Brettner Florian, Chappell Daniel, Schwartz Lisa, Lukasz Alexander, Kümpers Philipp, Becker Bernhard F, Reichart Bruno, Rehm Markus, Bruegger Dirk
Department of Anaesthesiology, University Hospital of Munich (LMU), Munich, Germany.
Walter-Brendel-Centre of Experimental Medicine, Ludwig-Maximilians-University Munich, Munich, Germany.
Eur Surg Res. 2017;58(5-6):354-368. doi: 10.1159/000480431. Epub 2017 Oct 26.
Cardiac surgery often causes ischemia and development of a systemic inflammatory response syndrome, which impairs vascular barrier function, normally maintained by the endothelial cell line and the endothelial glycocalyx (EG). The EG normally covers and protects healthy endothelial cells throughout the vasculature. The aim of the present study was to assess the disruption of the cellular part of the microvascular barrier by determining parameters of endothelial cell activation known to influence and reflect cell-cell junctional integrity. Particular attention was placed on angiopoietins and their important effects on endothelial gap junctions. Furthermore, comparative measurements were undertaken in patients undergoing on- and off-pump cardiac surgery, the latter group presumably experiencing less ischemic stress.
30 patients undergoing elective coronary artery bypass surgery were assigned to the conventional coronary artery bypass (CCAB) group (n = 15) or the off-pump coronary artery bypass grafting (OPCAB) group (n = 15). Blood samples were obtained for measuring angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), vascular endothelial (VE)-cadherin, and endocan at various time points.
There were significant increases in all measured parameters in both study groups versus the respective basal values. Maximal increases were as follows: Ang-1: CCAB +220%, OPCAB +166%, p < 0.05 each; Ang-2: CCAB +150%, OPCAB +20%, p < 0.05 each; VE-cadherin: CCAB +87%, OPCAB +66%, p < 0.05 each; endocan: CCAB +323%, OPCAB +72%, p < 0.05 each.
The present study demonstrates the activation of endothelial cells, shedding of cell-cell contacts and a potential intrinsic counterregulation by Ang-1 and endocan in patients undergoing major cardiac surgery. Quantitatively greater deviations of parameters in the CCAB than in the OPCAB group suggest a relation between the occurrence of ischemia/reperfusion and the extent of endothelial activation.
心脏手术常导致缺血及全身炎症反应综合征的发生，这会损害血管屏障功能，而该功能通常由内皮细胞系和内皮糖萼（EG）维持。EG通常覆盖并保护整个脉管系统中的健康内皮细胞。本研究的目的是通过测定已知会影响并反映细胞间连接完整性的内皮细胞活化参数，来评估微血管屏障细胞部分的破坏情况。特别关注血管生成素及其对内皮间隙连接的重要作用。此外，对接受体外循环和非体外循环心脏手术的患者进行了对比测量，后者可能经历较少的缺血应激。
30例行择期冠状动脉搭桥手术的患者被分为传统冠状动脉搭桥（CCAB）组（n = 15）和非体外循环冠状动脉搭桥术（OPCAB）组（n = 15）。在不同时间点采集血样以测量血管生成素-1（Ang-1）、血管生成素-2（Ang-2）、血管内皮（VE）-钙黏蛋白和内脂素。
与各自的基础值相比，两个研究组中所有测量参数均显著增加。最大增幅如下：Ang-1：CCAB组增加220%，OPCAB组增加166%，每组p < 0.05；Ang-2：CCAB组增加150%，OPCAB组增加20%，每组p < 0.05；VE-钙黏蛋白：CCAB组增加87%，OPCAB组增加66%，每组p < 0.05；内脂素：CCAB组增加323%，OPCAB组增加72%，每组p < 0.05。
本研究表明，在接受心脏大手术的患者中，内皮细胞被激活，细胞间接触减少，且Ang-1和内脂素可能存在内在的代偿调节。CCAB组参数的定量偏差比OPCAB组更大，这表明缺血/再灌注的发生与内皮激活程度之间存在关联。
