Role of collateral ventilation in ventilation-perfusion balance

1984 ◽  
Vol 56 (6) ◽  
pp. 1500-1506 ◽  
Author(s):  
T. Kuriyama ◽  
L. P. Latham ◽  
L. D. Horwitz ◽  
J. T. Reeves ◽  
W. W. Wagner
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Pulmonary Vasoconstriction ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia ◽  
Respiratory Mechanism ◽  
End Tidal ◽  
Arterial Po2 ◽  
Collateral Ventilation

Species with collateral ventilation have an auxiliary respiratory mechanism that could protect them, under certain circumstances, from regional alveolar hypoxia. Species without collateral ventilation may have a greater potential for routinely experiencing regional hypoxia; to maintain ventilation-perfusion balance they would have to rely on pulmonary vasoconstriction. We tested these ideas by ventilating a sublobar region of pig lung (no collateral ventilation) with 13% O2 while the rest of the lung was ventilated with 30% O2. Blood flow, as measured by radioactive microsphere distribution to the sublobar region, was reduced 50% during hypoxia. The hypoxia-induced vasoconstriction effectively defended arterial PO2. When a vasodilator was infused, regional blood flow increased to control levels; shunt fraction rose, and arterial PO2 fell. In dogs (collateral ventilation present) the same experimental maneuvers had no significant effect on regional end-tidal gases or on microsphere distribution, indicating that collateral ventilation was able to maintain ventilation-perfusion balance. When regional hypoxia was created in dogs by overcoming collateral ventilation with slightly positive airway pressure in the sublobar region, the dog acted like the pig and used hypoxic vasoconstriction to shift approximately 30% of the blood flow away from the hypoxic alveoli.

Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs

1995 ◽  
Vol 78 (4) ◽  
pp. 1509-1515 ◽  
Author(s):  
F. Grimminger ◽  
R. Spriestersbach ◽  
N. Weissmann ◽  
D. Walmrath ◽  
W. Seeger
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Sharp Drop ◽  
Pulmonary Vasoconstriction ◽  
Exhaled No ◽  
Pressor Responses ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia

Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs. J. Appl. Physiol. 78(4): 1509–1515, 1995.--We investigated the role of nitric oxide (NO) generation in hypoxic pulmonary vasoconstriction in buffer-perfused rabbit lungs. Exhaled NO was detected by chemiluminescence, and intravascular NO release was quantified as perfusate accumulation of nitrite, peroxynitrite, and nitrate (NOx). Under baseline conditions, exhaled NO was 45.3 +/- 4.1 parts per billion (1.8 +/- 0.2 nmol/min), and lung NOx release into the perfusate was 4.1 +/- 0.4 nmol/min. Alveolar hypoxia (alveolar PO2 of approximately 23 Torr) induced readily reproducible pressor responses preceded by a sharp drop in exhaled NO concentration. In contrast, perfusate NOx accumulation was not affected. Vasoconstrictor responses to U-46619 and angiotensin II were not accompanied by a decrease in NO exhalation. NG-monomethyl-L-arginine dose-dependently suppressed NO exhalation and amplified pressor responses to hypoxia > U-46619 and angiotensin II. In conclusion, portions of baseline NO generation originating from sites with ready access to the gaseous space sharply decrease in response to alveolar hypoxia, whereas the intravascular release of NO is unchanged. Such differential regulation of lung NO synthesis in response to hypoxia may suggest a complex role in the regulation or modulation of hypoxic pulmonary vasoconstriction.

Prostaglandin I2 supports blood flow to hypoxic alveoli in anesthetized dogs

1984 ◽  
Vol 56 (5) ◽  
pp. 1246-1251 ◽  
Author(s):  
R. S. Sprague ◽  
A. H. Stephenson ◽  
A. J. Lonigro
Keyword(s):  
Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Prostaglandin I2 ◽  
Flow Measurements ◽  
Pulmonary Vasoconstriction ◽  
Cyclooxygenase Activity ◽  
Hypoxic Vasoconstriction ◽  
Anesthetized Dogs ◽  
Alveolar Hypoxia ◽  
Mixed Venous

