nitrogen-dioxide and Methemoglobinemia

The extent of toxicity and adverse effects resulting from inhaled NO is poorly understood. Presumably, toxicity is low and adverse effects are rare at the doses commonly used to treat acute respiratory failure. Much remains to be learned about this important topic, however.

Topics: Administration, Inhalation; Blood Platelets; Humans; Hypertension, Pulmonary; Hypoxia; Methemoglobinemia; Nitric Oxide; Nitrogen Dioxide; Respiratory Insufficiency

To assess the dose-related effects of inhaled nitric oxide (I-NO) as a specific adjunct to early conventional therapy for term infants with persistent pulmonary hypertension (PPHN), with regard to neonatal outcome, oxygenation, and safety.. Randomized, placebo-controlled, double-masked, dose-response, clinical trial at 25 tertiary centers from April 1994 to June 1996. The primary endpoint was the PPHN Major Sequelae Index ([MSI], including the incidence of death, extracorporeal membrane oxygenation (ECMO), neurologic injury, or bronchopulmonary dysplasia [BPD]). Patients required a fraction of inspired oxygen [FIO2] of 1.0, a mean airway pressure >/=10 cm H2O on a conventional ventilator, and echocardiographic evidence of PPHN. Exogenous surfactant, concomitant high-frequency ventilation, and lung hypoplasia were exclusion factors. Control (0 ppm) or nitric oxide (NO) (5, 20, or 80 ppm) treatments were administered until success or failure criteria were met. Due to slowing recruitment, the trial was stopped at N = 155 (320 planned).. The baseline oxygenation index (OI) was 24 +/- 9 at 25 +/- 17 hours old (mean +/- SD). Efficacy results were similar among NO doses. By 30 minutes (no ventilator changes) the PaO2 for only the NO groups increased significantly from 64 +/- 39 to 109 +/- 78 Torr (pooled) and systemic arterial pressure remained unchanged. The baseline adjusted time-weighted OI was also significantly reduced in the NO groups (-5 +/- 8) for the first 24 hours of treatment. The MSI rate was 59% for the control and 50% for the NO doses (P = .36). The ECMO rate was 34% for control and 22% for the NO doses (P = .12). Elevated methemoglobin (>7%) and nitrogen dioxide (NO2) (>3 ppm) were observed only in the 80 ppm NO group, otherwise no adverse events could be attributed to I-NO, including BPD.. For term infants with PPHN, early I-NO as the sole adjunct to conventional management produced an acute and sustained improvement in oxygenation for 24 hours without short-term side effects (5 and 20 ppm doses), and the suggestion that ECMO use may be reduced.

Topics: Administration, Inhalation; Combined Modality Therapy; Dose-Response Relationship, Drug; Double-Blind Method; Extracorporeal Membrane Oxygenation; Female; Hemodynamics; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Male; Methemoglobinemia; Nitric Oxide; Nitrogen Dioxide; Oxygen; Persistent Fetal Circulation Syndrome; Treatment Outcome

Inhaled nitric oxide (iNO) is an advanced therapy typically managed by physicians and respiratory therapists in order to increase arterial oxygenation and decrease pulmonary arterial pressure. The Johns Hopkins Lifeline Critical Care Transportation Program (Lifeline) initiated a novel nurse-managed iNO protocol in order to optimize the oxygenation of critically ill patients during interfacility transport. This study was a retrospective chart review of adverse events associated with iNO initiation or continuation by Lifeline on patients transported from March 1, 2020, to August 1, 2022. Basic demographic data and adverse events were recorded. Recorded adverse events included hypotension defined as a mean arterial pressure (MAP) < 65 mm Hg, hypoxemia defined as a decrease of ≥ 10% arterial oxygenation saturation measured by pulse oximetry, new bradycardia or tachyarrhythmia, nitrogen dioxide (NO

Topics: Administration, Inhalation; COVID-19; Critical Care; Humans; Hypotension; Hypoxia; Methemoglobinemia; Nitric Oxide; Nitrogen Dioxide; Retrospective Studies; SARS-CoV-2

