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1.
Microvasc Res ; 137: 104188, 2021 09.
Article in English | MEDLINE | ID: covidwho-1237818

ABSTRACT

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been led to a pandemic emergency. So far, different pathological pathways for SARS-CoV-2 infection have been introduced in which the excess release of pro-inflammatory cytokines (such as interleukin 1 ß [IL-1ß], IL-6, and tumor necrosis factor α [TNFα]) has earned most of the attentions. However, recent studies have identified new pathways with at least the same level of importance as cytokine storm in which endothelial cell (EC) dysfunction is one of them. In COVID-19, two main pathologic phenomena have been seen as a result of EC dysfunction: hyper-coagulation state and pathologic angiogenesis. The EC dysfunction-induced hypercoagulation state seems to be caused by alteration in the levels of different factors such as plasminogen activator inhibitor 1 (PAI-1), von Willebrand factor (vWF) antigen, soluble thrombomodulin, and tissue factor pathway inhibitor (TFPI). As data have shown, these thromboembolic events are associated with severity of disease severity or even death in COVID-19 patients. Other than thromboembolic events, pathologic angiogenesis is among the recent findings. Furthermore, over-expression/higher levels of different proangiogenic factors such as vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1 α (HIF-1α), IL-6, TNF receptor super family 1A and 12, and angiotensin-converting enzyme 2 (ACE2) have been found in the lung biopsies/sera of both survived and non-survived COVID-19 patients. Also, there are some hypotheses regarding the role of nitric oxide in EC dysfunction and acute respiratory distress syndrome (ARDS) in SARS-CoV-2 infection. It has been demonstrated that different pathways involved in inflammation are generally common with EC dysfunction and angiogenesis. Altogether, considering the common possible upstream pathways in cytokine storm, pathologic angiogenesis, and EC dysfunction, it seems that targeting these molecules (such as nuclear factor κB) could be more effective in the management of patients with COVID-19.


Subject(s)
COVID-19/blood , COVID-19/physiopathology , Endothelial Cells/metabolism , Neovascularization, Pathologic , Angiotensin-Converting Enzyme 2/metabolism , Biomarkers/metabolism , Blood Coagulation , Cytokine Release Syndrome , Humans , Inflammation , Interleukin-1beta/metabolism , Interleukin-6/metabolism , Lipoproteins/metabolism , Nitric Oxide/metabolism , Plasminogen Activator Inhibitor 1/metabolism , SARS-CoV-2 , Tumor Necrosis Factor-alpha/metabolism , von Willebrand Factor/metabolism
2.
Panminerva Med ; 62(4): 252-259, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-1044555

ABSTRACT

BACKGROUND: Strong epidemiologic evidence has highlighted the role of pollution, on top of adverse climate features, as a novel cardiovascular risk factor. However, mechanistic proof that reducing pollution may be beneficial to prevent atherothrombotic events is limited. We aimed at appraising the impact of temporary traffic bans in a large metropolitan area on the risk of acute coronary syndromes. METHODS: Aggregate and anonymized data from 15 tertiary cardiac care centers were obtained detailing precoronavirus disease 2019 (COVID-19) daily cases of ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI), including those treated with percutaneous coronary intervention (PCI). Data on pollutants and climate were sought for the same days. Mixed level regression was used to compare the week before vs after the traffic ban (Fortnight analysis), the 3 days before vs. after (Weekly analysis) and the Sunday before vs. after (Sunday analysis). RESULTS: A total of 8 days of temporary traffic bans were included, occurring between 2017 and 2020, totaling 802 STEMI and 1196 NSTEMI in the Fortnight analysis, 382 STEMI and 585 in the Weekly analysis, and 148 STEMI and 210 NSTEMI in the Sunday analysis.Fortnight and Sunday analyses did not disclose a significant impact of traffic ban on STEMI or NSTEMI (all P>0.05). Conversely, Weekly analysis showed non-significant changes for STEMI, but a significant decrease in daily NSTEMI when comparing the 3 days before the traffic ban with the ban day (P=0.043), as well as the 3 days before vs. the 3 days after the ban (P=0.025). No statistically significant effect of traffic ban was found at Fortnight, Weekly or Sunday analyses for daily mean concentrations of benzene, carbon monoxide, nitric oxide, nitrogen dioxide, ozone, sulfur dioxide, particulate matter (PM) <2.5 µm or PM <10 µm (all P>0.05). However, minimum daily concentrations showed a significant reduction of ozone during the ban in comparison to the week preceding it (P=0.034), nitric oxide during the ban in comparison to the 3 days preceding it (P=0.046), and an increase in benzene during the ban in comparison to the Sunday before (P=0.039). CONCLUSIONS: Temporary traffic ban may favorably reduce coronary atherothrombotic events, and in particular NSTEMI, even if not globally and immediately impacting on environmental pollution. Further controlled studies are required to confirm and expand this hypothesis-generating results.


