UNASSIGNED:关于心脏手术后心包腔发生的炎症反应的数据很少。这项研究提供了对局部术后炎症反应的全面评估。
未经授权:43例患者接受了心脏切开术,抽取天然心包液,并与体外循环后4、24和48小时收集的术后心包流出物进行比较。流式细胞术用于确定特异性免疫细胞的水平和比例。还探测了样品中炎症细胞因子的浓度,基质金属蛋白酶(MMPs),和金属蛋白酶(TIMPs)的组织抑制剂。
未经批准:术前,心包间隙主要含有巨噬细胞和T细胞。然而,术后心包间隙主要由中性粒细胞组成,几乎占免疫细胞的80%,并在24小时达到峰值。当比较手术方法时,微创手术与术后4小时心包间隙中性粒细胞减少相关。对炎症介质的心包内浓度的分析显示,白细胞介素6,MMP-9和TIMP-1在手术后最高。随着时间的推移,MMP-9浓度显著降低,而TIMP-1水平升高,导致手术后MMP:TIMP的比率显着降低,提示活跃的炎症过程可能影响细胞外基质重塑。
未经证实:这些结果表明心脏手术引起心包空间免疫细胞谱的深刻改变。定义驱动心包特异性术后炎症过程的细胞和分子介质可以允许靶向治疗以减少免疫介导的并发症。
UNASSIGNED: There is a paucity of data on the inflammatory response that takes place in the pericardial space after cardiac surgery. This study provides a comprehensive assessment of the local postoperative inflammatory response.
UNASSIGNED: Forty-three patients underwent cardiotomy, where native pericardial fluid was aspirated and compared with postoperative pericardial effluent collected at 4, 24, and 48 hours\' postcardiopulmonary bypass. Flow cytometry was used to define the levels and proportions of specific immune cells. Samples were also probed for concentrations of inflammatory cytokines, matrix metalloproteinases (MMPs), and tissue inhibitors of metalloproteinases (TIMPs).
UNASSIGNED: Preoperatively, the pericardial space mainly contains macrophages and T cells. However, the postsurgical pericardial space was populated predominately by neutrophils, which constituted almost 80% of immune cells present, and peaked at 24 hours. When surgical approaches were compared, minimally invasive surgery was associated with fewer neutrophils in the pericardial space at 4 hours\' postsurgery. Analysis of the intrapericardial concentrations of inflammatory mediators showed interleukin-6, MMP-9, and TIMP-1 to be highest postsurgery. Over time, MMP-9 concentrations decreased significantly, whereas TIMP-1 levels increased, resulting in a significant reduction of the ratio of MMP:TIMP after surgery, suggesting that active inflammatory processes may influence extracellular matrix remodeling.
UNASSIGNED: These results show that cardiac surgery elicits profound alterations in the immune cell profile in the pericardial space. Defining the cellular and molecular mediators that drive pericardial-specific postoperative inflammatory processes may allow for targeted therapies to reduce immune-mediated complications.