Nitrogen dioxide /NO2/, is one of the basic photochemical atmospheric pollutants possessing both direct and indirect toxic effects. When inhaled NO2 affects directly the blood hemoglobin forming methemoglobin. The rate of effect depends on the level of the intra-erythrocyte redox systems and in the first place on the reduced glutathione. The systemic toxic effects of NO2 and is easy penetration through the hemato-alveolar barrier are well known. However the effects of NO2 on the organism during pregnancy have nor been studied. The present study has been designed to evaluate the effect of NO2 on the reduced oxidized glutathione and the level of methemoglobin in the blood of pregnant and nonpregnant female rats. Inhalation exposure of pregnant albino rats to NO2 in concentration of 10 and 1 mg/m3, 5 hours daily, throughout gestation /21 days/, induces an increased synthesis of glutathione and shifting towards the reduced form, which could be taken as a sign of adaptive mechanisms. The nonpregnant animals show no such effect, as they more easily compensate the oxidizing effect of NO2. At the age of 1 month the progeny of the NO2-exposed mothers show the same tendency to an elevated synthesis of glutathione and increase of its reduced form. When treated again with NO2 at the same dose levels during gestation, the F1 females show no changes in blood glutathione, but the level of methemoglobin is raised--an effect not observed in the parental generation.

Topics: Animals; Dose-Response Relationship, Drug; Environmental Exposure; Female; Glutathione; Methemoglobinemia; Nitrogen Dioxide; Oxidation-Reduction; Pregnancy; Pregnancy, Animal; Rats; Rats, Inbred Strains; Time Factors

A collective nitrous fumes poisoning (five cases) is reported. Two patients (case 3 and case 4) were comatose, in severe respiratory distress. Shock and slate blue cyanosis were noted. Physical examination and chest X ray revealed acute pulmonary edema-Methemoglobin levels were 71,3% (case 3) and 58% (case 4). Despite treatment both of them died from severe hypoxia resulting in cardiorespiratory arrest. Post-mortem examination was performed upon these four men. On admission the last one (case 5) was conscious, and in good hemodynamic condition. Acute pulmonary edema and cyanosis were present. Methemoglobin level was 37,3%. This patient recovered appropriate therapy. For case 1 and 2 acute anoxia due to methemoglobinemia seems to be cause of death. For cases 3 and 4 death is due to hypoxemia associated with pulmonary edema.

Topics: Accidents, Occupational; Bronchi; Cyanosis; Hemodynamics; Humans; Lung; Methemoglobinemia; Nitrates; Nitrogen Dioxide; Nitrogen Oxides; Occupational Diseases; Pulmonary Edema; Radiography; Water-Electrolyte Imbalance

Topics: Air Pollution; Carboxyhemoglobin; Female; Hemoglobins; Humans; Industry; Male; Methemoglobinemia; Middle Aged; Nitrates; Nitrogen Dioxide; Residence Characteristics; Smoking; Water Supply

Topics: Air Pollution; Anemia, Hemolytic; Animals; Bilirubin; Erythrocyte Count; Female; Hematocrit; Hemoglobins; Leukocyte Count; Male; Methemoglobinemia; Mice; Nitrogen Dioxide; Sex Factors

Topics: Animals; Chemical Phenomena; Chemistry; Dogs; Hemoglobins; Methemoglobinemia; Methylene Blue; Nitric Oxide; Nitrogen Dioxide; Oxygen; Spectrophotometry

Topics: Acidosis; Acidosis, Respiratory; Animals; Blood Pressure; Dogs; Electrocardiography; Heart Rate; Methemoglobinemia; Nitric Oxide; Nitrogen Dioxide; Oxygen; Polarography; Pulmonary Edema

Topics: Acid-Base Equilibrium; Animals; Dimercaprol; Humans; Methemoglobinemia; Methylene Blue; Nitrates; Nitric Oxide; Nitrogen Dioxide; Oxygen Inhalation Therapy; Pneumonia; Positive-Pressure Respiration

Topics: Biomedical Research; Dogs; Germany; Germany, West; Methemoglobin; Methemoglobinemia; Nitrogen; Nitrogen Dioxide; Occupational Medicine; Research; Toxicology