Hypothesis of COVID-19 Therapy with Sildenafil

Abstract

Backgound: Bacterial or viral infections often cause acute and severe systemic inflammation, which affects the lungs lipopolysaccharide (LPS), a pathogenic component of the membrane of gram-negative bacteria, stimulates active innate immune cells, monocytes, macrophages to produce inducible nitric oxide synthase (iNOS). Excess production of this compound occurs in COVID-19 resulting in inflammatory cascade and thromboembolism. We intend to propose the use of sildenafil to reduce this production.

Method: The analysis of biochemical pathways shows that viral infection produces a high amount of nitric oxide (NO), with an acute inflammatory process.

Results: In the case of COVID-19 infection we verified that numerous biochemical processes activate a cascade of inflammatory processes through the activation of iNOS with uncontrolled generation of (NO).

Conclusions: iNOS is the cause of damage to host cells with a consequent pulmonary thromboembolic lung phenomenon in a contest of interstitial pneumonia. This study proposes the use of sildenafil to counter the inflammatory cascade and thromboembolic episodes.

Keywords: COVID-19; nitric oxide; sildenafil citrate.

Figure 1

Metabolic pathways for no equilibrium restoration by activation of endothelial no synthase

Figure 2

AMPK in inflammatory cascade

Figure 3

Biochemical pathways of no in thromboembolisms