Subject(s)
Acute Coronary Syndrome/epidemiology , Motor Vehicles , Aged , COVID-19/epidemiology , COVID-19/virology , Female , Humans , Italy/epidemiology , Male , Middle Aged , Risk Factors , SARS-CoV-2/isolation & purification
3.
Ann Intensive Care ; 10(1): 151, 2020 Nov 04.
Article in English | MEDLINE | ID: covidwho-992558

ABSTRACT

BACKGROUND: In COVID-19 patients with severe acute respiratory distress syndrome (ARDS), the relatively preserved respiratory system compliance despite severe hypoxemia, with specific pulmonary vascular dysfunction, suggests a possible hemodynamic mechanism for VA/Q mismatch, as hypoxic vasoconstriction alteration. This study aimed to evaluate the capacity of inhaled nitric oxide (iNO)-almitrine combination to restore oxygenation in severe COVID-19 ARDS (C-ARDS) patients. METHODS: We conducted a monocentric preliminary pilot study in intubated patients with severe C-ARDS. Respiratory mechanics was assessed after a prone session. Then, patients received iNO (10 ppm) alone and in association with almitrine (10 µg/kg/min) during 30 min in each step. Echocardiographic and blood gases measurements were performed at baseline, during iNO alone, and iNO-almitrine combination. The primary endpoint was the variation of oxygenation (PaO2/FiO2 ratio). RESULTS: Ten severe C-ARDS patients were assessed (7 males and 3 females), with a median age of 60 [52-72] years. Combination of iNO and almitrine outperformed iNO alone for oxygenation improvement. The median of PaO2/FiO2 ratio varied from 102 [89-134] mmHg at baseline, to 124 [108-146] mmHg after iNO (p = 0.13) and 180 [132-206] mmHg after iNO and almitrine (p < 0.01). We found no correlation between the increase in oxygenation caused by iNO-almitrine combination and that caused by proning. CONCLUSION: In this pilot study of severe C-ARDS patients, iNO-almitrine combination was associated with rapid and significant improvement of oxygenation. These findings highlight the role of pulmonary vascular function in COVID-19 pathophysiology.

4.
Nitric Oxide ; 107: 11-18, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-949808

ABSTRACT

Nitric oxide, NO, has been explored as a therapeutic agent to treat thrombosis. In particular, NO has potential in treating mechanical device-associated thrombosis due to its ability to reduce platelet activation and due to the central role of platelet activation and adhesion in device thrombosis. Nitrite is a unique NO donor that reduces platelet activation in that it's activity requires the presence of red blood cells whereas NO activity of other NO donors is blunted by red blood cells. Interestingly, we have previously shown that red blood cell mediated inhibition of platelet activation by adenosine diphosophate (ADP) is dramatically enhanced by illumination with far-red light that is likely due to photolysis of red cell surface bound NO congeners. We now report the effects of nitrite, far-red light, and their combination on several measure of blood coagulation using a variety of agonists. We employed turbidity assays in platelet rich plasma, platelet activation using flow cytometry analysis of a fluorescently labeled antibody to the activated platelet fibrinogen binding site, multiplate impedance-based platelet aggregometry, and assessment of platelet adhesion to collagen coated flow-through microslides. In all cases, the combination of far-red light and nitrite treatment decreased measures of coagulation, but in some cases mono-treatment with nitrite or light alone had no effect. Perhaps most relevant to device thrombosis, we observed that platelet adhesions was inhibited by the combination of nitrite and light treatment while nitrite alone and far-red light alone trended to decrease adhesion, but the results were mixed. These results support the potential of combined far-red light and nitrite treatment for preventing thrombosis in extra-corporeal or shallow-tissue depth devices where the far-red light can penetrate. Such a combined treatment could be advantageous due to the localized treatment afforded by far-red light illumination with minimal systemic effects. Given the role of thrombosis in COVID 19, application to treatment of patients infected with SARS Cov-2 might also be considered.


