Modulating the Cardiac Autonomic Nervous System: Stay Close to My Heart or Keep Your Distance?
Modulating the Cardiac Autonomic Nervous System: Stay Close to My Heart or Keep Your Distance?
复制标题
调节心脏自主神经系统：靠近我的心还是保持距离？
DOI：
10.1097/aln.0000000000004529
复制
发表时间：
2023
期刊：
影响因子：
8.8
通讯作者：
Fox,AmandaA
中科院分区：
文献类型：
--
作者：
Bartels,Karsten;Fox,AmandaA
需要进行围手术期心脏保护研究，以确定如何预防和减轻可能导致心血管发病和死亡的心脏损伤。在本月的麻醉学版中，Howard-Quijano 博士等人。 1 报告了高胸段脊髓刺激对减少心脏交感神经刺激和相应室性心律失常的影响。这篇论文特别有意义的是，作者在约克夏猪身上进行了实验，以明确高位胸脊髓刺激对心脏产生有利影响的生物学原理。在他们的手稿中，作者报告了一系列优雅的实验结果，具体证明：1）心脏缺血期间的脊髓刺激治疗可减少室性心律失常，2）鞘内 GABAA 和 GABAB 受体阻断消除了脊髓刺激的保护作用，3）鞘内给予 GABA 转氨酶抑制剂以增加脊髓 GABA 浓度，可减少心肌交感兴奋和室性心律失常，其程度与脊髓刺激相似，并且4)脊髓刺激导致更多的GABAA受体表达，但没有GABAB受体表达。 1Howard-Quijano 博士等人的研究结果。 1 与使用慢性神经病理性疼痛模型的其他动物实验研究一致。啮齿类动物部分坐骨神经结扎后脊髓刺激可改善镇痛效果。 2 然而，鞘内注射 GABAA 和 GABAB 拮抗剂会消除脊髓刺激的镇痛作用。 2 因此，负责脊髓刺激介导的神经性疼痛镇痛的 GABA 能机制可能与负责脊髓刺激介导的缺血/再灌注引起的交感神经兴奋和室性心律失常的减弱的机制非常相似。
Perioperative cardiac protection research is needed to determine how to prevent and mitigate cardiac injury that can lead to cardiovascular morbidity and mortality. In this month’s edition of Anesthesiology, Dr. Howard-Quijano et al. 1 report effects of high thoracic spinal cord stimulation on decreasing sympathetic stimulation of the heart and corresponding ventricular arrhythmias. What is particularly meaningful about this paper is that the authors do experiments on Yorkshire pigs in order to define the biology underlying the favorable cardiac effects of high thoracic spinal cord stimulation. In their manuscript, the authors report findings from an elegant sequence of experiments demonstrating specifically that 1) spinal cord stimulation therapy during cardiac ischemia resulted in fewer ventricular arrhythmias, 2) intrathecal GABAA and GABAB receptor blockade eliminated the protective effects of spinal cord stimulation, 3) intrathecal administration of GABA transaminase inhibitor to increase spinal GABA concentrations resulted in less myocardial sympathoexcitation and ventricular arrhythmias to a similar degree as spinal cord stimulation, and 4) spinal cord stimulation resulted in more GABAA but not GABAB receptor expression. 1The findings of Dr. Howard-Quijano et al. 1 are concordant with other animal-experimental studies that use chronic neuropathic pain models. Spinal cord stimulation after partial sciatic nerve ligation in rodents results in improved analgesia. 2 Yet, analgesic effects of spinal cord stimulation are abolished by intrathecal administration of GABAA and GABAB antagonists. 2 Hence, the GABAergic mechanisms responsible for spinal cord stimulation-mediated analgesia for neuropathic pain may be quite similar to the mechanism responsible for spinal cord stimulation-mediated attenuation of ischemia/reperfusion-induced sympathoexcitation and ventricular arrhythmias.