Inhaled nitric oxide lowers pulmonary capillary pressure and changes longitudinal distribution of pulmonary vascular resistance in patients with acute lung injury

Abstract Background In acute lung injury, when pulmonary microvascular permeability is enhanced, transvascular fluid filtration mainly depends on pulmonary capillary pressure. Inhaled nitric oxide has been shown to decrease pulmonary capillary pressure. Therefore, the effect of inhaled nitric oxide at a concentration of 40 ppm on pulmonary transvascular albumin flux was studied in nine patients with acute lung injury.

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Effects of inhaled NO and inhibition of endogenous NO synthesis in oxidant-induced acute lung injury

Journal of Applied Physiology ◽

10.1152/jappl.1994.76.3.1324 ◽

1994 ◽

Vol 76 (3) ◽

pp. 1324-1329 ◽

Cited By ~ 100

Author(s):

B. P. Kavanagh ◽

A. Mouchawar ◽

J. Goldsmith ◽

R. G. Pearl

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Capillary Permeability ◽

Lung Weight ◽

Pulmonary Capillary ◽

Injury Model ◽

Pulmonary Capillary Pressure ◽

Inhaled No

Inhaled nitric oxide (NO) decreases pulmonary arterial pressure (Ppa) and improves oxygenation in the adult respiratory distress syndrome. Endogenous NO can modulate the development of acute tissue injury. We investigated the effects of inhaled NO and of inhibition of endogenous NO synthase in oxidant-induced acute lung injury in the isolated buffer-perfused rabbit lung. A rapid (45 min) and a more gradual (3 h) model of oxidant-induced acute lung injury were developed using the production of superoxide free radicals from the reaction of purine with low and high doses of xanthine oxidase, respectively. The effects of rapid injury included increases in Ppa, precapillary pulmonary vascular resistance, capillary filtration coefficient (Kfc), and lung weight. In the gradual-injury model, only lung weight and Kfc increased. Pretreatment with inhaled NO (90–120 ppm) prevented the rise in Ppa and precapillary pulmonary vascular resistance in the rapid-injury model and prevented elevation of Kfc in the gradual-injury model. Pretreatment with an inhibitor of endogenous NO synthase (NG-nitro-L-arginine methyl ester) resulted in increased pulmonary capillary pressure and postcapillary pulmonary vascular resistance in the rapid-injury model and increased peak Ppa, pulmonary capillary pressure, and pulmonary vascular resistance in the gradual-injury model. These data suggest that in oxidant-induced acute lung injury 1) inhaled NO may attenuate increases in capillary permeability and 2) endogenous NO may function as a modulator of pulmonary vascular tone without affecting capillary permeability.

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INTERRELATIONSHIPS AMONG PULMONARY “CAPILLARY” PRESSURE, BLOOD FLOW AND VALVE SIZE IN MITRAL STENOSIS. THE LIMITED REGULATORY EFFECTS OF THE PULMONARY VASCULAR RESISTANCE 1

Journal of Clinical Investigation ◽

10.1172/jci102703 ◽

1952 ◽

Vol 31 (12) ◽

pp. 1082-1088 ◽

Cited By ~ 40

Author(s):

Jorge Araujo ◽

Daniel S. Lukas

Keyword(s):

Blood Flow ◽

Capillary Pressure ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Mitral Stenosis ◽

Pulmonary Capillary ◽

Valve Size ◽

Pulmonary Capillary Pressure ◽

Regulatory Effects

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The Effect of Positive end Expiratory pressure on the Pulmonary Capillary Pressure in Acute Lung Injury Patients

Tuberculosis and Respiratory Diseases ◽

10.4046/trd.2000.49.5.594 ◽

2000 ◽

Vol 49 (5) ◽

pp. 594

Author(s):

Byung Chun Chung ◽

Chang Gyoo Byun ◽

Chang Youl Lee ◽

Hyung Jung Kim ◽

Chul Min An ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Capillary Pressure ◽

