Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.

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Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange

Journal of Applied Physiology ◽

10.1152/jappl.1996.81.4.1535 ◽

1996 ◽

Vol 81 (4) ◽

pp. 1535-1543 ◽

Cited By ~ 47

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.

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Hemodilution during Venous Gas Embolization Improves Gas Exchange, without Altering V̇A/Q̇ or Pulmonary Blood Flow Distributions

Anesthesiology ◽

10.1097/00000542-199912000-00041 ◽

1999 ◽

Vol 91 (6) ◽

pp. 1861-1861 ◽

Cited By ~ 12

Author(s):

Steven Deem ◽

Steven McKinney ◽

Nayak L. Polissar ◽

Richard G. Hedges ◽

Erik R. Swenson

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Lung Injury ◽

Partial Pressure ◽

Pulmonary Blood Flow ◽

Flow Distribution ◽

Arterial Oxygen ◽

Control Group ◽

Blood Flow Distribution ◽

Over Time

Background Isovolemic anemia results in improved gas exchange in rabbits with normal lungs but in relatively poorer gas exchange in rabbits with whole-lung atelectasis. In the current study, the authors characterized the effects of hemodilution on gas exchange in a distinct model of diffuse lung injury: venous gas embolization. Methods Twelve anesthetized rabbits were mechanically ventilated at a fixed rate and volume. Gas embolization was induced by continuous infusion of nitrogen via an internal jugular venous catheter. Serial hemodilution was performed in six rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; six rabbits were followed as controls over time. Measurements included hemodynamic parameters and blood gases, ventilation-perfusion (V(A)/Q) distribution (multiple inert gas elimination technique), pulmonary blood flow distribution (fluorescent microspheres), and expired nitric oxide (NO; chemoluminescence). Results Venous gas embolization resulted in a decrease in partial pressure of arterial oxygen (PaO2) and an increase in partial pressure of arterial carbon dioxide (PaCO2), with markedly abnormal overall V(A)/Q distribution and a predominance of high V(A)/Q areas. Pulmonary blood flow distribution was markedly left-skewed, with low-flow areas predominating. Hematocrit decreased from 30+/-1% to 11+/-1% (mean +/- SE) with hemodilution. The alveolar-arterial PO2 (A-aPO2) difference decreased from 375+/-61 mmHg at 30% hematocrit to 218+/-12.8 mmHg at 15% hematocrit, but increased again (301+/-33 mmHg) at 11% hematocrit. In contrast, the A-aPO2 difference increased over time in the control group (P < 0.05 between groups over time). Changes in PaO2 in both groups could be explained in large part by variations in intrapulmonary shunt and mixed venous oxygen saturation (SvO2); however, the improvement in gas exchange with hemodilution was not fully explained by significant changes in V(A)/Q or pulmonary blood flow distributions, as quantitated by the coefficient of variation (CV), fractal dimension, and spatial correlation of blood flow. Expired NO increased with with gas embolization but did not change significantly with time or hemodilution. Conclusions Isovolemic hemodilution results in improved oxygen exchange in rabbits with lung injury induced by gas embolization. The mechanism for this improvement is not clear.

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Effects of Unilateral Hypoxia and Hypercapnia on Pulmonary Blood Flow Distribution in the Dog

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1957.191.3.446 ◽

1957 ◽

Vol 191 (3) ◽

pp. 446-452 ◽

Cited By ~ 34

Author(s):

Hans G. Borst ◽

James L. Whittenberger ◽

Erik Berglund ◽

Maurice McGregor

Keyword(s):