In an animal model of unilateral alveolar hypoxia, inhibition of cyclooxygenase activity, estimates of immunoreactive 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and administration of prostaglandin I2 (PGI2) were used to evaluate the hypothesis that endogenous PGI2 opposes hypoxic pulmonary vasoconstriction, thereby producing redistribution of blood flow to hypoxic alveoli and reductions in systemic PO2. In anesthetized dogs, one lung was ventilated with 100% N2 and the other with 100% O2. Thermal dilution coupled with electromagnetic flow measurements permitted estimates of blood flow to each lung. Indomethacin or meclofenamate reduced flow to the N2-ventilated lungs (P less than 0.05) and increased systemic PO2 (P less than 0.05). Simultaneously, aortic concentrations of immunoreactive 6-keto-PGF1 alpha decreased 63 +/- 8% (P less than 0.001). Following cyclooxygenase inhibition, incremental doses of PGI2 (0.01, 0.025, and 0.10 micrograms X kg-1 X min-1) increased flow to the N2-ventilated lungs and reduced systemic PO2 (P less than 0.001) without affecting mixed venous PO2. These results suggest that systemic PO2 was reduced because of increased venous admixture. We conclude that PGI2 attenuates hypoxic vasoconstriction which allows flow to be maintained to hypoxic alveoli, resulting in reduced systemic PO2.

scholarly journals Regional pulmonary perfusion patterns in humans are not significantly altered by inspiratory hypercapnia

2019 ◽  
Vol 127 (2) ◽  
pp. 365-375
Author(s):  
Amran K. Asadi ◽  
Rui Carlos Sá ◽  
Tatsuya J. Arai ◽  
Rebecca J. Theilmann ◽  
Susan R. Hopkins ◽  
...  
Keyword(s):  
Blood Flow ◽  
Regional Perfusion ◽  
Spatiotemporal Variability ◽  
Pulmonary Perfusion ◽  
Relative Role ◽  
Alveolar Hypoxia ◽  
Dynamic Measures ◽  
End Tidal ◽  
The Right

Pulmonary vascular tone is known to be sensitive to both local alveolar Po2 and Pco2. Although the effects of hypoxia are well studied, the hypercapnic response is relatively less understood. We assessed changes in regional pulmonary blood flow in humans in response to hypercapnia using previously developed MRI techniques. Dynamic measures of blood flow were made in a single slice of the right lung of seven healthy volunteers following a block-stimulus paradigm (baseline, challenge, recovery), with CO2 added to inspired gas during the challenge block to effect a 7-Torr increase in end-tidal CO2. Effects of hypercapnia on blood flow were evaluated based on changes in spatiotemporal variability (fluctuation dispersion, FD) and in regional perfusion patterns in comparison to hypoxic effects previously studied. Hypercapnia increased FD 2.5% from baseline (relative to control), which was not statistically significant ( P = 0.07). Regional perfusion patterns were not significantly changed as a result of increased [Formula: see text] ( P = 0.90). Reanalysis of previously collected data using a similar protocol but with the physiological challenge replaced by decreased [Formula: see text] ([Formula: see text] = 0.125) showed marked flow redistribution ( P = 0.01) with the suggestion of a gravitational pattern, demonstrating hypoxia has the ability to affect regional change with a global stimulus. Taken together, these data indicate that hypercapnia of this magnitude does not lead to appreciable changes in the distribution of pulmonary perfusion, and that this may represent an interesting distinction between the hypoxic and hypercapnic regulatory response. NEW & NOTEWORTHY Although it is well known that the pulmonary circulation responds to local alveolar hypoxia, and that this mechanism may facilitate ventilation-perfusion matching, the relative role of CO2 is not well appreciated. This study demonstrates that an inspiratory hypercapnic stimulus is significantly less effective at inducing changes in pulmonary perfusion patterns than inspiratory hypoxia, suggesting that in these circumstances hypercapnia is not sufficient to induce substantial integrated feedback control of ventilation-perfusion mismatch across the lung.

