The Bronchial Circulation in COVID-19 Pneumonia.

The Bronchial Circulation in COVID-19 Pneumonia.
复制标题

DOI:
10.1164/rccm.202103-0594im
复制
发表时间:
2022-01-01
影响因子:
24.7
通讯作者:
Jonigk DD
Jonigk DD
中科院分区:
医学1区
文献类型:
--
作者:
Ackermann M;Tafforeau P;Wagner WL;Walsh CL;Werlein C;Kühnel MP;Länger FP;Disney C;Bodey AJ;Bellier A;Verleden SE;Lee PD;Mentzer SJ;Jonigk DD

文献摘要

被引文献

相似文献

严重冠状病毒病(新冠肺炎)的主要肺部疾病是以肺内皮炎、微血管病变和异常血管生成为特征的。虽然许多研究强调了肺循环中明显的微血管病变,但对支气管血管系统的影响还没有完全阐明。因此,我们综合分析了三名男性患者(年龄63.7614岁)的完整肺叶。2.通过常规CT、组织学、微血管铸型和分层相对比断层扫描,观察因严重新冠肺炎死亡的患者(2年;住院2261d,机械通气)。我们使用了三个来自身体捐赠者的对照肺(年龄,78.3613岁)。6岁,两名女性和一名男性死于中风或子宫癌。在肺CT血管成像中,我们发现了先前报道的新冠肺炎肺损伤的肺后遗症,表现为双侧周围磨玻璃样阴影、支气管周围实变和周围大血管充血[3](图1A和1B)。支气管周围和血管周围微血管(血管)明显扩张(图1C-1F)。支气管循环的这种肺内分流(图2A)解释了在各种呼吸道情况下持续灌流的原因,如炎症、急性呼吸窘迫综合征和慢性血栓栓塞症(3)。在重症新冠肺炎肺炎中,支气管周围血管的微血管构筑呈微血管构筑,有密集排列的异常血管束(图2B-2E)。管腔内皮组织柱(图2B-2D)(1,4,5)的出现证明了支气管周围神经丛的扩张主要是由肠套叠血管生成驱动的。应用分层相位对比断层扫描对新冠肺炎肺炎患者的支气管周围血管进行了空间分析,显示了支气管周围和血管周围的动静脉吻合扩张,并首次在第三维度上跨越单个次级肺小叶招募了“精动脉”(阻断动脉)(图3A和3B以及视频E1)。
The primary life-limiting pulmonary morbidity of severe coronavirus disease (COVID-19) is characterized by pulmonary endothelialitis, microangiopathy, and aberrant angiogenesis (1). Although numerous studies have highlighted the pronounced microangiopathy in pulmonary circulation, the impact of the bronchial vascular system has not been fully elucidated. Therefore, we comprehensively analyzed complete lung lobes from three male patients (age, 63.7614. 2 years; hospitalization time, 2261 days, mechanically ventilated) who succumbed to severe COVID-19 using conventional computed tomography, histology, microvascular corrosion casting, and hierarchical phase-contrast tomography (2). We used three control lungs from body donors (age, 78.3613. 6 yr; nonventilated, two females and one male died from cerebral stroke or uterine carcinoma). In pulmonary computed tomography angiography, we found the previously reported pulmonary sequelae of COVID-19 lung injury in the form of bilateral peripheral ground-glass opacities, peribronchial consolidations, and peripheral macrovascular congestion (3)(Figures 1A and 1B). Peribronchial and perivascular microvessels (vasa vasorum) were distinctly dilated (Figures 1C–1F). This intrapulmonary shunting by the bronchial circulation (Figure 2A) accounts for the continued perfusion in a variety of airway conditions, such as inflammation, acute respiratory distress syndrome, and chronic thromboembolism (3). In severe COVID-19 pneumonia, the microvascular architecture of the peribronchial vessels showed a microvascular architecture with densely packed aberrant bundles of blood vessels (Figures 2B–2E). The expansion of the peribronchial plexus is mainly driven by intussusceptive angiogenesis as evidenced by the appearance of transluminal endothelial tissue pillars (Figures 2B–2D)(1, 4, 5). A spatial analysis of peribronchial vessels in COVID-19 pneumonia by hierarchical phase-contrast tomography demonstrated the expansion of peribronchial and perivascular arteriovenous anastomoses and a recruitment of “Sperrarterien”(blockade arteries) across individual secondary pulmonary lobules in the third dimension for the first time (Figures 3A and 3B and Video E1 in