益心康泰胶囊联合硫氮唑酮对不稳定型心绞痛患者心功能及血清ET-1、Hcy、cTnT水平的影响

摘要 目的：探讨益心康泰胶囊联合硫氮唑酮对不稳定型心绞痛（UAP）患者心功能及血清ET-1、Hcy、cTnT水平的影响。方法：选择2019年3月到2021年3月期间在我院接受治疗的UAP患者84例,按照随机数字表法分为研究组和对照组各42例,对照组给予阿司匹林、硝酸酯类、?茁-受体阻滞剂及他汀类药物等常规治疗,研究组在其基础上给予益心康泰胶囊联合硫氮唑酮治疗,两组均治疗30 d。对比两组患者的心绞痛疗效、心功能指标、血清学指标、心绞痛发作次数和持续时间、不良反应发生率。结果：研究组临床总有效率高于对照组（P<0.05）。研究组治疗后的QT间期离散度(QTd)、左室舒张末径(LVEDD)、左室收缩末径(LVESD)均低于对照组,而左室射血分数(LVEF)高于对照组 (P<0.05)。治疗后研究组心绞痛发作次数和持续时间均低于对照组（P<0.05）。治疗后研究组患者的血管内皮素1(ET-1)、同型半胱氨酸(Hcy)、心肌肌钙蛋白T(cTnT)水平均低于对照组(P<0.05)。两组不良反应总发生率无明显差异（P>0.05）。结论：益心康泰胶囊联合硫氮唑酮治疗UAP患者疗效较好,能减少患者心绞痛持续时间和发作次数,增强患者的心功能,降低ET-1、Hcy、cTnT水平,且具有较好的安全性,具有一定临床应用价值。     

微血管减压术联合感觉根部分切断术对原发性三叉神经痛患者疼痛评分、生活质量及睡眠状况的影响

目的:探讨微血管减压术(MVD)联合感觉根部分切断术(PSR)对原发性三叉神经痛(TN)患者疼痛评分、生活质量及睡眠状况的影响。方法:回顾性分析2015年2月~2019年3月期间我院收治的80例原发性TN患者的临床资料,根据手术方式的不同将患者分为对照组(n=40,MVD治疗)和研究组(n=40,MVD联合PSR治疗),比较两组患者疼痛评分、生活质量、围术期指标、睡眠状况、并发症发生情况以及复发率。结果:两组患者治疗后视觉疼痛模拟量表(VAS)评分均较治疗前下降,且研究组低于对照组(P<0.05)。两组患者治疗后生活质量量表(SF-36)各维度评分均较治疗前升高,且研究组高于对照组(P<0.05)。两组患者治疗后匹兹堡睡眠质量指数表(PSQI)各项目评分均较治疗前升高,且研究组高于对照组(P<0.05)。研究组住院时间短于对照组,手术时间长于对照组(P<0.05);两组术中出血量比较无统计学差异(P>0.05)。研究组的并发症总发生率低于对照组(P<0.05)。两组随访期间复发率比较差异无统计学意义(P>0.05)。结论:MVD联合PSR治疗原发性TN,虽然手术时间较长,但是在减轻患者疼痛、改善患者生活质量及睡眠状况等方面效果显著,能够降低并发症发生率。     

Diagnostic value of exercise-induced changes in circulating high sensitive troponin T in stable chest pain patients

Abstract

Objective: We investigated the diagnostic value of exercise-induced increase in cardiac Troponin T (cTnT) in stable chest pain subjects.

Methods: CTnT was measured before and 20?h after an exercise test in 157 subjects suspected of coronary artery disease (CAD).

Results: CAD subjects (n?=?41) had higher baseline cTnT levels compared to non-CAD subjects (n?=?116), 6.39?ng/l and 3.00?ng/l, respectively, p?<?0.0001, and were more likely to increase in cTnT (70.7% versus 27.6%, p?<?0.0001). Net Reclassification Index for the combined variable was 19%, p?=?0.02.

Conclusions: Exercise-induced increase in cTnT was found to be associated with CAD and cTnT measurements improved the diagnostic evaluation.     

Serial measurements of high-sensitivity cardiac troponin T after exercise stress test in stable coronary artery disease

Abstract

Objective: The aim was to assess serial measurements of high-sensitivity cardiac troponin T (hs-cTNT) post-exercise in patients with stable coronary artery disease (CAD).

Methods: Twelve patients with positive coronary angiograms (CAD positives) and 12 controls performed an exercise stress test.