Cyclic hypoxic pulmonary vasoconstriction induced by concomitant carbon dioxide changes

1976 ◽  
Vol 41 (4) ◽  
pp. 466-469 ◽  
Author(s):  
J. L. Benumof ◽  
J. M. Mathers ◽  
E. A. Wahrenbrock
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lower Lobe ◽  
Co2 Concentration ◽  
Hypoxic Area ◽  
Pulmonary Vasoconstriction ◽  
End Tidal ◽  
End Tidal Co2

We examined the stability of acute lobar hypoxic pulmonary vasoconstriction. In 12 mongrel dogs the left lower lobe (LLL) was selectively ventilated with a constant minute molume with nitrogen and the electromagnetically measured fraction of the cardiac output perfusing the LLL and the LLL end-tidal CO2 concentration were observed for 1 h. We found that both the fraction of the cardiac output perfusing the LLL and the LLL end-tidal CO2 concentration initially decreased during LLL hypoxia and then oxcillated in a progressively damped fashion. When LLL end-tidal CO2 was kept constant by CO2 infusion during LLL hypoxia or when LLL hypoxia was induced by LLL atelectasis, no oscillations were observed. We conclude that if minute ventilation of a hypoxic area of lung is kept constant, then decreased regional blood flow decreases regional alveolar PCO2. As a consequence of these two opposinginfluences, blood flow to an acutely hypoxic area will be oscillatory.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

scholarly journals Perfusion magnetic resonance neuroimaging

2019 ◽  
Author(s):  
Adnan Šehić ◽  
Fuad Julardžija ◽  
Merim Jusufbegović ◽  
Deniz Bulja ◽  
Hadžan Konjo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Magnetic Resonance ◽  
Acute Stroke ◽  
Cerebral Perfusion ◽  
Technology Development ◽  
Regional Blood Flow ◽  
Mr Perfusion ◽  
Endovascular Recanalization

The clinical appliance of perfusion is being continuously developed and it is closely related to technology development. The role of perfusion neuroimaging in the management of acute stroke has been to prove reduced regional blood flow and to give the contribution in the identification of ischemic areas, respectively the regions of hypoperfusion that can be treated by thrombolytic and/or endovascular recanalization therapy. There are two main approaches to the measurement of cerebral perfusion by magnetic resonance. The aim of this article is to compare different measuring approaches of MR perfusion neuroimaging.

Regional distribution of blood flow in awake heat-stressed baboons

1979 ◽  
Vol 237 (6) ◽  
pp. H705-H712 ◽  
Author(s):  
J. R. Hales ◽  
L. B. Rowell ◽  
R. B. King
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Regional Blood Flow ◽  
Regional Distribution ◽  
Renal Vasoconstriction ◽  
Suitable Animal Model ◽  
Mean Pressure ◽  
Subcutaneous Adipose ◽  
Arterial Po2 ◽  
The Brain

Radioactive microspheres (containing six different nuclide labels) were used to measure blood flow (BF) to most major organs of eight conscious baboons during heat stress. Cardiac output (CO), arterial mean pressure, and arterial PO2, PCO2, and pH did not change, but heart rate increased and stroke volume fell as body temperature increased by as much as 2.56 degrees C. Skin BF increased in all regions sampled so that the fraction of CO distributed to skin (not including feet and hands) increased from 3% (control) to 14%. Increased skin BF was compensated for by decreases in splanchnic (intestines, stomach, pancreas, and spleen) (35%), renal (27%), and possibly muscle BF. There was no change in BF to the brain, spinal cord, coronary, or subcutaneous adipose tissue during heating. Therefore, baboons show a generalized redistribution of BF during heat stress, so that increments in skin BF are provided without increases in CO, whereas man depends on changes in both; despite this latter difference between the baboon and man, the similarity in magnitude of the splanchnic and renal vasoconstriction between the two primates may indicate that the baboon would be a suitable animal model for investigations into mechanisms of changes in regional blood flow in man during heat stress.

scholarly journals Evidence for a role of protein kinase C in hypoxic pulmonary vasoconstriction

1999 ◽  
Vol 276 (1) ◽  
pp. L90-L95 ◽  
Author(s):  
Norbert Weissmann ◽  
Robert Voswinckel ◽  
Thorsten Hardebusch ◽  
Simone Rosseau ◽  
Hossein Ardeschir Ghofrani ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Ang Ii ◽  
Pkc Inhibitor ◽  
Pulmonary Vasoconstriction ◽  
Pressor Responses ◽  
Hypoxic Vasoconstriction

