Inhaled nitric oxide reverses hypoxic pulmonary vasoconstriction without impairing gas exchange

1993 ◽  
Vol 74 (3) ◽  
pp. 1287-1292 ◽  
Author(s):  
U. Pison ◽  
F. A. Lopez ◽  
C. F. Heidelmeyer ◽  
R. Rossaint ◽  
K. J. Falke
Keyword(s):  
Nitric Oxide ◽  
Gas Exchange ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Pulmonary Gas Exchange ◽  
Blood Gas ◽  
Hemodynamic Effects ◽  
Pulmonary Vasoconstriction ◽  
Inhaled No

Nitric oxide (NO) is an endogenous endothelium-derived relaxing factor that participates in the regulation of vascular tone. We studied the effects of inhaled NO gas on transient hypoxic pulmonary vasoconstriction and normal lungs in mechanically ventilated sheep. We measured hemodynamics and pulmonary gas exchange. For gas exchange measurements we used conventional blood gas analysis and the multiple inert gas elimination technique to estimate ventilation-perfusion heterogeneity. Our hypotheses were 1) inhaled NO reverses hypoxic pulmonary vasoconstriction, 2) the hemodynamic effects of inhaled NO are limited to the pulmonary circulation, and 3) inhaled NO does not impair pulmonary gas exchange and may redistribute blood flow to better ventilated areas of the lungs. Hypoxic pulmonary vasoconstriction was induced by using a hypoxic inspiratory gas mixture. The addition of 20 ppm NO to the hypoxic inspiratory gases returned pulmonary arterial pressure to baseline values. Systemic hemodynamics and gas exchange indexes derived from conventional blood gas analysis remained constant. Gas exchange indexes for ventilation-perfusion ratios and gas dispersions improved. The addition of 20 ppm NO to medical air (21% O2) had no such significant effects on hemodynamics or pulmonary gas exchange. Our findings show that inhaled NO reverses transient hypoxic pulmonary vasoconstriction. The hemodynamic effects of NO are limited to the pulmonary circulation; it does not impair pulmonary gas exchange. Moreover, it redistributes blood flow to better ventilated alveoli. As such, NO has potential in the treatment of lung diseases associated with pulmonary hypertension.

Effect of anemia on intrapulmonary shunt during atelectasis in rabbits

1995 ◽  
Vol 79 (6) ◽  
pp. 1951-1957 ◽  
Author(s):  
S. Deem ◽  
M. J. Bishop ◽  
M. K. Alberts
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Left Lung ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Blood Gas ◽  
Intrapulmonary Shunt ◽  
Fluorescent Microspheres ◽  
Pulmonary Vasoconstriction ◽  
Arterial Po2 ◽  
Over Time

To elucidate the effects of anemia on intrapulmonary shunt, we studied a model of left lung atelectasis in anesthetized rabbits. In 10 rabbits, isovolemic anemia was produced by sequential hemodilution. Seven control rabbits were followed over time, without hemodilution. Intrapulmonary shunt (Qs/QT) was measured by using blood gas analysis and by quantitation of the percentage of blood flow to the collapsed left lung (QLl/QT) using fluorescent microspheres. In control rabbits, Qs/QT and QLl/QT decreased over time, whereas arterial PO2 increased. In hemodiluted rabbits, there was a trend toward increased Qs/QT and QLl/QT. There were significant differences in the behavior of Qs/QT, QLl/QT, and arterial PO2 between control and hemodiluted rabbits. Hemodynamic parameters, including cardiac output and pulmonary artery pressure, were not different between groups. In a third group of rabbits with pharmacologically induced acidosis but no hemodilution, Qs/QT and QLl/QT decreased over time, and arterial PO2 increased. We conclude that acute isovolemic anemia has a deleterious effect on pulmonary gas exchange, possibly through attenuation of hypoxic pulmonary vasoconstriction.

Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange

1996 ◽  
Vol 81 (4) ◽  
pp. 1535-1543 ◽  
Author(s):  
Serge Brimioulle ◽  
Philippe Lejeune ◽  
Robert Naeije
Keyword(s):  
Gas Exchange ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Gas Exchange ◽  
Lung Model ◽  
Arterial Oxygenation ◽  
Blood Gas ◽  
Stimulus Response ◽  
Pulmonary Vasoconstriction ◽  
Lung Compartment ◽  
Mixed Venous

Brimioulle, Serge, Philippe Lejeune, and Robert Naeije.Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange. J. Appl. Physiol. 81(4): 1535–1543, 1996.—Several reports have suggested that hypoxic pulmonary vasoconstriction (HPV) might result in deterioration of pulmonary gas exchange in severe hypoxia. We therefore investigated the effects of HPV on gas exchange in normal and diseased lungs. We incorporated a biphasic HPV stimulus-response curve observed in intact dogs (S. Brimioulle, P. Lejeune, J. L. Vachièry, M. Delcroix, R. Hallemans, and R. Naeije, J. Appl. Physiol. 77: 476–480, 1994) into a 50-compartment lung model (J. B. West, Respir. Physiol. 7: 88–110, 1969) to control the amount of blood flow directed to each lung compartment according to the local hypoxic stimulus. The resulting model accurately reproduced the blood gas modifications caused by HPV changes in dogs with acute lung injury. In single lung units, HPV had a moderate protective effect on alveolar oxygenation, which was maximal at near-normal alveolar[Formula: see text] (75–80 Torr), mixed venous[Formula: see text] (35 Torr), and[Formula: see text] at which hemoglobin is 50% saturated (24 Torr). In simulated diseased lungs associated with 40–60 Torr arterial [Formula: see text], however, HPV increased arterial [Formula: see text]by 15–20 Torr. We conclude that HPV can improve arterial oxygenation substantially in respiratory failure.

Improvement in Oxygenation by Phenylephrine and Nitric Oxide in Patients with Adult Respiratory Distress Syndrome 

1997 ◽  
Vol 87 (1) ◽  
pp. 18-25 ◽  
Author(s):  
Elana B. Doering ◽  
C. William Hanson ◽  
Daniel J. Reily ◽  
Carol Marshall ◽  
Bryan E. Marshall
Keyword(s):  
Nitric Oxide ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Adult Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Random Order ◽  
Pulmonary Vasoconstriction ◽  
Arterial Blood ◽  
Inhaled No

Background Inhaled nitric oxide (NO), a selective vasodilator, improves oxygenation in many patients with adult respiratory distress syndrome (ARDS). Vasoconstrictors may also improve oxygenation, possibly by enhancing hypoxic pulmonary vasoconstriction. This study compared the effects of phenylephrine, NO, and their combination in patients with ARDS. Methods Twelve patients with ARDS (PaO2/FIO2 <le> 180; Murray score <me> 2) were studied. Each patient received three treatments in random order: intravenous phenylephrine, 50-200 micrograms/min, titrated to a 20% increase in mean arterial blood pressure; inhaled NO, 40 ppm; and the combination (phenylephrine+NO). Hemodynamics and blood gas measurements were made during each treatment and at pre- and posttreatment baselines. Results All three treatments improved PaO2 overall. Six patients were "phenylephrine-responders" (delta PaO2 > 10 mmHg), and six were "phenylephrine-nonresponders." In phenylephrine-responders, the effect of phenylephrine was comparable with that of NO (PaO2 from 105 +/- 14 to 132 +/- 14 mmHg with phenylephrine, and from 110 +/- 14 to 143 +/- 19 mmHg with NO), and the effect of phenylephrine+NO was greater than that of either treatment alone (PaO2 from 123 +/- 13 to 178 +/- 23 mmHg). In phenylephrine-nonresponders, phenylephrine did not affect PaO2, and the effect of phenylephrine+NO was not statistically different from that of NO alone (PaO2 from 82 +/- 12 to 138 +/- 28 mmHg with NO; from 84 +/- 12 to 127 +/- 23 mmHg with phenylephrine+NO). Data are mean +/- SEM. Conclusions Phenylephrine alone can improve PaO2 in patients with ARDS. In phenylephrine-responsive patients, phenylephrine augments the improvement in PaO2 seen with inhaled NO. These results may reflect selective enhancement of hypoxic pulmonary vasoconstriction by phenylephrine, which complements selective vasodilation by NO.

