scholarly journals Effect of different doses of inhaled nitric oxide on pulmonary capillary pressure and on longitudinal distribution of pulmonary vascular resistance in ARDS

1998 ◽  
Vol 80 (4) ◽  
pp. 440-446 ◽  
Author(s):  
A Benzing ◽  
G Mols ◽  
J Guttmann ◽  
H Kaltofen ◽  
K Geiger
Keyword(s):  
Nitric Oxide ◽  
Capillary Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Inhaled Nitric Oxide ◽  
Longitudinal Distribution ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure ◽  
Different Doses

Pulmonary capillary pressure in intact dog lungs

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.

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 Impact of inhaled nitric oxide on pulmonary capillary pressure in ARDS patients

Critical Care ◽  
10.1186/cc419 ◽  
1999 ◽  
Vol 3 (Suppl 1) ◽  
pp. P044
Author(s):  
V Sramek ◽  
R Rokyta ◽  
I Novak ◽  
M Nalos ◽  
P Hora ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Capillary Pressure ◽  
Inhaled Nitric Oxide ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure

Inhaled nitric oxide does not alter the longitudinal distribution of pulmonary vascular resistance

1995 ◽  
Vol 78 (1) ◽  
pp. 341-348 ◽  
Author(s):  
D. M. Lindeborg ◽  
B. P. Kavanagh ◽  
K. Van Meurs ◽  
R. G. Pearl
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Dose Range ◽  
Venous Occlusion ◽  
Inhaled Nitric Oxide ◽  
Longitudinal Distribution ◽  
Perfused Lung ◽  
Inhaled No

Because the effects of inhaled nitric oxide (NO) may be localized to its site of delivery, we studied the effects of inhaled NO on the longitudinal distribution of pulmonary vascular resistance during pulmonary hypertension in perfused rabbit lungs. Before NO administration, pulmonary hypertension was produced by infusion of the thromboxane A2 mimetic U-46619 in all lungs. Pulmonary vascular resistance was divided into arterial, microvascular, and venous components by arterial and venous occlusion techniques. In the buffer-perfused lung, all doses of inhaled NO (5, 20, and 80 ppm) produced small decreases (approximately 3 mmHg) in pulmonary arterial pressure (Ppa), with equivalent proportional reductions in all segmental vascular resistances. Similar results were obtained after an extended inhaled NO dose range of 20, 80, and 240 ppm. In the buffer-perfused lung, inhibition of endogenous NO synthesis with NG-nitro-L-arginine methyl ester (L-NAME) potentiated the effects of U-46619. Subsequent inhaled NO administration produced larger decreases (approximately 7 mmHg) in Ppa with equivalent proportional reductions in all segmental vascular resistances. In the blood-perfused lung, L-NAME did not alter baseline pulmonary pressures. Administration of inhaled NO during U-46619-induced pulmonary hypertension produced dose-related decreases in Ppa. The highest dose (80 ppm) of inhaled NO decreased Ppa by 3.5 mmHg, with equivalent proportional reductions in all segmental vascular resistances.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Inhaled Nitric Oxide at Birth Reduces Pulmonary Vascular Resistance and Improves Oxygenation in Preterm Lambs

Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 378
Author(s):  
Satyan Lakshminrusimha ◽  
Sylvia F. Gugino ◽  
Krishnamurthy Sekar ◽  
Stephen Wedgwood ◽  
Carmon Koenigsknecht ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Preterm Infants ◽  
Vascular Resistance ◽  
Inhaled Nitric Oxide ◽  
Persistent Pulmonary Hypertension ◽  
Inhaled No ◽  
Birth Preterm

Resuscitation with 21% O2 may not achieve target oxygenation in preterm infants and in neonates with persistent pulmonary hypertension of the newborn (PPHN). Inhaled nitric oxide (iNO) at birth can reduce pulmonary vascular resistance (PVR) and improve PaO2. We studied the effect of iNO on oxygenation and changes in PVR in preterm lambs with and without PPHN during resuscitation and stabilization at birth. Preterm lambs with and without PPHN (induced by antenatal ductal ligation) were delivered at 134 d gestation (term is 147–150 d). Lambs without PPHN were ventilated with 21% O2, titrated O2 to maintain target oxygenation or 21% O2 + iNO (20 ppm) at birth for 30 min. Preterm lambs with PPHN were ventilated with 50% O2, titrated O2 or 50% O2 + iNO. Resuscitation with 21% O2 in preterm lambs and 50%O2 in PPHN lambs did not achieve target oxygenation. Inhaled NO significantly decreased PVR in all lambs and increased PaO2 in preterm lambs ventilated with 21% O2 similar to that achieved by titrated O2 (41 ± 9% at 30 min). Inhaled NO increased PaO2 to 45 ± 13, 45 ± 20 and 76 ± 11 mmHg with 50% O2, titrated O2 up to 100% and 50% O2 + iNO, respectively, in PPHN lambs. We concluded that iNO at birth reduces PVR and FiO2 required to achieve target PaO2.

scholarly journals Inhaled nitric oxide in patients with normal and increased pulmonary vascular resistance after cardiac surgery

1994 ◽  
Vol 72 (2) ◽  
pp. 185-189 ◽  
Author(s):  
D.J. SNOW ◽  
S.Y. GRAY ◽  
S. GHOSH ◽  
L. FOUBERT ◽  
A. ODURO ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Surgery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Inhaled Nitric Oxide

Phasic capillary pressure determined by arterial occlusion in intact dog lung lobes

1989 ◽  
Vol 67 (6) ◽  
pp. 2205-2211 ◽  
Author(s):  
Y. Yamada ◽  
M. Suzukawa ◽  
M. Chinzei ◽  
T. Chinzei ◽  
N. Kawahara ◽  
...  
Keyword(s):  
Capillary Pressure ◽  
Vascular Resistance ◽  
Control Period ◽  
Arterial Occlusion ◽  
Lung Lobe ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure ◽  
Lower Lung ◽  
Pulmonary Arterial ◽  
Electrocardiogram Ecg

In six open-chest dogs, electrocardiogram- (ECG) controlled pulmonary arterial occlusion was performed during the control period and during the infusions of serotonin and histamine. A temporal series of instantaneous pulmonary capillary pressure and the longitudinal distributions of vascular resistance and compliance were evaluated in the intact left lower lung lobe. In the control period, we found a significant phasic variation of pulmonary capillary pressure (Pc) with the cardiac cycle. The ratio of arterial to venous resistances (Ra/Rv) was 6:4, and the ratio of arterial to capillary compliances (Ca/Cc) was 1:11. During the infusions of serotonin and histamine, Pc showed similar phasic variations, despite significant hemodynamic changes induced by these agents. Serotonin predominantly increased Ra, whereas histamine predominantly increased Rv. The ratio of Rv to the total resistance decreased significantly from 0.42 to 0.32 during the infusion of serotonin and increased significantly to 0.62 during the infusion of histamine. The data suggest that phasic Pc determined by ECG-controlled arterial occlusion reflects the pulsatility in the pulmonary microvascular bed under control conditions and after alterations of the pulmonary vascular resistance by serotonin and histamine.

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