nitrogen-dioxide and Hypertension--Pulmonary

Nitric oxide (NO) is a biologically active molecule approved for the treatment of pulmonary hypertension in newborn patients. Commercially available NO delivery systems use pressurized cylinders as the source of NO and a sensor to control the concentrations of NO and nitrogen dioxide (NO

Topics: Administration, Inhalation; Humans; Hypertension, Pulmonary; Infant, Newborn; Nitric Oxide; Nitrogen Dioxide; Respiration, Artificial

Topics: Administration, Inhalation; Breath Tests; Critical Illness; High-Frequency Ventilation; Humans; Hypertension, Pulmonary; Intensive Care Units; Intubation, Intratracheal; Nitric Oxide; Nitrogen Dioxide; Vasodilator Agents

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

The response to inhaled nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS) varies. It is unclear which patients will respond favorably and whether the initial response persists over time. The authors defined a clinically useful response to inhaled NO as an increase of more than 20% of the ratio of the partial pressure of oxygen (Pa(O2)) to the inspiratory fraction of oxygen (FIO2), a decrease of more than 20% of pulmonary vascular resistance, or both. The authors hypothesized that patients who initially respond favorably are likely to show persistent improvements of gas exchange and hemodynamics after 48 h of NO inhalation.. The medical records and collected research data of 88 patients with ARDS who received 92 trials of NO inhalation between March 1991 and February 1996 were reviewed.. Fifty-three of the 92 trials (58%) produced a clinically significant response to NO. In the responding patients who continued to receive NO therapy (n = 43), the Pa(O2)/FiO2 ratio remained higher (120 +/- 46 vs. 89 +/- 32 mmHg before NO; P < 0.01) and the mean pulmonary artery pressure remained lower (35 +/- 8 vs. 40 +/- 12 mmHg before NO; P < 0.01) at 48 h. Only 33% of the patients with septic shock responded to inhaled NO compared with 64% of those without septic shock (P < 0.02).. Most patients with ARDS had clinically useful responses to NO inhalation. Patients with an initial favorable response maintained the improvement at 48 h. Patients with septic shock were less likely to respond favorably.

Topics: Administration, Inhalation; Humans; Hypertension, Pulmonary; Lung; Methemoglobin; Middle Aged; Nitric Oxide; Nitrogen Dioxide; Respiratory Distress Syndrome; Respiratory Insufficiency; Retrospective Studies; Vascular Resistance

The aim of the study was to evaluate the levels of cardiac biomarkers endothelin 1, B-natriuretic peptide (BNP), N-terminal pro-B-type natriuretic peptide (Nt-proBNP), NO

Topics: Biomarkers; COVID-19; Endothelin-1; Humans; Hypertension, Pulmonary; Natriuretic Peptide, Brain; Nitrates; Nitrites; Nitrogen Dioxide; Oxygen; Peptide Fragments

Model of chronic obstructive pulmonary disease (COPD) was induced in rats by nitrogen dioxide inhalation for 60 days. The effect of reagents-vasodilators on the isolated pulmonary arteries with a diameter less than 0.5 mm was studied in 15, 30 and 60 days of COPD induction. All vasodilators (beta-adrenoreceptor agonist izopreterenol, nitric oxide donor nitrosorbid, acetylcholine, activator of C-fibers capsaicin, corticosteroid beclometasone) dose-dependently decreased vascular tone of pulmonary arteries isolated from intact rats. On extension nitrogen dioxide exposure pulmonary arteries responded to the impact of all vasodilators by smaller relaxation. Dose-dependence of dilatation reaction disappeared. In the process of COPD model formation functioning of almost all pulmonary arterial wall neurotransmitter systems were broken. This led to decrease in vasodilators influence on vascular tone and could facilitate the development of pulmonary hypertension which is typical of COPD.

Topics: Acetylcholine; Animals; Dilatation; Disease Models, Animal; Humans; Hypertension, Pulmonary; Hypoxia; Male; Nitrogen Dioxide; Organ Culture Techniques; Pulmonary Artery; Pulmonary Disease, Chronic Obstructive; Rats; Rats, Wistar; Vasodilator Agents

