神经
词汇介绍
拓展阅读
解析
sympathectomy英 [,sɪmpə'θektəmɪ] 美 [,sɪmpə'θɛktəmi]
释 义 n. 交感神经切除术
例 句 Objective : To investigate the change of enzyme and twitch muscle fiber in spasmodic muscle after sympathectomy. 目的：探讨交感神经切断后，痉挛肌肉内酶与肌纤维结构的改变。
概述
概述
交感神经切断术是指通过外科手术的方法切断或切除一定部位的交感神经，治疗某些疾病。
手术指征
创伤后肢体痛：交感神经创伤后肢体痛中的灼痛。幻肢痛等传入神经阻滞痛不适于此于术。一般创伤后肢体灼痛能够自行缦解。如果长期不缓解，方考虑手术沿疗。
血管性病变：交感神经切除术对肢体血管痉挛性疾病效果较好。由于冷或者情感变化影响而导致的痉挛适于做交感神经切除术。由于血栓、脉管炎、胶原病引起的血管闭塞也适于手术。近年来对肢体近端大血管闭塞进行直接手术，如搭桥术和血管内膜剥脱术，配合交感神经节切除术能增加血管再通的成功率。
心绞痛：心绞痛是由于冠状动脉供血不足，造成心肌缺血而导致的。
诊断性交感神经节封闭术：在行交感神经切除术前，常规做相应节段的交感神经节封闭术。如果封闭有效，可以行切除术。封闭术完全控制症状者，可行反复封闭。如部分有效则行切除术。
并发症
交感神经节切除术后神经痛：其特点是术后7-10天起病，多发生在夜间，有时疼痛较严重。一般在术后1-3月内自行缀解，无须特殊处理。如果疼痛较重可使用镇痛剂对症处理。卡马西平可用来治疗术后神经痛。
盗血现象：对血管阻塞性疾患行交感神经切除后，造成动静脉短路而使血流增加,这样可能加重肢体缺血状况。因此肢体血管闭塞严重时，慎行交感神经节切除术。
复制标题严重低血糖诱导的致死性心律失常是由大鼠副交感神经系统介导的。
发表时间：2019-08-22
影响指数：7.2
作者： Candace M Reno
期刊：Diabetes
The contribution of the sympathetic (SNS) versus parasympathetic (PSNS) nervous system in mediating fatal cardiac arrhythmias during insulin-induced severe hypoglycemia is not well understood. Therefore, experimental protocols were performed in non-diabetic, Sprague Dawley rats to test SNS with 1) adrenal demedullation and 2) chemical sympathectomy, and to test PSNS with 3) surgical vagotomy, 4) nicotinic receptor (mecamylamine) and muscarinic receptor (AQ-RA 741) blockade, and 5) heart perfusions with normal or low glucose, acetylcholine and/or mecamylamine. In protocols 1-4, 3-hour hyperinsulinemic (0.2U·kg·min)-hypoglycemic (10-15 mg/dl) clamps were performed. Adrenal demedullation and chemical sympathectomy had no effect on mortality or arrhythmias during severe hypoglycemia compared to controls. Vagotomy led to a 6.9-fold decrease in mortality, reduced 1 and 2 degree heart block 4.6- and 4-fold, respectively, and prevented 3 degree heart block compared to controls. Pharmacological blockade of nicotinic receptors, but not muscarinic receptors, prevented heart block and mortality versus controls. heart perfusions demonstrated that neither low glucose nor acetylcholine alone caused arrhythmias, but their combination induced heart block that could be abrogated by nicotinic receptor blockade. Taken together, acetylcholine activation of nicotinic receptors via the vagus nerve is the primary mediator of severe hypoglycemia-induced fatal cardiac arrhythmias.
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