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节后神经刺激可诱导家兔窦房结兴奋性的短暂抑制。

Postganglionic nerve stimulation induces temporal inhibition of excitability in rabbit sinoatrial node.

作者信息

Fedorov Vadim V, Hucker William J, Dobrzynski Halina, Rosenshtraukh Leonid V, Efimov Igor R

机构信息

Department of Biomedical Engineering, Washington Univ., Campus Box 1097, One Brookings Drive, St. Louis, MO 63130, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2006 Aug;291(2):H612-23. doi: 10.1152/ajpheart.00022.2006. Epub 2006 Mar 24.

Abstract

Vagal stimulation results in complex changes of pacemaker excitability in the sinoatrial node (SAN). To investigate the vagal effects in the rabbit SAN, we used optical mapping, which is the only technology that allows resolving simultaneous changes in the activation pattern and action potentials morphologies. With the use of immunolabeling, we identified the SAN as a neurofilament 160-positive but connexin 43-negative region (n = 5). Normal excitation originated in the SAN center with a cycle length (CL) of 405 +/- 14 ms (n = 14), spread anisotropically along the crista terminalis (CT), and failed to conduct toward the septum. Postganglionic nerve stimulation (PNS, 400-800 ms) reduced CL by 74 +/- 7% transiently and shifted the leading pacemaker inferiorly (78%) or superiorly (22%) from the SAN center by 2-10 mm. In the intercaval region between the SAN center and the septal block zone, PNS produced an 8 +/- 1-mm(2) region of transient hyperpolarization and inexcitability. The first spontaneous or paced excitation following PNS could not enter this region for 500-1,500 ms. Immunolabeling revealed that the PNS-induced inexcitable region is located between the SAN center and the block zone and has a 2.5-fold higher density of choline acetyltransferase than CT but is threefold lower than the SAN center. The fact that the inexcitability region does not coincide with the most innervated area indicates that the properties of the myocytes themselves, as well as intercellular coupling, must play a role in the inexcitability induction. Optically mapping revealed that PNS resulted in transient loss of pacemaker cell excitability and unidirectional entrance conduction block in the periphery of SAN.

摘要

迷走神经刺激会导致窦房结(SAN)中起搏器兴奋性发生复杂变化。为了研究兔窦房结中的迷走神经效应,我们使用了光学标测技术,这是唯一能够解析激活模式和动作电位形态同时变化的技术。通过免疫标记,我们将窦房结确定为神经丝160阳性但连接蛋白43阴性的区域(n = 5)。正常兴奋起源于窦房结中心,周期长度(CL)为405±14毫秒(n = 14),沿终末嵴(CT)各向异性传播,且无法传向间隔。节后神经刺激(PNS,400 - 800毫秒)可使周期长度短暂缩短74±7%,并使主导起搏器从窦房结中心向下(78%)或向上(22%)移动2 - 10毫米。在窦房结中心与间隔阻滞区之间的腔静脉间区域,PNS产生了一个8±1平方毫米的短暂超极化和兴奋性丧失区域。PNS后第一个自发或起搏兴奋在500 - 1500毫秒内无法进入该区域。免疫标记显示,PNS诱导的兴奋性丧失区域位于窦房结中心与阻滞区之间,其胆碱乙酰转移酶密度比终末嵴高2.5倍,但比窦房结中心低三倍。兴奋性丧失区域与神经支配最密集区域不一致这一事实表明,心肌细胞自身的特性以及细胞间耦联必定在兴奋性丧失的诱导过程中发挥作用。光学标测显示,PNS导致窦房结周边起搏器细胞兴奋性短暂丧失以及单向传入传导阻滞。

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