Inhaled nitric oxide (NO) has the capacity to selectively dilate pulmonary blood vessels, and thus enhance the matching of ventilation and perfusion, improve oxygenation and decrease pulmonary hypertension. However, existing approaches for the administration of inhaled NO are associated with the co-delivery of potentially toxic concentrations of nitrogen dioxide (NO2) due to the oxidation of NO in oxygen rich environments. We tested the ability of a novel methodology for generating highly purified NO through the reduction of NO2 by ascorbic acid to reverse pulmonary hypertension. In vitro testing demonstrated that the NO output of the novel device is ultrapure and free of NO2. An in vivo hypoxemic swine model of pulmonary hypertension was used to examine the dose response to NO in terms of pulmonary pressures and pulmonary vascular resistance. Pulmonary hypertension was induced by lowering inspired oxygen to 15% prior to treatment with inhaled ultra purified NO (1, 5, 20, and 80PPM). Hypoxemia increased mean pulmonary artery pressures and pulmonary vascular resistance. Inhaled ultra purified NO doses (down to 1PPM) show a marked reduction of hypoxemia-induced pulmonary vascular resistance. These experiments demonstrate a simple and robust method to generate purified inhaled NO that is devoid of NO2 and capable of reversing hypoxemia induced pulmonary hypertension.

Topics: Administration, Inhalation; Animals; Ascorbic Acid; Disease Models, Animal; Hypertension, Pulmonary; Hypoxia; Nitric Oxide; Nitrogen; Nitrogen Dioxide; Oxygen; Pulmonary Artery; Swine; Vascular Resistance

A nitric oxide inhaling equipment cooperated with the ventilator synchronously, is introduced in this paper. This equipment monitors the inspiratory flow of the ventilator by a gas flow meter, and works out the flow value of NO on the therapeutic condition using the formula of gas dilution. Then its mass flow controller controls the flow of NO and delivers it to the respiratory circuit. At the same time, the concentrations of NO and NO2 are detected by the electrochemical NO/NO2 sensors before the therapeutic gas enters into the patient. The experimental result shows that this equipment can work with the ventilator in-phase periodically, the volume of E/(I+E) NO be saved, and the output of NO2 < or = 0.7 x 10(-6). Thus the equipment not only has realized the intellectual monitoring and gas-dispensing, but also has improved the precision of inhaled NO concentration with a better reliability and security during the therapy.

Topics: Equipment Design; Humans; Hypertension, Pulmonary; Monitoring, Physiologic; Nitric Oxide; Nitrogen Dioxide; Respiratory Therapy; Ventilators, Mechanical

Topics: Administration, Inhalation; Animals; Endothelium, Vascular; Epoprostenol; Hemoglobins; Humans; Hydroxyl Radical; Hypertension, Pulmonary; Nitrates; Nitric Oxide; Nitrogen Dioxide; Oxidation-Reduction; Pneumonia; Prostaglandin H2; Prostaglandins H; Signal Transduction; Superoxides; Tyrosine

To improve patients' quality of life and decrease pollution risks to medical personnel, we tested the usefulness of a nitric oxide (NO) inhalation system consisting of a nasal cannula and a demand valve in an open circuit system. To estimate the content of NO entering the lung with the open system, concentrations of NO and nitrogen dioxide (NO2) were measured in a mechanical lung model, and then nitrocylhaemoglobin (NO-Hb), methaemoglobin (Met-Hb), and nitrite (NO2-) + nitrate (NO3-) concentrations in venous blood were measured in eight healthy subjects. Exhaust NO and NO2 in the open system were also observed in 14 healthy subjects. In the lung model, NO concentration delivered with the open system was approximately 1/11 of that in the gas tank. Increases in Met-Hb and NO2- + NO3- with the open system showed that the concentration of delivered NO was approximately 1/9 of that in the gas tank. The open system reduced exhaust NO to 1/10 in human subjects. These data suggest that this NO inhalation system delivers sufficient NO to spontaneously breathing patients. In addition, these findings indicate that there is little environmental toxicity associated with the open circuit system.

Topics: Adult; Catheterization; Equipment Design; Female; Health Personnel; Humans; Hypertension, Pulmonary; Male; Nitric Oxide; Nitrogen Dioxide; Occupational Exposure; Quality of Life; Respiration, Artificial

