Inhaled nitric oxide in moderate-to-severe COVID-19 acute respiratory distress syndrome: a retrospective cohort study.

OBJECTIVE: In this study, we present the findings from a cohort of patients with COVID-19 with acute respiratory distress syndrome who underwent standard therapy, including prone positioning, with or without adjunctive inhalation of nitric oxide. Our investigation sought to determine whether inhaled nitric oxide administration yielded clinical enhancement in this population. Remarkably, nitric oxide administration elevated the PaO2/FiO2 ratio, which is indicative of improved oxygenation. Despite this improvement, discernible mortality benefits did not emerge in association with the inhaled nitric oxide treatment. To evaluate the responsiveness of COVID-19 acute respiratory distress syndrome patients to inhaled nitric oxide as part of their standard therapy. METHODS: This retrospective cohort study included critically ill adult patients with confirmed COVID-19 treated between March 2020 and May 2021. Eligible patients with moderate-to-severe acute respiratory distress syndrome due to COVID-19 were subsequently categorized into two groups based on inhaled nitric oxide use throughout their stay in the intensive care unit. The primary endpoints were overall mortality and improvement in oxygenation parameters 6 hours after inhaled nitric oxide use. RESULTS: A total of 481 patients admitted to the intensive care unit due to COVID-19 acute respiratory distress syndrome were screened, 105 of which were included. Among the 105 patients, inhaled nitric oxide therapy was used in 33 patients, will 72 did not undergo inhaled nitric oxide therapy. No significant difference in mortality was observed between the groups (67% for the treatment and 82% for the no-treatment groups respectively, p=0.173). Among the patients who used inhaled nitric oxide, 17 (51%) were considered responsive to therapy. There was no significant difference in the length of stay in the intensive care unit (p=0.324) or total hospitalization time (p=0.344). CONCLUSION: Inhaled nitric oxide rescue therapy improved oxygenation in patients with COVID-19 with moderate-to-severe acute respiratory distress syndrome but did not affect mortality.

Complications associated with the use of temporary pacemaker in patients waiting for definitive device implantation

ABSTRACT Objective To determine the rate of complications associated with the use of temporary pacemakers in patients in the waiting list for the definitive pacemaker implantation in a public hospital located in São Paulo, SP, Brazil. Methods Retrospective observational study based on data extracted from medical records of patients admitted to Hospital Municipal Dr. Moyses Deutsch, Hospital Israelita Albert Einstein from January 2014 to December 2018. Patients aged 18 years or older, diagnosed with high degree atrioventricular block upon admission and with indications for definitive pacemaker implantation were included. All-cause mortality, clinical and surgical complications and length of hospital stay while waiting for the procedure were defined as primary outcomes. Results The sample comprised 66 patient allocated to one of two groups: with and without the need of temporary pacemaker while in hospital (n=45 and n=21, respectively). The rate of complications was higher in patients who used a temporary pacemaker (p<0.001). These included primarily pneumonia (p=0.048) and length of hospital stay (p=0.029). Conclusion Patients who required a temporary pacemaker stayed longer in hospital. Longer hospital stay is associated with higher rates of general complications and all-cause mortality.

Ação hemodinâmica e metabolismo da bradicinina no fígado / Hemodynamic action and metabolism of bradykinin on the liver

Bradicinina (R1P2P3G4S6P7F8R9) infundida na veia porta provoca resposta hipertensiva via receptor B2 e, por outro lado, é eficientemente hidrolisada pelo fígado. A EC 3.4.24.15 é a principal enzima inativadora de BK in vitro e é liberada de fígados normais preservados ex vivo em líquido Braun Collins. Nossos objetivos foram: 1) estudar a liberação da EC 3.4.24.15 no reperfusato de fígados (normais e em fase aguda de inflamação) preservados ex vivo; 2) localizar a EC 3.4.24.15 no fígado; 3) caracterizar a interação entre bradicinina (BK) e fígado eluciando o local da ação do peptídeo e o papel das cininases ECA (enzima conversora de angiotensina) e EC 3.4.24.15 na sua inativação. Para tanto, fígados normais e inflamados foram preservados em líquido University of Wisconsin e reperfundidos após 8 ou 24 h. Alíquotas do reperfusato foram recolhidas para dosagens enzimáticas. BK, antagonista do receptor B2 (HOE-140), agonista do receptor B1 (des-R9-BK) e inibidores enzimáticos foram utilizados em perfusões monovascular (entrada pela veia porta) e bivascular (entrada pela veia porta e artéria hepática) de fígado e em ensaios com células hepáticas isoladas. Verificamos que a liberação da EC 3.4.24.15 no reperfusato de figados inflamados foi superior aos normais. Des-R9-BK não produz resposta hipertensiva portal (RHP); BK infundida na artéria hepática provocou RHP (cálcio-dependente) e resposta hipertensiva arterial (RHA) (cálcio-independente), esta quase abolida por naproxeno. Os produtos de hidrólise da BK infundida são R1-F5 e R1-P7; estes fragmentos não foram capazes de produzir RHP. ECA e EC 3.4.24.15 estão presentes no fígado e concentram-se na região perivenular (imuno-histoquímica); BK tem distribuição predominante no espaço extracelular e média de extração hepática de 8 por cento em condições estacionárias (diluição de indicadores); o receptor B2 concentra-se na região periportal em células sinusoidais (imuno-histoquímica), resultado confirmado com Cytosensor microphysiometer onde BK (mas não des-R9-BK) elicia mudanças na taxa de acidificação basal de células estreladas e da fração contendo células sinusoidais endoteliais/Kupffer, este efeito é inibido por HOE-140. Concluímos que a EC3.4.24.15 é indicador sensível do estado inflamatório de fígados preservados mas não indica disfunção do órgão; a seqüência de eventos é ação hipertensiva da BK em células sinusoidais da região periportal e sua hidrólise pela ECA e não pela EC 3.4.24.15...