The Effects of Localized Hypoventilation on Ventilation/Perfusion Ratios and Gas Exchange in the Dog Lung

1982 ◽  
Vol 63 (6) ◽  
pp. 497-503 ◽  
Author(s):  
A. J. Suggett ◽  
Gwenda R. Barer ◽  
F. H. Mohammed ◽  
G. W. Gill
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Artery ◽  
Oxygen Uptake ◽  
Pulmonary Artery Pressure ◽  
Dead Space ◽  
Respiratory Exchange Ratio ◽  
Plateau Phase ◽  
Flow Reduction ◽  
Co2 Output

1. Hypoventilation of one lobe of lung was studied in open-chest anaesthetized dogs. Lobar blood flow, pulmonary-artery pressure and gas exchange were measured, the latter from breath-by-breath analysis with a mass spectrometer. 2. Hypoventilation of the lobe by reducing the respiratory pump stroke led, at each step, to a reduction in blood flow to that lobe. The flow () reduction was variable, but always less than the ventilation () reduction, so that the ratio to the lobe was reduced. O2 tension and pH fell and CO2 tension rose in effluent blood. Thus regulation achieved by flow reduction varied between individuals and was of low gain. 3. Anatomical or series dead space (VD series) was reduced in proportion to ventilation. When VD series was less than the apparatus dead space, some gas exchange still took place. 4. Oxygen uptake () and CO2 output () were reduced during hypoventilation. fell more than , so that the respiratory exchange ratio (R) was reduced. 5. Whether the deterioration in gas tensions in effluent blood during hypoventilation of the lobe was due to shunt of blood past unventilated alveoli, or to mismatching, was not resolved. 6. The plateau phase of the CO2-output curves at low tidal volumes was usually regular; thus either hypoventilation was uniform, or some ventilation units were totally closed.

Unilateral hypoventilation produced in dogs by occluding one pulmonary artery

1961 ◽  
Vol 16 (1) ◽  
pp. 53-60 ◽  
Author(s):  
John W. Severinghaus ◽  
Edward W. Swenson ◽  
Theodore N. Finley ◽  
Michael T. Lategola ◽  
Jack Williams
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Gas Exchange ◽  
Pulmonary Artery ◽  
Dead Space ◽  
Airway Resistance ◽  
Artery Occlusion ◽  
Airway Closure ◽  
Residual Capacity ◽  
Unilateral Pulmonary Artery Occlusion

Temporary unilateral pulmonary artery occlusion resulted within 1 minute in a shift of tidal volume away from unperfused lungs in 14 anesthetized closed-chest dogs. The shift of ventilation was caused by bronchoconstriction following the decrease of CO2 on the occluded side. It was prevented by inhalation into that side of 6% CO2 in air, isoproterenol aerosol or 100% N2, but not by atropine or vagotomy. Airway resistance on the occluded side was doubled, and compliance fell 25%. Functional residual capacity fell variably (0–25%), and anatomic dead space decreased. When blood flow was restored, shunting was detected and ventilation returned slowly with normal inflation or immediately after hyperinflation of that lung. This suggests that terminal and respiratory bronchiolar smooth muscle constriction may lead to airway closure and atelectasis and that the gas exchange of the smooth muscle in smaller airways is carried out by direct diffusion to and from the airway rather than with blood. Submitted on June 9, 1960

Effects of changes in topographical distribution of lung blood flow on gas exchange

1965 ◽  
Vol 20 (5) ◽  
pp. 825-835 ◽  
Author(s):  
John B. West ◽  
Norman L. Jones
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Dead Space ◽  
Venous Blood ◽  
Uneven Distribution ◽  
Positive Pressure ◽  
Venous Admixture ◽  
Alveolar Dead Space ◽  
Artery Pressure

The left lung of a dog was suspended in a Lucite box, ventilated with negative pressure, and perfused with venous blood from another dog at 37 C. By varying the pulmonary artery pressure, it was possible to perfuse all the lung or leave increasing proportions of the upper and middle lobes unperfused. The mean Pco2 difference between end-tidal gas and pulmonary venous blood was 1.7 mm Hg (se mean 0.6) when all the lung was perfused, but steadily increased up to 17 mm Hg as more and more of the lung was unperfused. Alveolar dead space/alveolar tidal volume increased linearly with the proportion of lung unperfused. By contrast, the venous admixture component remained small as increasing amounts of lung were unperfused. The results were compared with calculations made on a theoretical model of the lung and it was concluded that the uneven distribution of blood flow caused by hydrostatic pressure differences down the lung may seriously interfere with CO2 exchange when the pulmonary artery pressure is low, but that this type of uneven distribution affects O2 exchange much less. isolated lung; hydrostatic effect; alveolar-arterial differences; physiologic dead space; alveolar dead space; shunt effect; venous admixture; increased acceleration; hypoxemia; hemorrhage; positive-pressure breathing Submitted on September 10, 1964

scholarly journals Progressive dysfunction of nitric oxide synthase in a lamb model of chronically increased pulmonary blood flow: a role for oxidative stress

