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Contribution of afferent pathway to vagal nerve stimulation-induced myocardial interstitial acetylcholine release in rats.
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology ( IF 2.8 ) Pub Date : 2020-09-09 , DOI: 10.1152/ajpregu.00080.2020
Toru Kawada 1 , Takashi Sonobe 2 , Takuya Nishikawa 1 , Yohsuke Hayama 1 , Meihua Li 1 , Can Zheng 1 , Kazunori Uemura 1 , Tsuyoshi Akiyama 2 , James T Pearson 2, 3 , Masaru Sugimachi 1
Affiliation  

Vagal nerve stimulation (VNS) has been explored as a potential therapy for chronic heart failure. The contribution of the afferent pathway to myocardial interstitial acetylcholine (ACh) release during VNS has yet to be clarified. In seven anesthetized Wistar-Kyoto rats, we implanted microdialysis probes in the left ventricular free wall and measured the myocardial interstitial ACh release during right VNS with the following combinations of stimulation frequency (F in Hz) and voltage readout (V in volts): F0V0 (no stimulation), F5V3, F20V3, F5V10, and F20V10. F5V3 did not affect the ACh level. F20V3, F5V10, and F20V10 increased the ACh level to 2.83 ± 0.47 (P < 0.01), 4.31 ± 1.09 (P < 0.001), and 4.33 ± 0.82 nM (P < 0.001), respectively, compared with F0V0 (1.76 ± 0.22 nM). After right vagal afferent transection (rVAX), F20V3 and F20V10 increased the ACh level to 2.90 ± 0.53 (P < 0.001) and 3.48 ± 0.63 nM (P < 0.001), respectively, compared with F0V0 (1.61 ± 0.19 nM) but F5V10 did not (2.11 ± 0.24 nM). The ratio of the ACh levels after rVAX relative to before was significantly less than 100% in F5V10 (59.4 ± 8.7%) but not in F20V3 (102.0 ± 8.7%). These results suggest that high-frequency and low-voltage stimulation (F20V3) evoked the ACh release mainly via direct activation of the vagal efferent pathway. By contrast, low-frequency and high-voltage stimulation (F5V10) evoked the ACh release in a manner dependent on the vagal afferent pathway.

中文翻译:

传入途径对迷走神经刺激引起的大鼠心肌间质乙酰胆碱释放的影响。

迷走神经刺激(VNS)已被研究作为治疗慢性心力衰竭的一种潜在疗法。VNS期间传入途径对心肌间质乙酰胆碱(ACh)释放的贡献尚未阐明。在七只麻醉的Wistar-Kyoto大鼠中,我们在左心室游离壁上植入了微透析探针,并通过以下刺激频率(F单位为Hz)和电压读数(V单位为伏)的组合测量了右VNS期间心肌间质ACh的释放:F0V0 (无刺激),F5V3,F20V3,F5V10和F20V10。F5V3不会影响ACh水平。与F0V0(1.76±0.22 nM)相比,F20V3,F5V10和F20V10将ACh水平分别提高到2.83±0.47(P <0.01),4.31±1.09(P <0.001)和4.33±0.82 nM(P <0.001)。 )。右迷走神经横切后(rVAX),与F0V0(1.61±0.19 nM)相比,F20V3和F20V10将ACh水平分别提高至2.90±0.53(P <0.001)和3.48±0.63 nM(P <0.001),但F5V10则没有(2.11±0.24 nM)。rVAX后相对于之前的ACh水平之比在F5V10中明显小于100%(59.4±8.7%),但在F20V3中则不小于100%(102.0±8.7%)。这些结果表明高频和低压刺激(F20V3)引起ACh释放主要是通过迷走神经传出途径的直接激活。相比之下,低频和高压刺激(F5V10)引起的ACh释放取决于迷走神经传入途径。rVAX后相对于之前的ACh水平比率在F5V10中显着小于100%(59.4±8.7%),但在F20V3中则不小于100%(102.0±8.7%)。这些结果表明高频和低压刺激(F20V3)引起ACh释放主要是通过迷走神经传出途径的直接激活。相比之下,低频和高压刺激(F5V10)引起的ACh释放取决于迷走神经传入途径。rVAX后相对于之前的ACh水平比率在F5V10中显着小于100%(59.4±8.7%),但在F20V3中则不小于100%(102.0±8.7%)。这些结果表明高频和低压刺激(F20V3)引起ACh释放主要是通过迷走神经传出途径的直接激活。相比之下,低频和高压刺激(F5V10)引起的ACh释放取决于迷走神经传入途径。
更新日期:2020-09-10
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