Carbon Dioxide ◽

Blood Flow ◽

Pulmonary Blood Flow ◽

Flow Distribution ◽

Blood Flow Distribution ◽

Low Oxygen ◽

Pulmonary Vasoconstriction ◽

Vasoconstrictor Response ◽

Flow Through ◽

Oxygen Gas

Effects of hypoxia and of hypercapnia on pulmonary blood flow distribution were examined in 19 dogs. The blood flow through each lung was continuously recorded; the test gas was administered to one lung, and the other lung was used as the control. Low oxygen gas mixtures were administered to one lung for periods of 2–47 minutes. When constriction occurred, it began within one-half minute after the gas administration was started and reached a plateau within 8–20 minutes. Vasodilation was never observed. In most animals no vasomotor effect of hypoxia was found early in the experiment (less than 6 hr. after induction of anesthesia), but seven of the early nonreactors became positive later in the experiment. After 6–8 hours from induction of anesthesia, all animals tested showed a vasoconstrictor response to hypoxia. The administration to one lung of 5 or 10% carbon dioxide for 2–10 minutes was always accompanied by vasoconstriction in that lung. In dogs that showed unilateral pulmonary vasoconstriction during hypoxia, further vasoconstriction was produced by adding 5% carbon dioxide. Some of the contradictory results of other investigators may be explained by the refractory period observed in these experiments.

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The intrarenal blood flow distribution and role of nitric oxide in diabetic rats

Metabolism ◽

10.1016/j.metabol.2005.01.023 ◽

2005 ◽

Vol 54 (6) ◽

pp. 788-792 ◽

Cited By ~ 3

Author(s):

Kazushige Nakanishi ◽

Shizuka Onuma ◽

Mariko Higa ◽

Yohko Nagai ◽

Toshiki Inokuchi

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Flow Distribution ◽

Diabetic Rats ◽

Blood Flow Distribution ◽

Intrarenal Blood Flow

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The role of cardiac output response in blood flow distribution during exercise in patients with chronic heart failure

European Heart Journal ◽

10.1093/oxfordjournals.eurheartj.a061030 ◽

1995 ◽

Vol 16 (7) ◽

pp. 951-960 ◽

Cited By ~ 9

Author(s):

H. YAMABE ◽

K. ITOH ◽

Y. YASAKA ◽

T. TAKATA ◽

M. YOKOYAMA

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Cardiac Output ◽

Chronic Heart Failure ◽

Flow Distribution ◽

Blood Flow Distribution ◽

Output Response

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Renal response of the new-born dog to a saline load: the role of intrarenal blood flow distribution

The Journal of Physiology ◽

10.1113/jphysiol.1974.sp010565 ◽

1974 ◽

Vol 239 (2) ◽

pp. 225-236 ◽

Cited By ~ 17

Author(s):

Leonard I. Kleinman ◽

John H. Reuter

Keyword(s):

Blood Flow ◽

Flow Distribution ◽

Blood Flow Distribution ◽

Renal Response ◽

New Born ◽

Intrarenal Blood Flow

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Effect of lung thromboxane generation on regional blood flow during sheep bypass

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1982.242.3.h462 ◽

1982 ◽

Vol 242 (3) ◽

pp. H462-H469

Author(s):

A. H. Schuette ◽

P. C. Huttemeier ◽

W. D. Watkins ◽

W. M. Zapol

Keyword(s):

Blood Flow ◽

Vascular Resistance ◽

Regional Blood Flow ◽

Flow Distribution ◽

Pulmonary Artery Hypertension ◽

Blood Flow Distribution ◽

Systemic Blood ◽

Systemic Blood Flow ◽

Pulmonary Vasoconstriction ◽

Potent Vasoconstrictor

Acute pulmonary artery hypertension and an increased plasma concentration of thromboxane B2 (TXB2), the stable metabolite of the potent vasoconstrictor thromboxane A2, occur within minutes of the onset of venovenous (VV) partial bypass in the awake sheep. To search for systemic vasoconstriction, we assessed systemic blood flow distribution by radioactive microspheres and correlated the changes to alterations in plasma TXB2 and 6-keto-F1 alpha concentration. In 10 control sheep mean plasma TXB2 concentration increased from 0.39 ng/ml prebypass to about 1.1 ng/ml at 8 and 16 min of bypass. Despite marked pulmonary vasoconstriction with a threefold elevated resistance, the blood flow to the heart, brain, and kidney were unchanged at 8 and 16 min of bypass. However, hepatic vascular resistance increased twofold at 8 min of bypass. Indomethacin treatment (10 mg/kg) of six sheep blocked the increase of both pulmonary and hepatic vascular resistance as well as reduced TXB2 levels below 0.1 ng/ml. Thus VV bypass induces transient and selective vasoconstriction of the lung and liver mediated by vasoconstrictor eicosanoids.

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