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1.
Am J Physiol Heart Circ Physiol ; 322(2): H319-H327, 2022 02 01.
Article in English | MEDLINE | ID: covidwho-1613119

ABSTRACT

Vascular dysfunction has been reported in adults who have recovered from COVID-19. To date, no studies have investigated the underlying mechanisms of persistent COVID-19-associated vascular dysfunction. Our purpose was to quantify nitric oxide (NO)-mediated vasodilation in healthy adults who have recovered from SARS-CoV-2 infection. We hypothesized that COVID-19-recovered adults would have impaired NO-mediated vasodilation compared with adults who have not had COVID-19. In methods, we performed a cross-sectional study including 10 (5 men/5 women, 24 ± 4 yr) healthy control (HC) adults who were unvaccinated for COVID-19, 11 (4 men/7 women, 25 ± 6 yr) healthy vaccinated (HV) adults, and 12 (5 men/7 women, 22 ± 3 yr) post-COVID-19 (PC, 19 ± 14 wk) adults. COVID-19 symptoms severity (survey) was assessed. A standardized 39°C local heating protocol was used to assess NO-dependent vasodilation via perfusion (intradermal microdialysis) of 15 mM NG-nitro-l-arginine methyl ester during the plateau of the heating response. Red blood cell flux was measured (laser-Doppler flowmetry) and cutaneous vascular conductance (CVC = flux/mmHg) was expressed as a percentage of maximum (28 mM sodium nitroprusside + 43°C). In results, the local heating plateau (HC: 61 ± 20%, HV: 60 ± 19%, PC: 67 ± 19%, P = 0.80) and NO-dependent vasodilation (HC: 77 ± 9%, HV: 71 ± 7%, PC: 70 ± 10%, P = 0.36) were not different among groups. Neither symptom severity (25 ± 12 AU) nor time since diagnosis correlated with the NO-dependent vasodilation (r = 0.46, P = 0.13; r = 0.41, P = 0.19, respectively). In conclusion, healthy adults who have had mild-to-moderate COVID-19 do not have altered NO-mediated cutaneous microvascular function.NEW & NOTEWORTHY Healthy young adults who have had mild-to-moderate COVID-19 do not display alterations in nitric oxide-mediated cutaneous microvascular function. In addition, healthy young adults who have COVID-19 antibodies from the COVID-19 vaccinations do not display alterations in nitric oxide-mediated cutaneous microvascular function.


Subject(s)
COVID-19/physiopathology , Microcirculation/physiology , Skin/blood supply , Vasodilation/physiology , Adult , COVID-19/metabolism , COVID-19/prevention & control , COVID-19 Vaccines/therapeutic use , Case-Control Studies , Enzyme Inhibitors/pharmacology , Female , Humans , Laser-Doppler Flowmetry , Male , Microcirculation/drug effects , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide/metabolism , SARS-CoV-2 , Severity of Illness Index , Vasodilation/drug effects , Young Adult
2.
Int J Antimicrob Agents ; 56(6): 106191, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-846626

ABSTRACT

Corona virus disease 2019 (COVID-19) is triggered by the Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV2) and has rapidly developed into a worldwide pandemic. Unlike other SARS viruses, SARS-CoV2 does not solely impact the respiratory system, but additionally leads to inflammation of endothelial cells, microvascular injuries and coagulopathies, thereby affecting multiple organs. Recent reports of patients who were infected with SARS-CoV2 suggest persistent health problems even months after the initial infection. The French maritime pine bark extract PycnogenolⓇ has demonstrated anti-inflammatory, vascular and endothelium-protective effects in over 90 human clinical studies. It is proposed that PycnogenolⓇ may be beneficial in supporting recovery and mitigating symptoms and long-term consequences resulting from a SARS-CoV2 infection in COVID-19 patients.


Subject(s)
COVID-19 Drug Treatment , Flavonoids/therapeutic use , Plant Extracts/therapeutic use , SARS-CoV-2 , Blood Platelets/drug effects , COVID-19/etiology , Endothelium, Vascular/drug effects , Flavonoids/adverse effects , Flavonoids/pharmacology , Humans , Microcirculation/drug effects , Plant Extracts/adverse effects , Plant Extracts/pharmacology
3.
Med Hypotheses ; 144: 109988, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-591493

ABSTRACT

Pentoxifylline (PTX) is a phosphodiesterase inhibitor that increases cyclic adenosine monophosphate levels, which in turn activate protein kinase, leading to a reduction in the synthesis of proinflammatory cytokines to ultimately influence the renin-angiotensin system (RAS) in vitro by inhibiting angiotensin 1 receptor (AT1R) expression. The rheological, anti-inflammatory, and renin-angiotensin axis properties of PTX highlight this drug as a therapeutic treatment alternative for patients with COVID-19 by helping reduce the production of the inflammatory cytokines without deleterious effects on the immune system to delay viral clearance. Moreover, PTX can restore the balance of the immune response, reduce damage to the endothelium and alveolar epithelial cells, improve circulation, and prevent microvascular thrombosis. There is further evidence that PTX can improve ventilatory parameters. Therefore, we propose repositioning PTX in the treatment of COVID-19. The main advantage of repositioning PTX is that it is an affordable drug that is already available worldwide with an established safety profile, further offering the possibility of immediately analysing the result of its use and associated success rates. Another advantage is that PTX selectively reduces the concentration of TNF-α mRNA in cells, which, in the case of an acute infectious state such as COVID-19, would seem to offer a more strategic approach.


Subject(s)
COVID-19 Drug Treatment , Drug Repositioning , Immunologic Factors/therapeutic use , Pandemics , Pentoxifylline/therapeutic use , Renin-Angiotensin System/drug effects , SARS-CoV-2/physiology , Alveolar Epithelial Cells/drug effects , Angiotensin II/physiology , Angiotensin-Converting Enzyme 2/metabolism , Animals , COVID-19/epidemiology , COVID-19/immunology , COVID-19/physiopathology , Complement Activation/drug effects , Cytokines/biosynthesis , Cytokines/genetics , Disease Models, Animal , Endothelial Cells/drug effects , Gene Expression Regulation/drug effects , Humans , Immunologic Factors/pharmacology , Inflammation , Lymphocyte Subsets/drug effects , Microcirculation/drug effects , Oxidative Stress , Pentoxifylline/pharmacology , Rats , Receptors, Virus/metabolism , Renin-Angiotensin System/physiology , Signal Transduction/drug effects , Venous Thromboembolism/etiology , Venous Thromboembolism/prevention & control
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