Results: CAD positive had higher baseline and peak concentrations of hs-cTNT than controls. Significant increases in hs-cTNT were seen in both groups after exercise. In two-third of patients the peak in hs-cTNT was above the 99th percentile.

Conclusion: hs-cTNT is higher in patients with stable coronary disease than in controls and exceeds the diagnostic cut-off value for myocardial infarction in a majority of patients with CAD after exercise.     

How calcium signals in myocytes and pericytes are integrated across in situ microvascular networks and control microvascular tone

The microcirculation is the site of gas and nutrient exchange. Control of central or local signals acting on the myocytes, pericytes and endothelial cells within it, is essential for health. Due to technical problems of accessibility, the mechanisms controlling Ca²⁺ signalling and contractility of myocytes and pericytes in different sections of microvascular networks in situ have not been investigated. We aimed to investigate Ca²⁺ signalling and functional responses, in a microcirculatory network in situ. Using live confocal imaging of ureteric microvascular networks, we have studied the architecture, morphology, Ca²⁺ signalling and contractility of myocytes and pericytes. Ca²⁺ signals vary between distributing arcade and downstream transverse and precapillary arterioles, are modified by agonists, with sympathetic agonists being ineffective beyond transverse arterioles. In myocytes and pericytes, Ca²⁺ signals arise from Ca²⁺ release from the sarcoplasmic reticulum through inositol 1,4,5-trisphosphate-induced Ca²⁺ release and not via ryanodine receptors or Ca²⁺ entry into the cell. The responses in pericytes are less oscillatory, slower and longer-lasting than those in myocytes. Myocytes and pericytes are electrically coupled, transmitting Ca²⁺ signals between arteriolar and venular networks dependent on gap junctions and Ca²⁺ entry via L-type Ca²⁺ channels. Endothelial Ca²⁺ signalling inhibits intracellular Ca²⁺ oscillations in myocytes and pericytes via L-arginine/nitric oxide pathway and intercellular propagating Ca²⁺ signals via EDHF. Increases of Ca²⁺ in pericytes and myocytes constrict all vessels except capillaries. These data reveal the structural and signalling specializations allowing blood flow to be regulated by myocytes and pericytes.     

SPA患者循环EPCs及SDF-1-alpha与冠状动脉侧支循环的相关性分析

目的：研究冠状动脉严重狭窄稳定型心绞痛(Stable angina pectoris, SPA)患者循环内皮祖细胞（endothelial progenitor cells, EPCs）及基质细胞衍生因子（SDF）-1-alpha与冠状动脉侧支循环（CCC）形成的相关性,以期为治疗冠心病提供新的思路。方法：选择 2012 年8 月到2014 年12月在我院就诊的88 例冠状动脉严重狭窄的稳定型心绞痛患者（CCC 良好40 例、不良48 例）,均采集 外周血测定EPC 数量、体外生成血管能力,并用ELISA 法检测其血浆SDF-1alpha 水平,采用直线相关和Pearson 检验分析CCC良好 与不良者各指标间及与CCC 分级的相关性;将所有入选病例随机分为6 组,并分离外周血单个核细胞并分别加入不同的培养 液,培养7 天后体外测定EPCs 数量以及生成血管的能力,并通过ELISA 法检测培养液上清中VEGF 的蛋白水平。结果：CCC 不 良组EPCs 数量、体外生成血管能力及SDF-1-alpha水平均明显低于CCC 良好组（P<0.05）。体外生成血管能力、循环EPCs 数量以及 SDF-1alpha水平均与CCC分级呈现显著的正相关性（r =0.72、0.67、0.79,均P<0.05）;循环EPCs 数量、SDF-1alpha水平以及体外生成血 管能力亦均呈现显著正相关性（r =0.78、0.62,均P<0.05）。与PBS、SDF-1alpha+ AMD3100 及SDF-1alpha+ KI8751 干预物质比较,SDF-1琢 能够呈剂量依赖性的明显提高EPCs 数量、增强其体外生成血管的能力及VEGF水平（P<0.05）。结论：冠状动脉严重狭窄稳定型 心绞痛患者循环EPCs及SDF-1琢与CCC 形成有关,VEGF可能参与该过程。     

Evidence that NO/cGMP/PKG signalling cascade mediates endothelium dependent inhibition of IP3R mediated Ca2+ oscillations in myocytes and pericytes of ureteric microvascular network in situ