Hypoxic pulmonary vasoconstriction (HPV) matches lung perfusion to ventilation, thus optimizing gas exchange. NADPH oxidase-related superoxide anion generation has been suggested as part of the signaling response to hypoxia. Because protein kinase (PK) C activation can occur during hypoxia and PKC activation is known to be critical for NADPH oxidase stimulation in different cell types, we probed the role of PKC in hypoxic vasoconstriction in intact rabbit lungs. Control vasoconstrictor responses were elicited by angiotensin II (ANG II) and the stable thromboxane analog U-46619. Portions of the experiments were performed while NO synthesis and prostanoid generation were blocked with N G-monomethyl-l-arginine and acetylsalicylic acid to avoid confounding effects due to interference with these vasoactive mediators. The PKC inhibitor H-7 (10–50 μM) caused dose-dependent inhibition of HPV, but this agent lacked specificity because ANG II- and U-46619-induced vasoconstrictions were correspondingly suppressed. In contrast, low concentrations of the specific PKC inhibitor bisindolylmaleimide I (BIM; 1–15 μM) strongly inhibited the hypoxic vasoconstriction without any interference with the responses to the pharmacological agents. Superimposable dose-inhibition curves were also obtained for BIM when lung NO synthesis and prostanoid generation were blocked throughout the experiments. Under either condition, BIM did not affect normoxic vascular tone. The PKC activator farnesylthiotriazole (FTT), ascertained to stimulate rabbit NADPH oxidase by provocation of alveolar macrophage superoxide anion generation in vitro, caused rapid-onset, transient pressor responses in normoxic lungs. After FTT, the hypoxic vasoconstrictor response was totally suppressed, in contrast to the largely maintained pressor responses to ANG II and U-46619. The lungs became refractory even to delayed hypoxic challenges after FTT application. In conclusion, these data support the concept that activation of PKC is involved in the transduction pathway forwarding pulmonary vasoconstriction in response to alveolar hypoxia.

Pulmonary hypoxic vasoconstriction: not affected by chemical sympathectomy

1979 ◽  
Vol 46 (3) ◽  
pp. 529-533 ◽  
Author(s):  
C. A. Hales ◽  
D. M. Westphal
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Systemic Blood Pressure ◽  
Lung Perfusion ◽  
Chemical Sympathectomy ◽  
Test Lung ◽  
Systemic Blood ◽  
Pulmonary Vasoconstriction ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia ◽  
6 Hydroxydopamine

The influence of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) on regional alveolar hypoxic vasconstriction and on global hypoxic pulmonary vasoconstriction was investigated. In eight dogs a double-lumened endotracheal tube allowed ventilation of one lung with nitrogen as an alveolar hypoxic challenge while ventilation of the other lung with 100% O2 maintained adequate systemic oxygenation. Distribution of perfusion to the two lungs was determined with 133Xe and external counters. Mean perfusion to the test lung was 50.9 +/- 4.9% of total lung perfusion on room air and decreased by 32.4% (P smaller than 0.01) during alveolar hypoxia. Following 6-OHDA the test lung continued to reduce perfusion during alveolar hypoxia by 27.3%. In five dogs global hypoxia induced a 106% increase in pulmonary vascular resistance (PVR) prior to 6-OHDA and a 90% increase in PVR after 6-OHDA. After 6-OHDA no rise in PRV or systemic blood pressure occurred in response to tyramine, confirming effective sympathectomy by the 6-OHDA. Thus, sympathectomy with 6-OHDA failed to substantially block regional alveolar hypoxic vasoconstriction or global hypoxic pulmonary vasconstriction.

Role of nitric oxide in the regulation of regional blood flow and metabolism in anaesthetized pigs

1998 ◽  
Vol 163 (4) ◽  
pp. 339-348 ◽  
Author(s):  
M. Licker ◽  
H. Boussairi ◽  
L. Hohn ◽  
D.R. Morel
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Regional Blood Flow
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