不同实验组内室性心律失常发生率及心脏间质去甲肾上腺素变化。每组动物均接受6阵HPS,其中β受体阻滞剂组、MNS组和阿片受体阻滞剂组于第3次HPS分别给予美托洛尔、MNS及纳络酮+MNS。实验过程中收集透析液,实验结束后确认微透析探针位置,灌流后取脑组织确认HPS位置。结果 HPS诱发持续稳定的室性心律失常发作。β受体阻滞剂静脉注射后抑制室性心律失常的发作。 MNS降低HPS诱发的室性心律失常发生率[第3、4次HPS时室性异位搏动分别为(0．5±1．0)个对(1．8±1．7)个,第1、2次HPS时室性异位搏动分别为(8．8±3．8)个对(8．0±4．2)个,P<0．05],延长首个室性异位搏动出现的时间。纳洛酮预处理后,MNS对于室性心律失常发生率和首个室性异位搏动出现时间的抑制作用消失。 HPS后心脏间质去甲肾上腺素含量明显增加,MNS抑制HPS引起的心脏间质去甲肾上腺素含量的升高[第3、4次HPS时去甲肾上腺素浓度分别为(0．9±0．2) ng/ml对(0．8±0．3) ng/ml,第1、2次HPS时去甲肾上腺素浓度分别为(1．4±0．3)ng/ml对(1．4±0．3)ng/ml,P<0．05],纳洛酮预处理后, MNS对于HPS诱发的去甲肾上腺素含量升高的抑制作用消失[第3、4次HPS时去甲肾上腺素浓度分别为(1．4±0．1)ng/ml对(1．3±0．1)ng/ml,第1、2次HPS时去甲肾上腺素浓度分别为(1．4±0．2)ng/ml对(1．5±0．1)ng/ml,P>0．05]。结论 MNS通过调节心脏交感神经的活性进而降低HPS诱发的室性心律失常的发生率。
目的：本研究假設正中神經刺激( MNS)通過調節交感神經的活性來影響室性心律失常的髮作。方法阜外醫院動物實驗中心提供新西蘭大白兔32隻隨機分為4組(對照組、β受體阻滯劑組、MNS組及阿片受體阻滯劑組,n=8)。採用下丘腦刺激(HPS)誘髮室性心律失常模型,比較不同實驗組內室性心律失常髮生率及心髒間質去甲腎上腺素變化。每組動物均接受6陣HPS,其中β受體阻滯劑組、MNS組和阿片受體阻滯劑組于第3次HPS分彆給予美託洛爾、MNS及納絡酮+MNS。實驗過程中收集透析液,實驗結束後確認微透析探針位置,灌流後取腦組織確認HPS位置。結果 HPS誘髮持續穩定的室性心律失常髮作。β受體阻滯劑靜脈註射後抑製室性心律失常的髮作。 MNS降低HPS誘髮的室性心律失常髮生率[第3、4次HPS時室性異位搏動分彆為(0．5±1．0)箇對(1．8±1．7)箇,第1、2次HPS時室性異位搏動分彆為(8．8±3．8)箇對(8．0±4．2)箇,P<0．05],延長首箇室性異位搏動齣現的時間。納洛酮預處理後,MNS對于室性心律失常髮生率和首箇室性異位搏動齣現時間的抑製作用消失。 HPS後心髒間質去甲腎上腺素含量明顯增加,MNS抑製HPS引起的心髒間質去甲腎上腺素含量的升高[第3、4次HPS時去甲腎上腺素濃度分彆為(0．9±0．2) ng/ml對(0．8±0．3) ng/ml,第1、2次HPS時去甲腎上腺素濃度分彆為(1．4±0．3)ng/ml對(1．4±0．3)ng/ml,P<0．05],納洛酮預處理後, MNS對于HPS誘髮的去甲腎上腺素含量升高的抑製作用消失[第3、4次HPS時去甲腎上腺素濃度分彆為(1．4±0．1)ng/ml對(1．3±0．1)ng/ml,第1、2次HPS時去甲腎上腺素濃度分彆為(1．4±0．2)ng/ml對(1．5±0．1)ng/ml,P>0．05]。結論 MNS通過調節心髒交感神經的活性進而降低HPS誘髮的室性心律失常的髮生率。
목적：본연구가설정중신경자격( MNS)통과조절교감신경적활성래영향실성심률실상적발작。방법부외의원동물실험중심제공신서란대백토32지수궤분위4조(대조조、β수체조체제조、MNS조급아편수체조체제조,n=8)。채용하구뇌자격(HPS)유발실성심률실상모형,비교불동실험조내실성심률실상발생솔급심장간질거갑신상선소변화。매조동물균접수6진HPS,기중β수체조체제조、MNS조화아편수체조체제조우제3차HPS분별급여미탁락이、MNS급납락동+MNS。실험과정중수집투석액,실험결속후학인미투석탐침위치,관류후취뇌조직학인HPS위치。결과 HPS유발지속은정적실성심률실상발작。β수체조체제정맥주사후억제실성심률실상적발작。 MNS강저HPS유발적실성심률실상발생솔[제3、4차HPS시실성이위박동분별위(0．5±1．0)개대(1．8±1．7)개,제1、2차HPS시실성이위박동분별위(8．8±3．8)개대(8．0±4．2)개,P<0．05],연장수개실성이위박동출현적시간。납락동예처리후,MNS대우실성심률실상발생솔화수개실성이위박동출현시간적억제작용소실。 HPS후심장간질거갑신상선소함량명현증가,MNS억제HPS인기적심장간질거갑신상선소함량적승고[제3、4차HPS시거갑신상선소농도분별위(0．9±0．2) ng/ml대(0．8±0．3) ng/ml,제1、2차HPS시거갑신상선소농도분별위(1．4±0．3)ng/ml대(1．4±0．3)ng/ml,P<0．05],납락동예처리후, MNS대우HPS유발적거갑신상선소함량승고적억제작용소실[제3、4차HPS시거갑신상선소농도분별위(1．4±0．1)ng/ml대(1．3±0．1)ng/ml,제1、2차HPS시거갑신상선소농도분별위(1．4±0．2)ng/ml대(1．5±0．1)ng/ml,P>0．05]。결론 MNS통과조절심장교감신경적활성진이강저HPS유발적실성심률실상적발생솔。