2008 ◽  
Vol 295 (5) ◽  
pp. L756-L766 ◽  
Author(s):  
Peter E. Oishi ◽  
Dean A. Wiseman ◽  
Shruti Sharma ◽  
Sanjiv Kumar ◽  
Yali Hou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Lung Tissue ◽  
Pulmonary Blood Flow ◽  
Artery Pressure ◽  
Oxide Synthase ◽  
Inhaled No

Cardiac defects associated with increased pulmonary blood flow result in pulmonary vascular dysfunction that may relate to a decrease in bioavailable nitric oxide (NO). An 8-mm graft (shunt) was placed between the aorta and pulmonary artery in 30 late gestation fetal lambs; 27 fetal lambs underwent a sham procedure. Hemodynamic responses to ACh (1 μg/kg) and inhaled NO (40 ppm) were assessed at 2, 4, and 8 wk of age. Lung tissue nitric oxide synthase (NOS) activity, endothelial NOS (eNOS), neuronal NOS (nNOS), inducible NOS (iNOS), and heat shock protein 90 (HSP90), lung tissue and plasma nitrate and nitrite (NOx), and lung tissue superoxide anion and nitrated eNOS levels were determined. In shunted lambs, ACh decreased pulmonary artery pressure at 2 wk ( P < 0.05) but not at 4 and 8 wk. Inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). In control lambs, ACh and inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). Total NOS activity did not change from 2 to 8 wk in control lambs but increased in shunted lambs (ANOVA, P < 0.05). Conversely, NOxlevels relative to NOS activity were lower in shunted lambs than controls at 4 and 8 wk ( P < 0.05). eNOS protein levels were greater in shunted lambs than controls at 4 wk of age ( P < 0.05). Superoxide levels increased from 2 to 8 wk in control and shunted lambs (ANOVA, P < 0.05) and were greater in shunted lambs than controls at all ages ( P < 0.05). Nitrated eNOS levels were greater in shunted lambs than controls at each age ( P < 0.05). We conclude that increased pulmonary blood flow results in progressive impairment of basal and agonist-induced NOS function, in part secondary to oxidative stress that decreases bioavailable NO.

Unilateral lung edema: effects on pulmonary gas exchange, hemodynamics, and pulmonary perfusion distribution

2000 ◽  
Vol 89 (4) ◽  
pp. 1513-1521 ◽  
Author(s):  
Klaus Slama ◽  
Mareike Gesch ◽  
Johannes C. Böck ◽  
Sylvia M. Pietschmann ◽  
Walter Schaffartzik ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Artery ◽  
Venous Pressure ◽  
Pulmonary Gas Exchange ◽  
The Other ◽  
Lung Edema ◽  
Pulmonary Perfusion ◽  
Central Venous ◽  
Fluorescent Microspheres

Two types of unilateral lung edema in sheep were characterized regarding their effects on pulmonary gas exchange, hemodynamics, and distribution of pulmonary perfusion. One edema type was induced with aerosolized HCl (0.15 M, pH 1.0) and the other with NaCl (0.15 M, pH 7.4). Both aerosols were nebulized continuously for 4 h into left lungs. In HCl-treated animals, pulmonary gas exchange deteriorated [from a partial arterial O2 pressure-to-inspired O2 fraction ratio (PaO2 /Fi O2 ) of 254 at baseline to 187 after 4 h HCl]. In addition, pulmonary artery pressure and total pulmonary vascular resistance increased (from 16 to 19 mmHg and from 133 to 154 dyn · s · cm−5, respectively). In NaCl-treated animals, only the central venous pressure significantly increased (from 7 to 9 mmHg). Distribution of pulmonary perfusion (measured with fluorescent microspheres) changed differently in both groups. After HCl application, 6% more blood flow was directed to the treated lung, whereas, after NaCl, 5% more blood flow was directed to the untreated lung. HCl and NaCl treatment both induce an equivalent lung edema, but only HCl treatment is associated with gas exchange alteration and tissue damage. Redistribution of pulmonary perfusion maintains gas exchange during NaCl treatment and decreases it during HCl inhalation.

Impaired pulmonary gas exchange efficiency, but normal pulmonary artery pressure increases, with hypoxia in men and women with a patent foramen ovale

2020 ◽  
Vol 105 (9) ◽  
pp. 1648-1659
Author(s):  
Joseph W. Duke ◽  
Kara M. Beasley ◽  
Julia P. Speros ◽  
Jonathan E. Elliott ◽  
Steven S. Laurie ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Patent Foramen Ovale ◽  
Pulmonary Gas Exchange ◽  
Foramen Ovale ◽  
Men And Women ◽  
Artery Pressure

Physiological alterations in increased pulmonary blood flow with and without pulmonary hypertension

1961 ◽  
Vol 16 (2) ◽  
pp. 305-308 ◽  
Author(s):  
Lois T. Ellison ◽  
David P. Hall ◽  
Thomas Yeh ◽  
H. Mobarhan ◽  
Joseph Rossi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Function ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Artery Hypertension ◽  
Systolic Pulmonary Artery Pressure ◽  
Venous Admixture ◽  
Artery Pressure ◽  
Physiological Alterations