Subject(s)
Blood Coagulation/drug effects , Blood Coagulation/radiation effects , Nitric Oxide Donors/pharmacology , Nitrites/pharmacology , Blood Platelets/drug effects , Blood Platelets/radiation effects , COVID-19/drug therapy , COVID-19/radiotherapy , Humans , Light , Nitric Oxide/metabolism , Platelet Activation/drug effects , Platelet Activation/radiation effects , Platelet Adhesiveness/drug effects , Platelet Adhesiveness/radiation effects , Platelet Aggregation/drug effects , Platelet Aggregation/radiation effects , SARS-CoV-2/drug effects
5.
ESC Heart Fail ; 8(1): 714-718, 2021 02.
Article in English | MEDLINE | ID: covidwho-932426

ABSTRACT

AIMS: This study aims to analyse whether inhaled nitric oxide (iNO) was beneficial in the treatment of coronavirus disease 2019 (COVID-19) patients with pulmonary hypertension. METHODS AND RESULTS: Five critically ill COVID-19 patients with pulmonary hypertension designated Cases 1-5 were retrospectively included. Clinical data before and after iNO treatment were serially collected and compared between patients with or without iNO treatment. The five cases experienced pulmonary artery systolic pressure (PASP) elevation (≥50 mmHg) at 30, 24, 33, 23, and 24 days after illness onset (d.a.o), respectively. Cases 1-3 received iNO treatment on the 24th, 13th, and 1st day after the first elevation of PASP, with concentrations varied from 10 to 20 ppm based on the changes of PASP and blood pressure for 10, 9, and 5 days, respectively. Upon iNO treatment, PASP of Cases 1 and 2 returned to normal on the 10th day and 1st day, and maintained between 50 and 58 mmHg in Case 3. Pa02 /Fi02 increased from 88 to 124, 51 to 118, and 146 to 244, respectively. SPO2 increased from 91% to 97% for Case 1 and maintained a high level above 97% for Case 2. Cardiac function remained normal in the three patients after treatment. Moreover, Cases 1 and 3 survived from severe acute respiratory syndrome coronavirus 2 infection, while Case 2 finally died on the 36th day after the first elevation of PASP due to severe complications. Both cases who did not receive iNO treatment experienced a sudden decrease of PASP and Pa02 /Fi02 due to right heart failure and then died. CONCLUSIONS: Inhaled nitric oxide treatment was beneficial in reducing and stabilizing the PASP and might also reduce the risk of right heart failure in COVID-19 with pulmonary hypertension.


Subject(s)
COVID-19/drug therapy , Hypertension, Pulmonary/drug therapy , Nitric Oxide/therapeutic use , Administration, Inhalation , COVID-19/complications , Humans , Hypertension, Pulmonary/etiology , Middle Aged , Nitric Oxide/administration & dosage , Retrospective Studies
6.
Heart Lung Circ ; 30(1): 36-44, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-912219

ABSTRACT

It is now 30 years since Japanese investigators first described Takotsubo Syndrome (TTS) as a disorder occurring mainly in ageing women, ascribing it to the impact of multivessel coronary artery spasm. During the intervening period, it has become clear that TTS involves relatively transient vascular injury, followed by prolonged myocardial inflammatory and eventually fibrotic changes. Hence symptomatic recovery is generally slow, currently an under-recognised issue. It appears that TTS is induced by aberrant post-ß2-adrenoceptor signalling in the setting of "surge" release of catecholamines. Resultant activation of nitric oxide synthases and increased inflammatory vascular permeation lead to prolonged myocardial infiltration with macrophages and associated oedema formation. Initially, the diagnosis of TTS was made via exclusion of relevant coronary artery stenoses, plus the presence of regional left ventricular hypokinesis. However, detection of extensive myocardial oedema on cardiac MRI imaging offers a specific basis for diagnosis. No adequate methods are yet available for definitive diagnosis of TTS at hospital presentation. Other major challenges remaining in this area include understanding of the recently demonstrated association between TTS and antecedent cancer, the development of effective treatments to reduce risk of short-term (generally due to shock) and long-term mortality, and also to accelerate symptomatic recovery.