Objective To test the hypothesis that the inhibitory effect of median nerve stimulation on ventricular arrhythmias ( VA) was associated with the modulation of cardiac sympathetic neural activity. Meth-ods Thirty-two anesthetized Newzeland white rabbits were randomly divided into four groups(n=8):the con-trol group, the β-receptor blocker group, the median nerve stimulation( MNS) group and the opioid receptor blocker group. This study was to compare the incidence of ventricular arrhythmias and the qualitative change of cardiac interstitial norepinephrine in different groups with hypothalamus stimulation induced ventricular arrhyth-mias animal model. Each animal underwent 6 episodes of hypothalamus stimulation ( HPS ) with 30 min interval and animals in theβ-receptor blocker group, the MNS group and the opioid receptor blocker group were pre-treated with metoprolol, MNS and naloxone plus MNS before the third HPS episode separately. Dialysate was collected during the experiment and the site of microdialysis probe and HPS was confirmed after the experi-ment. Results HPS induced reliable occurrence of VA. Metoprolol infusion significantly reduced the incidence of HPS-induced VA. In the MNS group, the concurrent MNS during the third and fourth HPS episode signifi-cantly reduced VA incidence compared to the episodes without MNS (0. 5±1. 0) beats vs. (1. 8±1. 7) beats for the third and fourth HPS episode vs. (8. 8±3. 8) beats vs. (8. 0±4. 2) beats for the first and second HPS episode, P<0. 05) and postponed the time of the occurrence of the first ventricular arrhythmic beat during the HPS. However, after pretreatment with naloxone, the number of arrhythmic beats induced by hypothalamus stimulation didn’ t showed a significant decrease during the concurrent MNS and the retarding effect on the oc-currence of the first ventricular arrhythmic beat was blocked. The concentration of interstitial norepinephrine was significantly increased after HPS intervention and this effect was blocked after the concurrent MNS intervention (0. 9±0. 2)ng/ml vs. (0. 8±0. 3)ng/ml for the third and fourth HPS episode vs. (1. 4±0. 3)ng/ml vs. (1. 4± 0. 3)ng/ml for the first and second HPS episode,P<0. 05). After pretreatment with naloxone, the inhibitory effect of MNS on interstitial norepinephrine induced by HPS was disappeared ( 1. 4 ± 0. 1 ) ng/ml vs. ( 1. 3 ± 0. 1)ng/ml for the third and fourth HPS episode vs. (1. 4±0. 2)ng/ml vs. (1. 5±0. 1)ng/ml for the first and second HPS episode, P>0. 05). Conclusion MNS reduced the incidence of hypothalamus stimulation-induced VA via modulating cardiac neural activity in rabbits.