In ureteric microvessels the antagonistic relationship between Ca²⁺ signalling in endothelium and Ca²⁺ oscillations in myocytes and pericytes of arterioles and venules involves nitric oxide (NO), but the underlying mechanisms are not well understood. In the present study we investigated the effects of carbachol and NO donor SNAP on Ca²⁺ signalling and vasomotor responses of arterioles and venules in intact urteric microvascular network in situ using confocal microscopy. Vasomotor responses of arterioles and venules induced by AVP correlated with the occurrence of Ca²⁺ oscillations in the myocytes and pericytes and were not abolished by the removal of Ca²⁺ from extracellular fluid. Carbachol-induced rise of intracellular Ca²⁺ in endothelium was accompanied by the termination of the Ca²⁺ oscillations in myocytes and pericytes. This carbachol-induced inhibitory effect on Ca²⁺ oscillations in myocytes and pericytes was reversed by ODQ, an inhibitor of soluble guanylyl cyclase (sGC) and by Rp-8-pCPT-cGMPS, an inhibitor of protein kinase G (PKG). Ca²⁺ oscillations in myocytes and pericytes were also effectively blocked by NO donor SNAP. An Inhibitory effect of SNAP was markedly enhanced by zaprinast, a selective inhibitor of cGMP-specific phosphodiesterase-5, and reversed by sGC inhibitor, ODQ and PKG inhibitor, Rp-8-pCPT-cGMPS. The cGMP analogue and selective PKG activator 8pCPT-cGMP also induced inhibition of the AVP-induced Ca²⁺ oscillations in myocytes and pericytes. SNAP had no effects on Ca²⁺ oscillations induced by caffeine in distributing arcade arterioles. Consequently, we conclude that NO- mediated inhibition of Ca²⁺ oscillations in myocytes and pericytes predominantly recruits the cGMP/PKG dependent pathway. The inhibitory effect of NO/cGMP/PKG cascade is associated with suppressed Ca²⁺ release from the SR of myocytes and pericytes selectively via the inositol triphosphate receptor (IP₃R) channels.     

ERM蛋白在微血管内皮细胞通透性调控中的研究进展

埃兹蛋白(Ezrin)/根蛋白(Radixin)/膜突蛋白(Moesin)(ERM)是细胞膜与胞内骨架的连接蛋白,具有高度同源性。细胞外刺激因子可通过多种信号通路磷酸化ERM蛋白,使细胞骨架重构,从而调控微血管内皮细胞通透性,在感染、炎症、代谢异常等病理过程中发挥作用。ERM功能调节的一个重要环节就是其羧基末端苏氨酸残基磷酸化后引起ERM构象的改变,暴露的羧基末端尾部的肌动蛋白(actin)-细胞骨架结合位点;故通过ERM的桥接作用,可将肌动蛋白微丝与细胞膜相连,使血管内皮细胞屏障功能发生变化。目前已知能使ERM磷酸化的激酶有蛋白激酶C(PKC)、促分裂原活化蛋白激酶(MAPK)、Rho相关激酶(ROCK),分别通过p38-MAPK、Rho/ROCK、PKC信号通路参与微血管内皮屏障功能的调控。本文旨在阐述ERM及其相关信号通路在微血管内皮细胞通透性调控中发挥的作用。     

前列腺素E1治疗冠状动脉微血管病变的临床研究

目的:本研究旨在探索前列腺素E1(PGE1)对冠状动脉微血管病变(CMVD)治疗的效果及其可能的机制。方法:92例CMVD患者随机分为PGE1治疗组(47例)及常规治疗组(45例)。PGE1治疗组给予PGE1静脉注射,10μg/次,一日一次。常规治疗组给予等剂量生理盐水静脉注射,一日一次。两组治疗时间均为10天。通过治疗前后各组的西雅图心绞痛量表评分、血清血栓调节蛋白(TM)水平、血清超氧化物歧化酶(SOD)水平观察PGE1对CMVD的治疗效果。结果:PGE1治疗组在西雅图心绞痛量表中的5个维度(躯体活动受限程度、心绞痛频率、心绞痛稳定状态、治疗的满意程度、疾病认识)评分均高于常规治疗组(P均0.05)。此外,PGE1治疗组患者血清TM水平较常规治疗组显著下调(PGE1治疗组18.25±7.84 vs常规治疗组23.1±9.11,P0.05),血清SOD水平两组间无统计学差异(PGE1治疗组78.23±18.61 vs常规治疗组71.01±19.1,P=0.07)。结论:PGE1能够缓解CMVD患者的心绞痛状态,提高CMVD患者的生活质量,其机制可能与下调血清TM水平、保护冠状动脉微血管内皮细胞有关。