Positive End Expiratory Pressure ◽

Pulmonary Capillary ◽

Pulmonary Capillary Pressure

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Pulmonary capillary pressure during acute lung injury in dogs

Critical Care Medicine ◽

10.1097/00003246-200202000-00023 ◽

2002 ◽

Vol 30 (2) ◽

pp. 403-409 ◽

Cited By ~ 10

Author(s):

Andrew A. Pellett ◽

Kevin C. Lord ◽

Michael S. Champagne ◽

Bennett P. deBoisblanc ◽

Royce W. Johnson ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Capillary Pressure ◽

Pulmonary Capillary ◽

Pulmonary Capillary Pressure

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Pulmonary capillary pressure in intact dog lungs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.235.5.h569 ◽

1978 ◽

Vol 235 (5) ◽

pp. H569-H573

Author(s):

J. C. Gabel ◽

R. E. Drake

Keyword(s):

Capillary Pressure ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Pressure Range ◽

Gravimetric Method ◽

Average Value ◽

Pulmonary Capillary ◽

Pulmonary Capillary Pressure

We used a gravimetric method to determine the ratio (gamma) of pulmonary venous to total pulmonary vascular resistance in intact dog lungs. From this ratio, pulmonary capillary pressure (Pc) can be calculated. The average value of gamma was 0.50 +/- 0.06 (mean +/- SD) in 10 dogs. We found no correlation between gamma and PO2, PCO2, pH, or hematocrit in the narrow ranges of these experiments. Over the capillary pressure range of 22.4--35.2 mmHg we found no correlation between gamma and Pc. The value of gamma found in this study is not significantly different from the value found in isolated perfused lungs.

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Unintended Inhalation of Nitric Oxide by Contamination of Compressed Air

Anesthesiology ◽

10.1097/00000542-199910000-00013 ◽

1999 ◽

Vol 91 (4) ◽

pp. 945-945 ◽

Cited By ~ 9

Author(s):

Albert Benzing ◽

Torsten Loop ◽

Georg Mols ◽

Klaus Geiger

Keyword(s):

Nitric Oxide ◽

Acute Respiratory Distress Syndrome ◽

Acute Lung Injury ◽

Lung Injury ◽

Pulmonary Vascular Resistance ◽

Oxygen Tension ◽

Vascular Resistance ◽

Arterial Oxygen Tension ◽

Compressed Air ◽

Arterial Oxygen

Background Compressed air from a hospital's central gas supply may contain nitric oxide as a result of air pollution. Inhaled nitric oxide may increase arterial oxygen tension and decrease pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. Therefore, the authors wanted to determine whether unintentional nitric oxide inhalation by contamination of compressed air influences arterial oxygen tension and pulmonary vascular resistance and interferes with the therapeutic use of nitric oxide. Methods Nitric oxide concentrations in the compressed air of a university hospital were measured continuously by chemiluminescence during two periods (4 and 2 weeks). The effects of unintended nitric oxide inhalation on arterial oxygen tension (n = 15) and on pulmonary vascular resistance (n = 9) were measured in patients with acute lung injury and acute respiratory distress syndrome by changing the source of compressed air of the ventilator from the hospital's central gas supply to a nitric oxide-free gas tank containing compressed air. In five of these patients, the effects of an additional inhalation of 5 ppm nitric oxide were evaluated. Results During working days, compressed air of the hospital's central gas supply contained clinically effective nitric oxide concentrations (> 80 parts per billion) during 40% of the time. Change to gas tank-supplied nitric oxide-free compressed air decreased the arterial oxygen tension by 10% and increased pulmonary vascular resistance by 13%. The addition of 5 ppm nitric oxide had a minimal effect on arterial oxygen tension and pulmonary vascular resistance when added to hospital-supplied compressed air but improved both when added to tank-supplied compressed air. Conclusions Unintended inhalation of nitric oxide increases arterial oxygen tension and decreases pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. The unintended nitric oxide inhalation interferes with the therapeutic use of nitric oxide.

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