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停止使用 ACEI 和 ARB 类药物对 COVID-19 患者的潜在有害影响。

Potential harmful effects of discontinuing ACE-inhibitors and ARBs in COVID-19 patients.

机构信息

Hypertension Unit -Department of Medicine-DIMED, University of Padova, Padova, Italy.

International PhD Program in Arterial Hypertension and Vascular Biology (ARHYVAB)- University of Padua, Padua, Italy.

出版信息

Elife. 2020 Apr 6;9:e57278. doi: 10.7554/eLife.57278.

Abstract

The discovery of angiotensin converting enzyme-2 (ACE-2) as the receptor for SARS- CoV-2 (Severe Acute Respiratory Syndrome Coronavirus-2) has implicated the renin-angiotensin-aldosterone system in acute respiratory distress syndrome (ARDS) and respiratory failure in patients with coronavirus disease-19 (COVID-19). The angiotensin converting enzyme-1-angiotensin II-angiotensin AT receptor pathway contributes to the pathophysiology of ARDS, whereas activation of the ACE-2-angiotensin(1-7)-angiotensin AT receptor and the ACE-2-angiotensin(1-7)-Mas receptor pathways have been shown to be protective. Here we propose and discuss therapeutic considerations how to increase soluble ACE-2 in plasma in order for ACE-2 to capture and thereby inactivate SARS-CoV-2. This could be achieved by administering recombinant soluble ACE-2. We also discuss why and how ACEIs and ARBs provide cardiovascular, renal and also pulmonary protection in SARS-CoV-2- associated ARDS. Discontinuing these medications in COVID-19 patients may therefore potentially be harmful.

摘要

血管紧张素转换酶 2(ACE-2)作为严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的受体被发现,这表明肾素-血管紧张素-醛固酮系统在新型冠状病毒疾病 19(COVID-19)患者的急性呼吸窘迫综合征(ARDS)和呼吸衰竭中起作用。血管紧张素转换酶 1-血管紧张素 II-血管紧张素 AT 受体途径有助于 ARDS 的病理生理学,而 ACE-2-血管紧张素(1-7)-血管紧张素 AT 受体和 ACE-2-血管紧张素(1-7)-Mas 受体途径的激活已被证明具有保护作用。在这里,我们提出并讨论了治疗方面的考虑因素,即如何增加血浆中的可溶性 ACE-2,以使 ACE-2能够捕获并失活 SARS-CoV-2。这可以通过给予重组可溶性 ACE-2 来实现。我们还讨论了为什么血管紧张素转换酶抑制剂(ACEIs)和血管紧张素受体阻滞剂(ARBs)在 SARS-CoV-2 相关 ARDS 中提供心血管、肾脏和肺部保护,以及在 COVID-19 患者中停用这些药物可能潜在有害的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d6/7198232/a1e55238ecbb/elife-57278-fig1.jpg

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