Let it rip Unconventional maybe I know the Co.
I think there may be a backdoor Covid pay to this XAIR. I have read on some of these weird sites that one of the crazy self-treatments for Covid is Nitric Oxide...
So I searched and I did find an important peer reviewed case---
It is with this backdrop that, in this issue of the
Journal, Zamanian and colleagues (pp.
130–132) present an interesting and compelling
case of a patient with pulmonary arterial hypertension (PAH) who was treated remotely in an ambulatory setting with inhaled nitric oxide (iNO) (
5).
This patient with well-controlled vasoreactive PAH lived in a remote area more than 300 miles away from their center and experienced symptoms of worsening breathlessness after being diagnosed with COVID-19. Considering her concerns about traveling the long distance to their center to receive care, and with recognition of her prior confirmed responsiveness to iNO,
they established a plan to support her with an ambulatory iNO system while monitoring her symptoms, vital signs, and functional capacity remotely. The patient had rapid and sustained improvement in her 6-minute-walk distance, as assessed by her caregiver, and symptom score, and she recovered over several days without having to engage emergency department or hospital care.
This case report raises many questions. How might iNO have benefited this patient? Would we expect the benefit to be unique to iNO, or could other therapies that increase signaling along the NO axis also be helpful, such as NO donors, NO precursors, or phosphodiesterase 5 inhibitors? Can NO be safely administered to a patient in their own home, potentially helping to unburden overwhelmed healthcare systems?
NO is a free radial gas that functions as an important signaling molecule in human physiology. Its canonical receptor, guanylate cyclase, is highly expressed vascular smooth muscle cells, where it becomes activated once NO binds to its heme moiety, significantly increasing its enzymatic conversion of guanosine-5′-triphosphate to cyclic guanosine monophosphate, which
subsequently promotes vasorelaxation. As a gas, it has unique pharmacological properties including its delivery into well-ventilated lung units where
it promotes local vasodilatation. When NO enters the blood stream, it rapidly reacts with intraerythrocytic Hb, thus inactivating the NO, resulting in an extremely short half-life, which limits its systemic effects. By preferentially vasodilating pulmonary arterioles in well-ventilated lung units, it decreases the relative blood flow to poorly ventilated lung units and enhancesV./Q.matching, increasing oxygenation (
6). NO also induces mild bronchodilation, and inhibits neutrophil-mediated oxidative burst (
6). These properties have been well known for decades and have led to U.S. Food and Drug Administration approval for the treatment of persistent pulmonary hypertension of the newborn,
as well as various trials of iNO for patients with myriad conditions including ARDS, right ventricular failure after cardiac surgery, acute pulmonary embolism, and more recently pulmonary fibrosis in patients requiring long-term oxygen therapy (
6–
10). In patients with SARS, iNO was associated with improvements in oxygenation in a severity-matched observational cohort (
11). Both endogenous and exogenous NO were shown to inhibit SARS-CoV viral replication (
12). While iNO has not been shown to reduce the time on mechanical ventilation or mortality in adults with ARDS,
iNO does significantly improve oxygenation in ARDS patients and leads to reduction in pulmonary vascular resistance (
6) (
Figure 1).
These therapeutic responses suggest that iNO could be used early in the course of COVID-19 infection to reduce the need for invasive mechanical ventilation. <--- HEY ROBIN HOOD!!!!