Subject(s)
Heart Ventricles/physiopathology , Magnetic Resonance Imaging, Cine/methods , Takotsubo Cardiomyopathy/physiopathology , Ventricular Function, Left/physiology , Heart Ventricles/diagnostic imaging , Humans , Takotsubo Cardiomyopathy/diagnosis
7.
Ageing Res Rev ; 64: 101201, 2020 12.
Article in English | MEDLINE | ID: covidwho-907102

ABSTRACT

The COVID-19 pandemic poses an imminent threat to humanity, especially to the elderly. The molecular mechanisms underpinning the age-dependent disparity for disease progression is not clear. COVID-19 is both a respiratory and a vascular disease in severe patients. The damage endothelial system provides a good explanation for the various complications seen in COVID-19 patients. These observations lead us to suspect that endothelial cells are a barrier that must be breached before progression to severe disease. Endothelial intracellular defences are largely dependent of the activation of the interferon (IFN) system. Nevertheless, low type I and III IFNs are generally observed in COVID-19 patients suggesting that other intracellular viral defence systems are also activated to protect the young. Intriguingly, Nitric oxide (NO), which is the main intracellular antiviral defence, has been shown to inhibit a wide array of viruses, including SARS-CoV-1. Additionally, the increased risk of death with diseases that have underlying endothelial dysfunction suggest that endothelial NOS-derived nitric oxide could be the main defence mechanism. NO decreases dramatically in the elderly, the hyperglycaemic and the patients with low levels of vitamin D. However, eNOS derived NO occurs at low levels, unless it is during inflammation and co-stimulated by bradykinin. Regrettably, the bradykinin-induced vasodilation also progressively declines with age, thereby decreasing anti-viral NO production as well. Intriguingly, the inverse correlation between the percentage of WT eNOS haplotype and death per 100K population could potentially explain the disparity of COVID-19 mortality between Asian and non-Asian countries. These changes with age, low bradykinin and NO, may be the fundamental reasons that intracellular innate immunity declines with age leading to more severe COVID-19 complications.


Subject(s)
Aging/metabolism , COVID-19/metabolism , COVID-19/mortality , Nitric Oxide Synthase Type III/metabolism , Nitric Oxide/metabolism , Age Factors , Bradykinin , COVID-19/enzymology , COVID-19/genetics , Endothelial Cells/metabolism , Endothelium, Vascular/cytology , Endothelium, Vascular/metabolism , Haplotypes , Humans , Immunity, Innate , Nitric Oxide Synthase Type III/genetics , SARS-CoV-2/pathogenicity
8.
BMC Pulm Med ; 20(1): 269, 2020 Oct 16.
Article in English | MEDLINE | ID: covidwho-873971

ABSTRACT

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has spread to almost 100 countries, infected over 31 M patients and resulted in 961 K deaths worldwide as of 21st September 2020. The major clinical feature of severe COVID-19 requiring ventilation is acute respiratory distress syndrome (ARDS) with multi-functional failure as a result of a cytokine storm with increased serum levels of cytokines. The pathogenesis of the respiratory failure in COVID-19 is yet unknown, but diffuse alveolar damage with interstitial thickening leading to compromised gas exchange is a plausible mechanism. Hypoxia is seen in the COVID-19 patients, however, patients present with a distinct phenotype. Intracellular levels of nitric oxide (NO) play an important role in the vasodilation of small vessels. To elucidate the intracellular levels of NO inside of RBCs in COVID-19 patients compared with that of healthy control subjects. METHODS: We recruited 14 COVID-19 infected cases who had pulmonary involvement of their disease, 4 non-COVID-19 healthy controls (without pulmonary involvement and were not hypoxic) and 2 hypoxic non-COVID-19 patients subjects who presented at the Masih Daneshvari Hospital of Tehran, Iran between March-May 2020. Whole blood samples were harvested from patients and intracellular NO levels in 1 × 106 red blood cells (RBC) was measured by DAF staining using flow cytometry (FACS Calibour, BD, CA, USA). RESULTS: The Mean florescent of intensity for NO was significantly enhanced in COVID-19 patients compared with healthy control subjects (P ≤ 0.05). As a further control for whether hypoxia induced this higher intracellular NO, we evaluated the levels of NO inside RBC of hypoxic patients. No significant differences in NO levels were seen between the hypoxic and non-hypoxic control group. CONCLUSIONS: This pilot study demonstrates increased levels of intracellular NO in RBCs from COVID-19 patients. Future multi-centre studies should examine whether this is seen in a larger number of COVID-19 patients and whether NO therapy may be of use in these severe COVID-19 patients.