Inhaled nitric oxide (NO) is increasingly being used in the treatment of diseases characterized by hypoxemia and pulmonary hypertension. To avoid complications, accurate quantitative analysis of NO and NO2 is necessary during this therapy. We evaluated the accuracy of electrochemical NO and nitrogen dioxide (NO2) analyzers suitable for use during mechanical ventilation.. We evaluated six electrochemical NO analyzer brands (Bedfont, B & W, Dräger, EIT, Pulmonox, Saan). All were calibrated and used per manufacturer's specifications. An adult mechanical ventilator was used to produce serial dilutions of NO with O2 for [NO] of 0-80 ppm. F1O2 settings of 0.90, 0.70, 0.50, 0.30, and 0.21 were used. Settings of low, moderate, and high ventilation pressures were evaluated. Gas was sampled from the inspiratory limb of the ventilator circuit using either a sidestream or mainstream technique. [NO] was also measured using a calibrated chemiluminescence analyzer. For the analyzers that measured NO2, serial dilutions of 8.5 ppm NO2 with O2 were analyzed using chemiluminescence and the electrochemical analyzers.. Bias +/- precision for [NO] by individual devices ranged from 1.8 +/- 1.9 ppm to -1.0 +/- 0.7 ppm. There were significant differences in the bias between analyzers (P < 0.001), pressure settings (P < 0.001), and NO level (P < 0.017). The difference in bias between levels of F1O2 was not significant (P = 0.062). Bias +/- precision for NO2 ranged from 0.18 +/- 0.12 ppm to -0.14 +/- 0.13 ppm, with a significant difference between analyzers (P < 0.001).. The bias and precision of these analyzers was acceptable for clinical use. The devices tended to be most accurate at [NO] < or = 20 ppm-the clinical conditions at which NO is most commonly used.

Topics: Administration, Inhalation; Adult; Electrochemistry; Evaluation Studies as Topic; Humans; Hypertension, Pulmonary; Hypoxia; Luminescent Measurements; Monitoring, Physiologic; Nitric Oxide; Nitrogen Dioxide; Respiration, Artificial

Topics: Administration, Inhalation; Adult; Child; Environmental Monitoring; Humans; Hypertension, Pulmonary; Infant, Newborn; Luminescent Measurements; Nitric Oxide; Nitrogen Dioxide; Respiratory Insufficiency

Inhaled nitric oxide (NO) is a selective pulmonary vasodilator, potentially useful in the treatment of pulmonary hypertension and ventilation-perfusion mismatch. High doses of inhaled NO and its oxidative product nitrogen dioxide (NO2) may cause acute lung injury. Using a standard infant ventilator, ventilator circuit and test lung, an administration and monitoring strategy has been defined for inhaled NO and these observations validated in eight ventilated infants. In 90% oxygen, doses of inhaled NO > or = 80 parts per million may result in toxic NO2 concentrations.

Topics: Administration, Inhalation; Drug Administration Schedule; Humans; Hypertension, Pulmonary; Infant; Models, Biological; Nitric Oxide; Nitrogen Dioxide; Respiration, Artificial

Pulmonary hypertension and transient graft dysfunction may complicate the postoperative course of patients undergoing lung transplantation. We report the acute effect of inhaled nitric oxide (80 ppm) on hemodynamics and gas exchange in 6 patients (median age, 14 years; range, 5 to 21 years) after lung transplantation as well as the effect of extended treatment over 40 to 69 hours in 2 patients. In 5 patients with pulmonary hypertension nitric oxide lowered mean pulmonary artery pressure (from 38.4 +/- 1.6 to 29.4 +/- 3.1 mm Hg; p < 0.05), pulmonary vascular resistance index (from 9.3 +/- 1.4 to 6.4 +/- 1.3 Um2; p < 0.05), and intrapulmonary shunt fraction (from 28.6% +/- 8.3% to 21.0% +/- 5.7%; p < 0.05). There was a 28.4% +/- 7.2% reduction in transpulmonary pressure gradient with only minor accompanying effects on the systemic circulation. Mean arterial pressure decreased only 2.7% +/- 5% (from 76.4 +/- 2.2 to 74 +/- 2.3 mm Hg; p = not significant), and systemic vascular resistance index by 4.2% +/- 9.7% (from 21.7 +/- 3.1 to 20.6 +/- 3.6 Um2; p = not significant). Cardiac index was unchanged (from 3.5 +/- 0.8 to 3.6 +/- 0.7 L.min-1.m-2; p = not significant). Nitric oxide caused a sustained improvement in oxygenation and pulmonary artery pressure during extended therapy at doses of 10 ppm. There were no major side effects. However, transient methemoglobinemia (9%) developed in 1 patient after 10 hours of nitric oxide treatment. Nitric oxide may be useful in the treatment of pulmonary hypertension and the impaired gas exchange that occurs after lung transplantation.

Topics: Acetylcholine; Administration, Inhalation; Adolescent; Adult; Breath Tests; Child; Child, Preschool; Female; Hemodynamics; Humans; Hypertension, Pulmonary; Infusions, Intra-Arterial; Lung Transplantation; Male; Methemoglobin; Nitric Oxide; Nitrogen Dioxide; Pulmonary Circulation; Pulmonary Gas Exchange