scholarly journals The role of pulmonary capillary pressure in the oxygen free radical- induced acute lung injury.

1992 ◽  
Vol 39 (6) ◽  
pp. 474-483
Author(s):  
Chul Gyu Yoo ◽  
Young Whan Kim ◽  
Sung Koo Han ◽  
Young Soo Shim ◽  
Keun Youl Kim ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Free Radical ◽  
Lung Injury ◽  
Capillary Pressure ◽  
Oxygen Free Radical ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure

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

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

Pulmonary capillary pressure during acute lung injury in dogs

2002 ◽  
Vol 30 (2) ◽  
pp. 403-409 ◽  
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

Inhaled Nitric Oxide Reduces Pulmonary Transvascular Albumin Flux in Patients with Acute Lung Injury

1995 ◽  
Vol 83 (6) ◽  
pp. 1153-1161 ◽  
Author(s):  
A. Benzing ◽  
P. Brautigam ◽  
K. Geiger ◽  
T. Loop ◽  
U. Beyer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Capillary Pressure ◽  
Microvascular Permeability ◽  
Inhaled Nitric Oxide ◽  
Fluid Filtration ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure

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.

scholarly journals The role of reactive oxygen free radical in the pathogenetic mechan- ism of endotoxin-induced acute lung injury in domestic pigs.

1991 ◽  
Vol 38 (4) ◽  
pp. 357-371
Author(s):  
Young Whan Kim ◽  
Chul Gyu Yoo ◽  
Ki Ho Jeong ◽  
Hyung Seok Choi ◽  
Hyuk Pyo Lee ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Free Radical ◽  
Lung Injury ◽  
Reactive Oxygen ◽  
Oxygen Free Radical ◽  
Domestic Pigs

scholarly journals Oxygen free radical involvement in acute lung injury induced by H5N1 virus in mice

2013 ◽  
Vol 7 (6) ◽  
pp. 945-953 ◽  
Author(s):  
Guimei He ◽  
Changgui Dong ◽  
Zhihua Luan ◽  
Bronwyn M. McAllan ◽  
Tong Xu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Free Radical ◽  
Lung Injury ◽  
H5n1 Virus ◽  
Oxygen Free Radical

Pulmonary vasoreactivity to serotonin during hypoxia is modulated by ATP-sensitive potassium channels

1997 ◽  
Vol 83 (2) ◽  
pp. 569-574 ◽  
Author(s):  
Scott A. Barman
Keyword(s):  
Potassium Channels ◽  
Capillary Pressure ◽  
Pressor Response ◽  
Vascular Occlusion ◽  
Large Vessel ◽  
Channel Modulation ◽  
Hypoxic Conditions ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure

Barman, Scott A. Pulmonary vasoreactivity to serotonin during hypoxia is modulated by ATP-sensitive potassium channels. J. Appl. Physiol. 83(2): 569–574, 1997.—The role of ATP-sensitive K+-channel modulation in the canine pulmonary vascular response to serotonin during hypoxia was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured by using vascular occlusion techniques. Under normoxia, serotonin (10−5 M) significantly increased precapillary and postcapillary resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. During hypoxia, the effect of serotonin was potentiated on both precapillary and postcapillary resistance and capillary pressure, as well as on microvascular compliance and large-vessel compliance. Under normoxia, the ATP-sensitive K+-channel opener cromakalim (10−5 M) inhibited the serotonergic response on postcapillary resistance and microvascular compliance, whereas during hypoxia cromakalim inhibited the potentiated effect of serotonin on both precapillary and postcapillary resistance, capillary pressure, and both microvascular and large-vessel compliances. These results indicate that canine pulmonary vasoreactivity to serotonin is heightened under hypoxic conditions and that ATP-sensitive K+ channels modulate the pressor response to serotonin, an effect that is more pronounced during hypoxia.

Contributions of vascular flow and pulmonary capillary pressure to ventilator-induced lung injury

2006 ◽  
Vol 34 (4) ◽  
pp. 1106-1112 ◽  
Author(s):  
Josefina López-Aguilar ◽  
Enrique Piacentini ◽  
Ana Villagrá ◽  
Gastón Murias ◽  
Sara Pascotto ◽  
...  
Keyword(s):  
Lung Injury ◽  
Capillary Pressure ◽  
Ventilator Induced Lung Injury ◽  
Vascular Flow ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure

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

1994 ◽  
Vol 76 (3) ◽  
pp. 1324-1329 ◽  
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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