Subject(s)
Carbon Dioxide/metabolism , Coronavirus Infections/metabolism , Erythrocytes/metabolism , Hypoxia/metabolism , Nitric Oxide/metabolism , Oxygen/metabolism , Pneumonia, Viral/metabolism , Adult , Aged , Aged, 80 and over , Asymptomatic Diseases , Betacoronavirus , Blood Gas Analysis , COVID-19 , Case-Control Studies , Coronavirus Infections/blood , Coronavirus Infections/complications , Female , Flow Cytometry , Humans , Hypoxia/blood , Hypoxia/etiology , Male , Middle Aged , Pandemics , Partial Pressure , Pilot Projects , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pulmonary Disease, Chronic Obstructive/blood , Pulmonary Disease, Chronic Obstructive/complications , Pulmonary Disease, Chronic Obstructive/metabolism , SARS-CoV-2 , Vasodilation , Young Adult
9.
Free Radic Biol Med ; 161: 15-22, 2020 12.
Article in English | MEDLINE | ID: covidwho-816474

ABSTRACT

Amelioration of immune overactivity during sepsis is key to restoring hemodynamics, microvascular blood flow, and tissue oxygenation, and in preventing multi-organ dysfunction syndrome. The systemic inflammatory response syndrome that results from sepsis ultimately leads to degradation of the endothelial glycocalyx and subsequently increased vascular leakage. Current fluid resuscitation techniques only transiently improve outcomes in sepsis, and can cause edema. Nitric oxide (NO) treatment for sepsis has shown promise in the past, but implementation is difficult due to the challenges associated with delivery and the transient nature of NO. To address this, we tested the anti-inflammatory efficacy of sustained delivery of exogenous NO using i.v. infused NO releasing nanoparticles (NO-np). The impact of NO-np on microhemodynamics and immune response in a lipopolysaccharide (LPS) induced endotoxemia mouse model was evaluated. NO-np treatment significantly attenuated the pro-inflammatory response by promoting M2 macrophage repolarization, which reduced the presence of pro-inflammatory cytokines in the serum and slowed vascular extravasation. Combined, this resulted in significantly improved microvascular blood flow and 72-h survival of animals treated with NO-np. The results from this study suggest that sustained supplementation of endogenous NO ameliorates and may prevent the morbidities of acute systemic inflammatory conditions. Given that endothelial dysfunction is a common denominator in many acute inflammatory conditions, it is likely that NO enhancement strategies may be useful for the treatment of sepsis and other acute inflammatory insults that trigger severe systemic pro-inflammatory responses and often result in a cytokine storm, as seen in COVID-19.


