正中神经刺激降低兔室性心律失常发生率机制研究
Median nerve stimulation reduces cardiac interstitial norepinephrine and inhibits ventricular arrhyth-mias in rabbit
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。
更多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.
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