Alterations in pulmonary function and in hemodynamics were studied in dogs with high pulmonary blood flow resulting from systemic pulmonary artery shunts. In order to facilitate elevation in pulmonary artery pressure, the vascular bed was reduced in some cases by obstructing branches of the pulmonary artery with Teflon clips or by lobectomy. Results in 30 control dogs and in 30 animals that survived 5–36 months (average 16) following creation of shunts indicated that pulmonary function was not significantly altered by increased pulmonary blood flow until pulmonary artery hypertension developed. When systolic pulmonary artery pressure exceeded 40 mm Hg, there was a decrease in arterial Po2, an increase in venous admixture percentage of cardiac output, and an increase in the A-a O2 difference during three levels of O2 breathing, indicating both abnormal venous admixture and abnormal diffusion. Possible explanations for these findings are presented. Evidence in one dog suggests that these alterations are reversible. Submitted on August 10, 1960

scholarly journals Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

1971 ◽  
Vol 50 (4) ◽  
pp. 827-837 ◽  
Author(s):  
Richard S. Kronenberg ◽  
Peter Safar ◽  
Joseph Lee ◽  
Fred Wright ◽  
William Noble ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Artery Pressure ◽  
Alveolar Gas Exchange

Pressure-Flow Relationships in the Dog Lung During Acute, Subtotal Pulmonary Vascular Occlusion

1958 ◽  
Vol 192 (3) ◽  
pp. 613-619 ◽  
Author(s):  
Michael T. Lategola
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Vascular Occlusion ◽  
Percentage Change ◽  
Artery Pressure ◽  
Vascular Bed ◽  
Change In Mean ◽  
Pulmonary Vascular Bed

The relationship of pulmonary artery pressure to pulmonary blood flow was studied in the dog by means of occlusive shifting of blood flow within the pulmonary vascular bed. All experiments were performed using the closed-chest preparation. The range of blood flow increases studied was 25–388%. A graphical plot of the percentage change in blood flow versus the percentage change in mean pulmonary artery pressure is presented. A visually estimated curve of this latter data is presented, discussed and compared to four other curves from previous pulmonary vascular studies. A comparison of these curves suggests that the relative maximum capacity of the pulmonary vascular bed of man and dog are similar. These curves plus certain assumptions allow the speculative delineation of a graphical area representing the ‘active’ vasomotor component of exercise at different levels of pulmonary blood flow increase.

Abstract 102: Inhaled Nitric Oxide Mitigates Pulmonary Hypertension and Improves Cerebral Hemodynamics During Prolonged Cardiopulmonary Pesuscitation in a Swine Model of Pediatric Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Constantine D Mavroudis ◽  
Ryan W Morgan ◽  
Tiffany S Ko ◽  
Marco M Hefti ◽  
William P Landis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Systemic Hemodynamics ◽  
Swine Model ◽  
Pulmonary Vasodilation

Introduction: Pulmonary hypertension may play a role in preventing ROSC during prolonged CPR. Targeted pulmonary vasodilation with inhaled nitric oxide (iNO) during CPR may improve pulmonary blood flow and improve outcomes. The purpose of this study was to study the effects of iNO in a randomized, blinded, placebo controlled, pediatric swine model of asphyxial cardiac arrest. Hypothesis: Animals treated with iNO will have lower pulmonary artery pressure, improved systemic hemodynamics, and increased cerebral blood flow during prolonged CPR compared to control. Methods: Four-week-old piglets (n=10) that underwent seven minutes of asphyxia, induction of VF, and 10 minutes of CPR were randomized to either iNO (20 ppm) or placebo in a blinded fashion starting one min into CPR and needed more than 1 defibrillation attempt. Defibrillation was attempted after 10 minutes of CPR. Animals that did not achieve ROSC by 20 minutes were euthanized. Invasive pulmonary and systemic hemodynamics, and both invasive and noninvasive cerebral hemodynamics were continuously measured. Data described as mean ± SD and compared using a generalized estimating equation regression model. Results: All 5 iNO-treated animals and 2/5 placebo-treated animals achieved ROSC. Those treated with iNO had lower mean pulmonary artery pressures (29.5 ± 9.1 vs. 48.3 ± 5.6 mmHg, p=0.04); higher mean aortic pressures (51.9 ± 6.4 vs. 35.5 ± 4.4 mmHg, p=0.01); higher cerebral blood flow (invasive: 230.4 ± 57.4 vs. 28.7 ± 42.1 % baseline, p<0.001; noninvasive: 58.4 ± 10.9 vs. 32.4 ± 8.1 % baseline, p=0.02); and higher cerebral tissue oxygenation (invasive: 33.1 ± 13.0 vs. 1.2 ± 9.8 mmHg, p=0.01; noninvasive: 38.0 ± 4.2 vs. 26.2 ± 3.1%, p=0.005) compared with placebo. Conclusions: Treatment with iNO during prolonged CPR results in lower pulmonary artery pressure, improved systemic hemodynamics, and increased cerebral blood flow and oxygenation. Pulmonary vasodilation may have an important role during prolonged CPR for asphyxial cardiac arrests.

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