Subject(s)
Endotoxemia/drug therapy , Nitric Oxide/therapeutic use , Sepsis/drug therapy , Systemic Inflammatory Response Syndrome/drug therapy , Animals , Blood Circulation/drug effects , COVID-19/pathology , Cytokine Release Syndrome/prevention & control , Cytokines/blood , Delayed-Action Preparations/therapeutic use , Disease Models, Animal , Hemodynamics/drug effects , Lipopolysaccharides/toxicity , Macrophages/immunology , Male , Mice , Mice, Inbred BALB C , Nanoparticles/therapeutic use , SARS-CoV-2/immunology
10.
J Investig Med High Impact Case Rep ; 8: 2324709620946621, 2020.
Article in English | MEDLINE | ID: covidwho-690444

ABSTRACT

Little is known about the effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on pregnant women, fetuses, and neonates, especially when the virus is contracted early in pregnancy. The literature is especially lacking on the effects of SARS-CoV-2 on extremely preterm (<28 weeks gestation) infants who have underdeveloped immune systems. We report the case of an extremely preterm, 25-week 5-days old infant, born to a mother with severe COVID-19 (coronavirus disease-2019) pneumonia. In this case, there is no evidence of vertical transmission of SARS-CoV-2 based on reverse transcription-polymerase chain reaction testing, despite extreme prematurity. However, it appears that severe maternal COVID-19 may have been associated with extremely preterm delivery, based on observed histologic chorioamnionitis. This is the first reported case of an extremely preterm infant born to a mother with severe COVID-19 pneumonia who required intubation, and was treated with hydroxychloroquine, azithromycin, remdesivir, tocilizumab, convalescent plasma, inhaled nitric oxide, and prone positioning for severe hypoxemic respiratory failure prior to and after delivery of this infant. The infant remains critically ill with severe respiratory failure on high-frequency ventilation, inotropic support, hydrocortisone for pressor-resistant hypotension, and inhaled nitric oxide for severe persistent pulmonary hypertension with a right to left shunt across the patent ductus arteriosus and foramen ovale. Pregnant women or women planning to get pregnant should take all precautions to minimize exposure to SARS-CoV-2 to decrease adverse perinatal outcomes.


Subject(s)
Coronavirus Infections/complications , Coronavirus Infections/therapy , Infant, Extremely Premature , Pneumonia, Viral/complications , Pneumonia, Viral/therapy , Pregnancy Complications, Infectious/therapy , Pregnancy Complications, Infectious/virology , Premature Birth/therapy , Premature Birth/virology , COVID-19 , Female , Humans , Infant, Newborn , Pandemics , Pregnancy , Young Adult
11.
Pharmacol Rep ; 72(6): 1509-1516, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-662484

ABSTRACT

Cepharanthine (CEP) is a naturally occurring alkaloid derived from Stephania cepharantha Hayata and demonstrated to have unique anti-inflammatory, antioxidative, immunomodulating, antiparasitic, and antiviral properties. Its therapeutic potential as an antiviral agent has never been more important than in combating COVID-19 caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) virus. Cepharanthine suppresses nuclear factor-kappa B (NF-κB) activation, lipid peroxidation, nitric oxide (NO) production, cytokine production, and expression of cyclooxygenase; all of which are crucial to viral replication and inflammatory response. Against SARS-CoV-2 and homologous viruses, CEP predominantly inhibits viral entry and replication at low doses; and was recently identified as the most potent coronavirus inhibitor among 2406 clinically approved drug repurposing candidates in a preclinical model. This review critically analyzes and consolidates available evidence establishing CEP's potential therapeutic importance as a drug of choice in managing COVID-19 cases.


Subject(s)
Antiviral Agents/therapeutic use , Benzylisoquinolines/therapeutic use , COVID-19/drug therapy , Animals , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Antiviral Agents/pharmacology , Benzylisoquinolines/pharmacology , COVID-19/virology , Drug Repositioning , Humans , Inflammation/drug therapy , Inflammation/virology , Japan , SARS-CoV-2/drug effects , SARS-CoV-2/isolation & purification , Virus Replication/drug effects
12.
Nitric Oxide ; 103: 1-3, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-611235

