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脑死亡对供体肺微血管的影响:实验模型研究。

Brain death effects on lung microvasculature in an experimental model of lung donor.

机构信息

Laboratório Cirúrgico de Pesquisa Cardiovascular, Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo (SP) Brasil.

出版信息

J Bras Pneumol. 2020 Feb 21;46(2):e20180299. doi: 10.36416/1806-3756/e20180299. eCollection 2020.

DOI:10.36416/1806-3756/e20180299
PMID:32130341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8651258/
Abstract

OBJECTIVE

Brain death (BD) triggers important hemodynamic and inflammatory alterations, compromising the viability of organs suitable for transplantation. To better understand the microcirculatory alterations in donor lungs caused by BD. The present study investigated the pulmonary microcirculation in a rodent model of BD via intravital microscopy.

METHODS

Male Wistar rats were anaesthetized and mechanically ventilated. They were trepanned and BD was induced through the increase in intracranial pressure. As control group, sham-operated (SH) rats were trepanned only. In both groups, expiratory O2 and CO2 were monitored and after three hours, a thoracotomy was performed, and a window was created to observe the lung surface using an epi-fluorescence intravital microscopy. Lung expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) was evaluated by immunohistochemistry, and cytokines were measured in lung samples.

RESULTS

Three hours after the surgical procedures, pulmonary perfusion was 73% in the SH group. On the other hand, BD animals showed an important decrease in organ perfusion to 28% (p = 0.036). Lung microcirculatory compromise after BD induction was associated with an augmentation of the number of leukocytes recruited to lung tissue, and with a reduction in eNOS expression and an increase in ICAM-1 expression on lung endothelial cells. BD rats showed higher values of expiratory O2 and lower values of CO2 in comparison with SH animals after three hours of monitoring.

CONCLUSION

Data presented showed that BD triggers an important hypoperfusion and inflammation in the lungs, compromising the donor pulmonary microcirculation.

摘要

目的

脑死亡(BD)会引发重要的血流动力学和炎症改变,从而影响适合移植的器官的存活能力。为了更好地了解 BD 引起的供体肺的微循环改变,本研究通过活体显微镜观察研究了 BD 啮齿动物模型中的肺微循环。

方法

雄性 Wistar 大鼠接受麻醉并进行机械通气。他们被钻孔,通过颅内压升高来诱导 BD。作为对照组,仅进行假手术(SH)的大鼠被钻孔。在两组中,监测呼气中的 O2 和 CO2,三小时后进行开胸手术,在肺表面创建一个窗口,使用荧光显微镜观察。通过免疫组织化学评估肺细胞间黏附分子(ICAM)-1 和内皮型一氧化氮合酶(eNOS)的表达,并测量肺组织中的细胞因子。

结果

在手术程序后三小时,SH 组的肺灌注为 73%。另一方面,BD 动物的器官灌注明显下降至 28%(p = 0.036)。BD 诱导后肺微循环受损与肺组织中募集的白细胞数量增加有关,并且 eNOS 表达减少,肺内皮细胞上的 ICAM-1 表达增加。与 SH 动物相比,BD 大鼠在监测三小时后表现出更高的呼气 O2 值和更低的 CO2 值。

结论

所呈现的数据表明,BD 会引发肺部重要的低灌注和炎症,从而影响供体肺的微循环。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/dec53a1c47b4/jbpneu-46-2-e20180299-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/1fe8538ef23b/jbpneu-46-2-e20180299-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/2a01f07545aa/jbpneu-46-2-e20180299-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/a9bd18879580/jbpneu-46-2-e20180299-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/dec53a1c47b4/jbpneu-46-2-e20180299-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/1fe8538ef23b/jbpneu-46-2-e20180299-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/2a01f07545aa/jbpneu-46-2-e20180299-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/a9bd18879580/jbpneu-46-2-e20180299-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e78e/8651258/dec53a1c47b4/jbpneu-46-2-e20180299-g04.jpg

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