探討求證一下武漢肺炎的病理

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首先聲明一下，我不是醫生。甚至基礎性科學方麵生物生理知識都有限，不過是喜歡可以讀一些科學文章。所以想和大家探討求證一下這個武漢肺炎的病理。

昨晚補了一下ACE2的作用。得出這樣的理解：

Ace 和ace2是腎素-血管收縮素係統裏互相製衡的。實驗證明ACE2在肺纖毛表麵細胞上有很高的表達。在肺裏，它幫助調節循環係統裏麵腎素和血管收縮的素的平衡。（有文獻依據）
以下是我個人的理解，
如果一個人的心肺功能差，體內氧氣不足，ACE2在肺部就會過分表達顯露出來，這樣冠狀病毒和Ace2的接觸概率就增加了。
我認為，如果病毒複製幹擾到ACE2正常的功能，會進一步妨礙肺部的氧氣吸收能力。
如果人體免疫係統去消滅這些被病毒感染的細胞，實際上把ACE 2也消滅了。這些ACE2表達出來的細胞實際上為了人體要提高肺部的吸收能力，致使Ace增加，為了輔助ACE保護肺部細胞不纖化，Ace2也同時增加了。本來Ace2是保護肺細胞的，但是反而被免疫係統一起消滅了。所以病毒對本來心肺功能差，體內氧氣含量低的人，傷害更大。是雙重打擊。
那麽，作為健康的人，我們是不是應該多到空曠的室外，呼吸新鮮的空氣，心情平靜地避免給自己的心肺功能造成不必要的stress.

這到應了:正氣不足，邪氣當道。正氣內存，邪不可幹。

以下是學術文章的摘要：

ACE2 is more abundantly expressed on the apical surface of polarized epithelia, and we show for the first time that well-differentiated cells support viral replication with viral entry and egress occurring primarily from the apical surface. Thus, SARS-CoV preferentially infects well-differentiated ciliated epithelial cells expressing ACE2. Since ACE2 is also the receptor for the coronavirus NL63 (12), these findings are relevant to the biology of infection with this more common human pathogen.

ACE2 Receptor Expression and Severe Acute Respiratory Syndrome Coronavirus Infection Depend on Differentiation of Human Airway Epithelia

Hong Peng Jia, Dwight C. Look, [...], and Paul B. McCray, Jr

RAS activity is intrinsically high in the lung, which is a major source of ACE and therefore a major site of systemic Ang II synthesis. ACE2 is also highly expressed in the lung. Pulmonary ACE2 appears to have a role in regulating the balance of circulating Ang II/Ang 1–7 levels. (ACE2在肺部有很高的表達。在肺裏，它幫助調節循環係統裏麵腎素和血管收縮的素的平衡）Ang II induces pulmonary vasoconstriction in response to hypoxia, which is important in preventing shunting in patients with pneumonia or lung injury [59]. Locally increased Ang II production also triggers increasing vascular permeability facilitating pulmonary edema [60]. In Acute respiratory distress syndrome (ARDS), the RAS appears crucial in maintaining oxygenation, possibly as widespread lung injury would otherwise result in complete pulmonary shutdown. Certainly in ARDS models, ACE2 knockout mice displayed more severe symptoms of this disease compared with wild-type mice [60] while overexpression appears protective (see below). Interestingly, ACE2 protein also appears to be the entry-point receptor for the severe acute respiratory syndrome (SARS) coronavirus [61, 62].

Review Article | Open Access

Volume 2012 |Article ID 256294 | 8 pages | https://doi.org/10.1155/2012/256294