Influence of G-suit abdominal bladder inflation on gas exchange during +GZ stress

1985 ◽  
Vol 58 (2) ◽  
pp. 506-513
Author(s):  
H. I. Modell ◽  
P. Beeman ◽  
J. Mendenhall
Keyword(s):  
Gas Exchange ◽  
Time Course ◽  
Venous Blood ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Mixed Venous Blood ◽  
Blood Gas ◽  
Series Of Experiments ◽  
Spontaneously Breathing ◽  
Arterial Po2

Available data relating duration of +GZ stress to blood gas exchange status is limited. Furthermore, studies focusing on pulmonary gas exchange during +GZ stress when abdominal restriction is imposed have yielded conflicting results. To examine the time course of blood gas changes occurring during exposure to +GZ stress in dogs and the influence of G-suit abdominal bladder inflation on this time course, seven spontaneously breathing pentobarbital-anesthetized adult mongrel dogs were exposed to 60 s of up to +5 GZ stress with and without G-suit abdominal bladder inflation. Arterial and mixed venous blood were sampled for blood gas analysis during the first and last 20 s of the exposure and at 3 min postexposure. Little change in blood gas status was seen at +3 GZ regardless of G-suit status. However, with G-suit inflation, arterial PO2 fell by a mean of 14.7 Torr during the first 20 s at +4 Gz (P less than 0.01, t test) and 20.6 Torr at +5 GZ (P less than 0.01). It continued to fall an additional 10 Torr during the next 40 s at both +4 and +5 GZ. Arterial PO2 was still 5–10 Torr below control values (P less than 0.05) 3 min postexposure. A second series of experiments paralleling the first focused on blood gas status during repeated exposure to acceleration. Blood gas status was assessed in five dogs during the late 20 s of two 60-s exposures separated by 3 min at 0 GZ. No significant differences between the initial and repeated exposures were detected. The data indicate that G-suit abdominal bladder inflation promotes increased venous admixture.

Nitric oxide inhalation: effects on the ovine neonatal pulmonary and systemic circulations

1996 ◽  
Vol 8 (3) ◽  
pp. 431 ◽  
Author(s):  
V DeMarco ◽  
JW Skimming ◽  
TM Ellis ◽  
S Cassin
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Minimum Concentration ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Inhaled No

Others have shown that inhaled nitric oxide causes reversal of pulmonary hypertension in anaesthetized perinatal sheep. The present study examined haemodynamic responses to inhaled NO in the normal and constricted pulmonary circulation of unanaesthetized newborn lambs. Three experiments were conducted on each of 7 lambs. First, to determine a minimum concentration of NO which could reverse acute pulmonary hypertension caused by infusion of the thromboxame mimic U46619, the haemodynamic effects of 5 different doses of inhaled NO were examined. Second, the effects of inhaling 80 ppm NO during hypoxic pulmonary vasoconstriction were examined. Finally, to determine if tachyphalaxis occurs during NO inhalation, lambs were exposed to 80 ppm NO for 3 h during which time pulmonary arterial pressure was doubled by infusion of U46619. Breathing NO (80 ppm) caused a slight but significant decrease in pulmonary vascular resistance (PVR) in lambs with normal pulmonary arterial pressure (PAP). Nitric oxide, inhaled at concentrations between 10 and 80 ppm for 6 min (F1O2 = 0.60), caused decreases in PVR when PAP was elevated with U46619. Nitric oxide acted selectively on the pulmonary circulation, i.e. no changes occurred in systemic arterial pressure or any other measured variable. Breathing 80 ppm NO for 6 min reversed hypoxic pulmonary vasoconstriction. In the chronic exposure study, inhaling 80 ppm NO for 3 h completely reversed U46619-induced pulmonary hypertension. Although arterial methaemoglobin increased during the 3-h exposure to 80 ppm NO, there was no indication that this concentration of NO impairs oxygen loading. These data demonstrate that NO, at concentrations as low as 10 ppm, is a potent, rapid-action, and selective pulmonary vasodilator in unanaesthetized newborn lambs with elevated pulmonary tone. Furthermore, these data support the use of inhaled NO for treatment of infants with pulmonary hypertension.

Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man

1987 ◽  
Vol 68 (1) ◽  
pp. 11-27 ◽  
Author(s):  
Christian Mélot ◽  
Robert Naeije ◽  
Roger Hallemans ◽  
Philippe Lejeune ◽  
Pierre Mols
Keyword(s):  
Gas Exchange ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Gas Exchange ◽  
Pulmonary Vasoconstriction ◽  
Normal Man

Pulmonary effects of intravenous atropine induce ventilation perfusion mismatch

2014 ◽  
Vol 92 (5) ◽  
pp. 399-404 ◽  
Author(s):  
Romolo J. Gaspari ◽  
David Paydarfar
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Blood Flow ◽  
Gas Analysis ◽  
Pulmonary Gas Exchange ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Anticholinergic Medications ◽  
Arterial Blood ◽  
Intravenous Atropine

Atropine is used for a number of medical conditions, predominantly for its cardiovascular effects. Cholinergic nerves that innervate pulmonary smooth muscle, glands, and vasculature may be affected by anticholinergic medications. We hypothesized that atropine causes alterations in pulmonary gas exchange. We conducted a prospective interventional study with detailed physiologic recordings in anesthetized, spontaneously breathing rats (n = 8). Animals breathing a normoxic gas mixture titrated to a partial arterial pressure of oxygen of 110–120 were exposed to an escalating dose of intravenous atropine (0.001, 0.01, 0.1, 5.0, and 20.0 mg/kg body mass). Arterial blood gas measurements were recorded every 2 min (×5) at baseline, and following each of the 5 doses of atropine. In addition, the animals regional pulmonary blood flow was measured using neutron-activated microspheres. Oxygenation decreased immediately following intravenous administration of atropine, despite a small increase in the volume of inspired air with no change in respiratory rate. Arterial blood gas analysis showed an increase in pulmonary dysfunction, characterized by a widening of the alveolar–arteriole gradient (p < 0.003 all groups except for the lowest dose of atropine). The microsphere data demonstrates an abrupt and marked heterogeneity of pulmonary blood flow following atropine treatment. In conclusion, atropine was found to decrease pulmonary gas exchange in a dose-dependent fashion in this rat model.

Effects of inhaled nitric oxide on pulmonary hemodynamics and gas exchange in an ovine model of ARDS

1994 ◽  
Vol 76 (1) ◽  
pp. 345-355 ◽  
Author(s):  
I. Rovira ◽  
T. Y. Chen ◽  
M. Winkler ◽  
N. Kawai ◽  
K. D. Bloch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Soluble Guanylate Cyclase ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vasodilation ◽  
Pulmonary Vasoconstriction ◽  
Selective Pulmonary Vasodilation

Inhaling low concentrations of nitric oxide (NO) gas causes selective pulmonary vasodilation of ventilated lung regions. NO activates soluble guanylate cyclase, increasing guanosine 3′,5′-cyclic monophosphate (cGMP). Inhibition of NO synthesis enhances hypoxic pulmonary vasoconstriction. Therefore we examined independent and combined effects of NO inhalation and infusion of NG-nitro-L-arginine methyl ester (L-NAME), an NO synthesis inhibitor, on pulmonary vascular pressure-flow relationships, gas exchange, and plasma cGMP levels in anesthetized and mechanically ventilated sheep with acute lung injury induced by bilateral lavage. After lavage, inhaling 60 ppm by volume of NO decreased pulmonary arterial pressure (PAP) and resistance without any systemic hemodynamic effects, increased arterial PO2, and decreased venous admixture (Qva/QT; all P < 0.05) without altering cardiac output (QT), mixed venous PO2, or O2 uptake, major determinants of intrapulmonary shunt. During NO inhalation, PAP-left atrial pressure gradient (PAP-LAP) and Qva/QT were reduced (both P < 0.05) independently of QT, which was varied mechanically. L-NAME infusion produced systemic and pulmonary vasoconstriction and increased PAP-LAP gradient across the entire range of QT, whereas Qva/QT, was not changed. NO inhalation after L-NAME infusion produced pulmonary vasodilation and decreased Qva/QT to the same degree as NO inhalation alone. Five to 10 min after inhalation of 60 ppm NO, before and after L-NAME infusion, arterial plasma cGMP levels were increased by 80% (both P < 0.05). With NO breathing after L-NAME, we measured a consistent transpulmonary cGMP arteriovenous gradient [31 +/- 8 and 33 +/- 7 (SE) pmol/ml at 5 and 10 min, respectively; both P < 0.05]. NO inhalation before or after L-NAME administration in this acute lung injury model reduced Qva/QT, most likely by increasing cGMP concentration in ventilated lung regions and causing selective pulmonary vasodilation.

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