In DepthCOVID-19

Blood vessel injury may spur disease's fatal second phase

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Science  05 Jun 2020:
Vol. 368, Issue 6495, pp. 1039-1040
DOI: 10.1126/science.368.6495.1039

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  • Is Covid-19 a nitric oxide deficiency disease?

    SARS-CoV-2 infects endothelial cells throughout the body with associated endothelial dysfunction, disseminated thrombosis, and endotheliitis. A hallmark of endothelial dysfunction, thrombosis, and localized inflammation is suppressed endothelial nitric oxide synthase with concomitant nitric oxide deficiency. In healthy vessels, the endothelium releases the vasodilator and antithrombotic factor, nitric oxide. Whereas in injured vessels, nitric oxide is impaired contributing to vascular collapse and thrombus formation. Jump starting endothelial nitric oxide synthase is likely time-dependent and in the case of late-stage Covid-19, endogenous nitric oxide synthase is unlikely to be up-regulated. However, providing an exogenous nitric oxide gas or stimulating the inducible nitric oxide synthase pathway early in the disease process may prove to be restorative and lifesaving. Clinicals for inhaled nitric oxide are underway and we await the outcomes.

    Nitric oxide is as vital as oxygen; without it, oxygen is not delivered to our brain, muscles and organs. Nitric oxide is a pleotropic molecule: at a minimum, it lowers blood pressure and increases antimicrobial activity. As we grow older, we lose the ability to make it. And this loss of nitric oxide is further exacerbated in individuals with comorbidities, in particular, hypertension. With the onset of nitric oxide deficiencies, we see an increase in cardiometabolic problems and weakening of our innate arm of the i...

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    Competing Interests: None declared.

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