The Combination of Inhaled Nitric Oxide and Pulmonary Artery Balloon Inflation Improves Oxygenation During Whole-Lung Lavage

2004 ◽  
Vol 99 (3) ◽  
pp. 676-679 ◽  
Author(s):  
Marie-Josée Nadeau ◽  
Dany Côté ◽  
Jean S. Bussières
1998 ◽  
Vol 84 (1) ◽  
pp. 107-115 ◽  
Author(s):  
Zenaide M. N. Quezado ◽  
Charles Natanson ◽  
Waheedullah Karzai ◽  
Robert L. Danner ◽  
Cezar A. Koev ◽  
...  

Quezado, Zenaide M. N., Charles Natanson, Waheedullah Karzai, Robert L. Danner, Cezar A. Koev, Yvonne Fitz, Donald P. Dolan, Steven Richmond, Steven M. Banks, Laura Wilson, and Peter Q. Eichacker.Cardiopulmonary effects of inhaled nitric oxide in normal dogs and during E. coli pneumonia and sepsis. J. Appl. Physiol. 84(1): 107–115, 1998.—We investigated the effect of inhaled nitric oxide (NO) at increasing fractional inspired O2concentrations ([Formula: see text]) on hemodynamic and pulmonary function during Escherichia coli pneumonia. Thirty-eight conscious, spontaneously breathing, tracheotomized 2-yr-old beagles had intrabronchial inoculation with either 0.75 or 1.5 × 1010 colony-forming units/kg of E. coli 0111:B4 (infected) or 0.9% saline (noninfected) in one or four pulmonary lobes. We found that neither the severity nor distribution (lobar vs. diffuse) of bacterial pneumonia altered the effects of NO. However, in infected animals, with increasing[Formula: see text] (0.08, 0.21, 0.50, and 0.85), NO (80 parts/million) progressively increased arterial[Formula: see text] [−0.3 ± 0.6, 3 ± 1, 13 ± 4, 10 ± 9 (mean ± SE) Torr, respectively] and decreased the mean arterial-alveolar O2 gradient (0.5 ± 0.3, 4 ± 2, −8 ± 7, −10 ± 9 Torr, respectively). In contrast, in noninfected animals, the effect of NO was significantly different and opposite; NO progressively decreased mean[Formula: see text] with increasing[Formula: see text] (2 ± 1, −5 ± 3, −2 ± 3, and −12 ± 5 Torr, respectively; P < 0.05 compared with infected animals) and increased mean arterial-alveolar O2 gradient (0.3 ± 0.04, 2 ± 2, 1 ± 3, 11 ± 5 Torr; P< 0.05 compared with infected animals). In normal and infected animals alike, only at [Formula: see text]≤0.21 did NO significantly lower mean pulmonary artery pressure, pulmonary artery occlusion pressure, and pulmonary vascular resistance index (all P < 0.01). However, inhaled NO had no significant effect on increases in mean pulmonay artery pressure associated with bacterial pneumonia. Thus, during bacterial pneumonia, inhaled NO had only modest effects on oxygenation dependent on high[Formula: see text] and did not affect sepsis-induced pulmonary hypertension. These data do not support a role for inhaled NO in bacterial pneumonia. Further studies are necessary to determine whether, in combination with ventilatory support, NO may have more pronounced effects.


2005 ◽  
Vol 150 (4) ◽  
pp. 725-728 ◽  
Author(s):  
Richard A. Krasuski ◽  
Andrew Wang ◽  
J. Kevin Harrison ◽  
Victor F. Tapson ◽  
Thomas M. Bashore

2021 ◽  
Vol 8 ◽  
Author(s):  
Driss Laghlam ◽  
Ghilas Rahoual ◽  
Julien Malvy ◽  
Philippe Estagnasié ◽  
Alain Brusset ◽  
...  

Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is manifested by an acute respiratory distress syndrome (ARDS) with intense inflammation and endothelial dysfunction leading to particularly severe hypoxemia. We hypothesized that an impaired hypoxic pulmonary vasoconstriction aggravates hypoxemia. The objective of the study was to test the effect of two pulmonary vasoactive drugs on patient oxygenation.Methods: Observational, single-center, open-label study in one intensive care unit (ICU) of the Paris area, realized in April 2020. Eligible patients had coronavirus disease 2019 (COVID-19) and moderate to severe ARDS [arterial partial pressure of oxygen/fraction of inspired oxygen (PaO2/FiO2) &lt;200 mmHg] despite conventional protective ventilation. Exclusion criteria included pulmonary artery hypertension defined by a pulmonary artery systolic pressure (PAPs) &gt;45 mmHg. The assessment of oxygenation was based on PaO2/FiO2 at (1) baseline, then after (2) 30 min of inhaled nitric oxide (iNO) 10 ppm alone, then (3) 30 min combination of iNO + almitrine infusion 8 μg/kg/min, then (4) 30 min of almitrine infusion alone.Results: Among 20 patients requiring mechanical ventilation during the study period, 12 met the inclusion criteria. Baseline PaO2/FiO2 was 146 ± 48 mmHg. When iNO was combined with almitrine, PaO2/FiO2 rose to 255 ± 90 mmHg (+80 ± 49%, p = 0.005), also after almitrine alone: 238 ± 98 mmHg (+67 ± 75%, p = 0.02), but not after iNO alone: 185 ± 73 mmHg (+30 ± 5%, p = 0.49). No adverse events related to almitrine infusion or iNO was observed.Conclusion: Combining iNO and infused almitrine improved the short-term oxygenation in patients with COVID-19-related ARDS. This combination may be of interest when first-line therapies fail to restore adequate oxygenation. These findings argue for an impaired pulmonary hypoxic vasoconstriction in these patients.


Heart ◽  
2001 ◽  
Vol 86 (1) ◽  
pp. e1-e1
Author(s):  
C J McMahon ◽  
J Kadkin ◽  
M R Nihill

A 14 month old child presented for investigation of tachypnoea. No parenchymal lung disease was shown on chestx ray. On echocardiography there was normal intracardiac anatomy with significant pulmonary hypertension. At cardiac catheterisation the presence of primary pulmonary hypertension was confirmed, with a partial response to inhaled nitric oxide (80 ppm) and 100% oxygen. The child was referred for assessment for heart–lung transplantation while maintained on oxygen, inhaled nitric oxide, and nifedipine. Repeat cardiac catheterisation two months after presentation showed complete normalisation of the pulmonary artery pressures.


1999 ◽  
Vol 5 (5) ◽  
pp. 381-387 ◽  
Author(s):  
James Y. Findlay ◽  
Barry A. Harrison ◽  
David J. Plevak ◽  
Michael J. Krowka

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