急性心肌梗死引起无菌性炎症后心脏和脾脏的形态学反应:临床病理研究

Harsa Mihai Iuliu, B. Nándor, Horváth Emőke
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摘要

作为无菌炎症诱导的急性缺血过程的结果,许多脾细胞进入循环系统并迁移到病变处,保护组织免受缺血扩散或增强坏死。目的探讨脾形态学对无菌性炎症性心肌梗死的治疗作用。材料与方法对106例急性心肌梗死死亡患者的心脏和脾脏进行重量和结构检查。这些数据与人口统计(个人)和流行病学数据以及病史相关。在对存档的心肌和脾组织标本进行形态学调查后,采用数字形态计量学方法对急性缺血引起的脾组织结构改变进行定量分析。将结果与心肌缺血系数进行比较。通过定义巨噬细胞的免疫表型(M1 vs. M2)来表征缺血诱导细胞类型分布的变化。无缺血史患者脾脏标本作为对照。结果脾脏重量的改变与外周血白细胞水平升高有关。形态学分析证实缺血系数与脾脏重量下降呈正相关。脾组织结构分析显示红髓窦塌陷,白髓边缘区明显缩小(p<0.05),滤泡减少,边缘不规则,无明显萌发中心。同时,随着粒细胞的增殖,心肌中M1巨噬细胞增多,脾滤泡边缘区M1/M2比值升高。结论在急性缺血的背景下,时间对脾的动态结构变化起关键作用。随着减少边缘区,针对其细胞成分的免疫调节将是未来可能的治疗方法。
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The morphological response of the heart and spleen following acute myocardial infarction-induced sterile inflammation: a clinicopathological study
Abstract Introduction as an outcome of sterile inflammation-inducing acute ischemic processes, many splenic cells enter the circulatory system and migrate into the lesion, defending tissues against the spread of ischemia or enhancing necrosis. Objective investigating the therapeutic effect of splenic morphological response to sterile inflammation-inducing myocardial infarction. Material and method We examined the weight and structure of the heart and spleen of 106 patients deceased due to acute myocardial infarction. These data were correlated with demographic (personal) and epidemiological data, and disease history. After morphological investigation of archived myocardial and splenic tissue samples, the acute ischemia-induced structural alterations of splenic samples were quantified using a digital morphometric method. Results were evaluated in comparison to the myocardial ischemia coefficient. Changes in distribution of ischemia-induced cell types were characterized by defining the immunological phenotypes of macrophages (M1 vs. M2). Spleen samples from patients without history of ischemia were used as controls. Results The modification of the spleen weight was associated with an increase in peripheral blood leucocyte levels. Our morphological analysis proved a positive correlation between the ischemia coefficient and the decrease of spleen weight. Structural analysis of splenic tissue revealed the collapse of red pulp sinusoids, a significant size decrease of the white pulp marginal zone (p<0.05), and depleted follicles with irregular margins without any distinct germinative centers. Concurrently, with the proliferation of granulocytes, the increase of M1 macrophages was observed in the myocardium, and a higher M1/M2 ratio was detected in the marginal zone of splenic follicles. Conclusion On the background of acute ischemia, time critically determines the dynamic structural changes of the spleen. Along with reducing the marginal zone, immunomodulation targeting its cellular composition will be a putative therapeutic approach in the future.
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