Spinal Anesthesia Reduces Myocardial Ischemia-triggered Ventricular Arrhythmias by Suppressing Spinal Cord Neuronal Network Interactions in Pigs.
Spinal Anesthesia Reduces Myocardial Ischemia-triggered Ventricular Arrhythmias by Suppressing Spinal Cord Neuronal Network Interactions in Pigs.
复制标题
脊髓麻醉通过抑制脊髓神经元网络相互作用减少猪心肌缺血触发的室性心律失常。
DOI：
10.1097/aln.0000000000003662
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发表时间：
2021-03-01
期刊：
影响因子：
8.8
通讯作者：
Mahajan A
中科院分区：
文献类型：
--
作者：
Omura Y;Kipke JP;Salavatian S;Afyouni AS;Wooten C;Herkenham RF;Maoz U;Lashgari E;Dale EA;Howard-Quijano K;Mahajan A
心脏交感神经兴奋导致室性心律失常。脊髓麻醉调节交感神经输出，可以保护心脏。然而，其对背角（DH）心脏传入神经元和调节交感神经输出的中间外侧核（IML）交感神经元中的心脊髓反射和网络相互作用的影响尚不清楚。我们假设，脊髓布比卡因减少心脏神经元的放电和网络的相互作用，在DH-DH和DH-IML，产生交感神经兴奋心肌缺血，减弱心室肌。在约克郡猪（N=9）中，使用插入T2脊髓的64通道高密度穿透微阵列电极同时记录来自DH和IML神经元的细胞外神经元信号。在鞘内注射布比卡因的心肌缺血和心脏负荷依赖性扰动过程中，评价了DH和IML神经相互作用和已知的心脏血管生成标志物。根据它们对心肌缺血和心脏负荷依赖性扰动的反应来鉴定心脏脊髓神经元。脊髓布比卡因没有改变DH或IML的心脏神经元的基础活动。布比卡因给药后，心肌缺血时心脏神经元活动增加的百分比降低。心肌缺血和心脏负荷依赖性应激增加了DH和DH之间的短期相互作用（1189对中有324对至931对相关，p<0.0001），以及DH和IML神经元之间的短期相互作用（1135对中有11对至69对相关，p<0.0001）。布比卡因减少了这种网络反应，并增强了DH-DH（1189对中的931对至38对相关对，p<0.0001）和IML-DH神经元（1135对中的69对至1对相关对，p<0.0001）之间的相互作用。脊髓布比卡因可减少急性缺血时心室激动恢复间期缩短和复极离散度，并减少心室肌再生。脊髓麻醉减少心肌缺血期间脊髓中DH-DH和DH-IML心脏神经元之间的网络相互作用。阻断脊髓中局部传入-传出心脏神经元之间的短期协调有助于减少心脏交感兴奋和心室肌生成。
Cardiac sympathoexcitation leads to ventricular arrhythmias. Spinal anesthesia modulates sympathetic output and can be cardioprotective. However, its effect on the cardio-spinal reflexes and network interactions in the dorsal horn (DH) cardiac afferent neurons and the intermediolateral nucleus (IML) sympathetic neurons that regulate sympathetic output is not known. We hypothesize that spinal bupivacaine reduces cardiac neuronal firing and network interactions in the DH-DH and DH-IML that produce sympathoexcitation during myocardial ischemia, attenuating ventricular arrhythmogenesis. Extracellular neuronal signals from the DH and IML neurons were simultaneously recorded in Yorkshire pigs (N=9) using a 64-channel high-density penetrating microarray electrode inserted at the T2 spinal cord. DH and IML neural interactions and known markers of cardiac arrhythmogenesis were evaluated during myocardial ischemia and cardiac load-dependent perturbations with intrathecal bupivacaine. Cardiac spinal neurons were identified based on their response to myocardial ischemia and cardiac load-dependent perturbations. Spinal bupivacaine did not change the basal activity of cardiac neurons in the DH or IML. After bupivacaine administration, the percentage of cardiac neurons that increased their activity in response to myocardial ischemia was decreased. Myocardial ischemia and cardiac-load dependent stress increased the short-term interactions between the DH and DH (324 to 931 correlated pairs out of 1189 pairs, p<0.0001), and DH and IML neurons (11 to 69 correlated pairs out of 1135 pairs, p<0.0001). Bupivacaine reduced this network response and augmentation in the interactions between DH-DH (931 to 38 correlated pairs out of 1189 pairs, p<0.0001) and IML-DH neurons (69 to 1 correlated pairs out of 1135 pairs, p<0.0001). Spinal bupivacaine reduced shortening of ventricular activation recovery interval and dispersion of repolarization, with decreased ventricular arrhythmogenesis during acute ischemia. Spinal anesthesia reduces network interactions between DH-DH and DH-IML cardiac neurons in the spinal cord during myocardial ischemia. Blocking short-term coordination between local afferent-efferent cardiac neurons in the spinal cord contributes to a decrease in cardiac sympathoexcitation and reduction of ventricular arrhythmogenesis.