ABSTRACT

It has long been suggested that NO may inhibit an early stage in viral replication. Furthermore, in vitro tests have shown that NO inhibits the replication cycle of severe acute respiratory syndrome coronavirus. Despite smoking being listed as a risk factor to contract Covid-19, only a low proportion of the smokers suffered from SARS-corona infection in China 2003, and from Covid-19 in China, Europe and the US. We hypothesize, that the intermittent bursts of high NO concentration in cigarette smoke may be a mechanism in protecting against the virus. Mainstream smoke from cigarettes contains NO at peak concentrations of between about 250 ppm and 1350 ppm in each puff as compared to medicinal use of no more than 80 to a maximum of 160 ppm. The diffusion of NO through the cell wall to reach the virus should be significantly more effective at the very high NO concentration in the smoke, according to classic laws of physics. The only oxide of nitrogen in the mainstream smoke is NO, and the NO2 concentration that is inhaled is very low or undetectable, and methemoglobin levels are lower in smokers than non-smokers, reasonably explained by the breaths of air in between the puffs that wash out the NO. Specialized iNO machines can now be developed to provide the drug intermittently in short bursts at high concentration dose, which would then provide both a preventative drug for those at high risk, as well as an effective treatment, without the health hazards associated with smoking.


Subject(s)
Betacoronavirus/drug effects , Coronavirus Infections/prevention & control , Nitric Oxide/pharmacology , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Protective Agents/pharmacology , Administration, Inhalation , COVID-19 , Coronavirus Infections/drug therapy , Female , Humans , Male , Nitric Oxide/administration & dosage , Protective Agents/administration & dosage , SARS-CoV-2 , Smokers , Smoking
13.
Indian J Otolaryngol Head Neck Surg ; 72(3): 395-397, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-324638

ABSTRACT

The Coronavirus (2019-Cov-2) infection Covid-19 is highly contagious caused by single stranded RNA virus (+ssRNA) with nucleocapsid and spreading widely all across the world and responsible for more than 3.6 million morbidity and 0.25 million mortality No specific treatment is available till date. The clinical symptoms are mainly upper respiratory leading to diffuse viral pneumonia and multiple organ failure involving. Kidney, Liver and Heart along with coagulopathies. During 2004 (SARS-CoV) pandemic role of nitric oxide in its management is well demonstrated. Nitric Oxide (NO) reversed pulmonary hypertension. Improved severe hypoxia and shortened the stay in ICU and ventilatory support. Nitric Oxide increased the survival rate. The genetic composition of Corona Virus (SARS-CoV) is almost similar to Covid-19, thus indicates good chances of effectiveness or enhancement in results by Nitric Oxide along with other modes in treatment of Covid-19. It has been proved by studies by serendipity humming increases NO Expression dramatically.It is estimated that humming increases the endogenous generation of nitric oxide level by 15-fold. Hypoxia in ARD Syndrome leads to blood coagulation by depression of body defence anticoagulatory and fibrolytic properties along with metabolic acidosis. If we go into hypoxic hypercapnic state no hyper coagulation takes place. Hence Bhramari by enhancing the expression of Nitric Oxide and increased Carbon dioxide by extended exhalation and alkaline pH prevents coagulopathies and morbidity due to Covid-19.

14.
Microbes Infect ; 22(4-5): 168-171, 2020.
Article in English | MEDLINE | ID: covidwho-275089

ABSTRACT

The nasal cavity and turbinates play important physiological functions by filtering, warming and humidifying inhaled air. Paranasal sinuses continually produce nitric oxide (NO), a reactive oxygen species that diffuses to the bronchi and lungs to produce bronchodilatory and vasodilatory effects. Studies indicate that NO may also help to reduce respiratory tract infection by inactivating viruses and inhibiting their replication in epithelial cells. In view of the pandemic caused by the novel coronavirus (SARS-CoV-2), clinical trials have been designed to examine the effects of inhaled nitric oxide in COVID-19 subjects. We discuss here additional lifestyle factors such as mouth breathing which may affect the antiviral response against SARS-CoV-2 by bypassing the filtering effect of the nose and by decreasing NO levels in the airways. Simple devices that promote nasal breathing during sleep may help prevent the common cold, suggesting potential benefits against coronavirus infection. In the absence of effective treatments against COVID-19, the alternative strategies proposed here should be considered and studied in more detail.


Subject(s)
Betacoronavirus , Coronavirus Infections/drug therapy , Nitric Oxide/administration & dosage , Nitric Oxide/therapeutic use , Pneumonia, Viral/drug therapy , Administration, Intranasal , Betacoronavirus/drug effects , COVID-19 , Coronavirus Infections/prevention & control , Humans , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , SARS-CoV-2 , Viral Load/drug effects
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