Leukotriene inhibitors do not block hypoxic pulmonary vasoconstriction in dogs

1987 ◽  
Vol 62 (5) ◽  
pp. 1808-1813 ◽  
Author(s):  
D. P. Schuster ◽  
D. R. Dennis
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lower Lobe ◽  
Left Lower Lobe ◽  
The Other ◽  
Pulmonary Vasoconstriction ◽  
Other Hand ◽  
Alveolar Hypoxia

We studied whether intravenously administered inhibitors of leukotriene synthesis (diethylcarbamazine, DEC) or end-organ effect (FPL-55712) would change the distribution of regional pulmonary blood flow (rPBF) caused by left lower lobe (LLL) alveolar hypoxia in dogs. Both drugs failed to alter rPBF. In addition, the pressor response to whole-lung hypoxia was not blocked by an FPL-55712 infusion. On the other hand, nitroprusside, as a nonspecific vasodilator also administered intravenously, was able to partially reverse the effects of LLL hypoxia on rPBF. Thus our data do not support a role for leukotriene mediation of hypoxic pulmonary vasoconstriction in dogs.

Mechanism of decreased blood flow to atelectatic lung

1979 ◽  
Vol 46 (6) ◽  
pp. 1047-1048 ◽  
Author(s):  
J. L. Benumof
Keyword(s):  
Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lower Lobe ◽  
Transpulmonary Pressure ◽  
Left Lower Lobe ◽  
Mechanical Forces ◽  
Relative Contribution ◽  
Pulmonary Vasoconstriction ◽  
Blood Flow Reduction ◽  
Increased Blood Flow

This study examined the relative contribution of passive mechanical forces vs. hypoxic pulmonary vasoconstriction as mechanisms of blood flow reduction through atelectatic canine lung. Selective atelectasis of the left lower lobe caused the electromagnetically measured lobar blood flow to decrease 59% from control levels. Reexpansion and ventilation of the left lower lobe with 95% N2–5% CO2, which should terminate any passive mechanical contribution to the decreased test lobe blood flow, did not cause any significant increase in left lower lobe blood flow. Ventilation of the left lower lobe with 100% O2, which should terminate any hypoxic pulmonary vasoconstriction contribution to the decreased test lobe blood flow, increased blood flow back to levels not significantly different from control. Differences between degree of hypoxia, magnitude of transpulmonary pressure, and absolute pulmonary vascular pressure during left lower lobe atelectasis and ventilation with N2 were considered to be minor influences. I conclude that the mechanism of decreased blood flow to an atelectatic lobe is hypoxic pulmonary vasoconstriction.

Predicting The Influence Of Hypoxic Pulmonary Vasoconstriction On The Distribution Of Pulmonary Blood Flow

2011 ◽  
Author(s):  
Kelly S. Burrowes ◽  
Annalisa J. Swan ◽  
Alys R. Clark ◽  
Quentin P.P. Croft ◽  
Keith L. Dorrington ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction

Dependency of hypoxic pulmonary vasoconstriction on temperature

1977 ◽  
Vol 42 (1) ◽  
pp. 56-58 ◽  
Author(s):  
J. L. Benumof ◽  
E. A. Wahrenbrock
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Temperature Change ◽  
Vascular Resistance ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lower Lobe ◽  
Effect Of Temperature ◽  
Hypoxic Response ◽  
Pulmonary Vasoconstriction ◽  
Mechanism Of Inhibition

We studied the effect of temperature change on hypoxic pulmonary vasoconstriction. Selective hypoxia on the left lower lobe of the lung in open-chested dogs at 37 degrees C caused the electromagnetically measured blood flow to the lobe to decrease 51 +/- 5 (SE)% and its vascular resistance to increase 155 +/- 25%. Testing hypoxic response. The hypoxic response at 31.1 +/- 0.4 degrees C was only a 26 +/- 6% decrease in lobar blood flow compared to the hypoxic response at 40.0 +/- 0.5 degrees C which was a 60 +/- 5% decrease in lobar blood flow. Hypothermia itself was associated with a significant increase in pulmonary vascular resistance. We conclude that hypothermia inhibits and hyperthermia enhances hypoxic pulmonary vasoconstriction. The mechanism of inhibition may involve prehypoxic vasoconstriction.

Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures

1975 ◽  
Vol 38 (5) ◽  
pp. 846-850 ◽  
Author(s):  
J. L. Benumof ◽  
E. A. Wahrenbrock
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Main Pulmonary Artery ◽  
Lower Lobe ◽  
Respiratory Alkalosis ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pulmonary Vasoconstriction ◽  
Lung Vessels

We tested the hypothesis that increased pressures within the lung vessels would inhibit hypoxic pulmonary vasoconstriction at all levels of alveolar CO2 tension. Selective hypoxia of the left lower lobe of the lung in open chested dogs caused the electromagnetically measured blood flow to the lobe to decrease 51 plus or minus 4 (SE) percent and its vascular resistance to increase 132 plus or minus 13 percent. Pressure and blood flow in the main pulmonary artery and left atrial pressure did not change during the hypoxic response. Stepwise increments in left artrial and pulmonary arterial pressures induced either by inflating a left atrial balloon or infusing dextran, progressively diminished the vasoconstrictive response to hypoxia. The response was usually abolished when left atrial pressure reached 25 mmHg. For all vascular pressures, hypoxic vasoconstriction was blunted by hypocapnic alkalosis but not enhanced by hypercapnia. We conclude that the redistribution of blood flow away from an hypoxic lobe of the lung to lobes with high Po2 was greatly attenuated by increasing pressures within lung vessels or by inducing respiratory alkalosis.

Dynamic response of local pulmonary blood flow to alveolar gas tensions: analysis

1983 ◽  
Vol 54 (2) ◽  
pp. 445-452 ◽  
Author(s):  
B. J. Grant ◽  
A. M. Schneider
Keyword(s):  
Experimental Data ◽  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Lower Lobe ◽  
Time Constants ◽  
Vasodilator Effect ◽  
Vasoconstrictor Effect ◽  
Exponential Decrease ◽  
Oscillatory Response ◽  
Alveolar Hypoxia

It has been reported that left lower lobe pulmonary blood flow (Q) and alveolar CO2 decrease then oscillate in a progressively damped manner when the lobar inspirate is changed from pure O2 to N2. This damped oscillatory response of lobar Q is abolished by maintaining lobar CO2 constant. We set out to develop the simplest mathematical model that can simulate these experimental results by using techniques derived from control theory. Different models were tested. The simplest model that predicts the experimental data incorporates an exponential decrease of lobar Q to local alveolar hypoxia (time constant 3 min) and a damped oscillatory response of lobar Q to local alveolar hypocapnia. The response to hypocapnia has two components: a vasodilator effect possibly related to intracellular [H+] and a vasoconstrictor effect possibly related to changes of molar CO2. Both these components (time constants of 4.8 min) interact with each other by cross-coupled elements (time constants of 4.8 min). This model can be used to forecast results so that its validity can be tested by experiment.

Hypoxic pulmonary vasoconstriction in dogs: effects of lung segment size and oxygen tension

1981 ◽  
Vol 51 (6) ◽  
pp. 1543-1551 ◽  
Author(s):  
B. E. Marshall ◽  
C. Marshall ◽  
J. Benumof ◽  
L. J. Saidman
Keyword(s):  
Oxygen Tension ◽  
Standard Error ◽  
Perfusion Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Left Lung ◽  
Lower Lobe ◽  
Left Lower Lobe ◽  
Physiological Basis ◽  
Test Segment ◽  
Pulmonary Vasoconstriction

Six pentobarbital-anesthetized dogs were prepared with endobronchial tubes and electromagnetic flow probes. The effects of changing inspired oxygen concentrations (FIO2 = 1, 0.21, 0.15, 0.1, 0.075, 0.05, and 0) were tested on test segments of different size corresponding to left lower lobe, left upper lobe-lingula, left lung, right lung, right lung plus left lower lobe, right lung plus left upper lobe-lingula, and whole lung. In each test the rest of the lung received oxygen. Hypoxic pulmonary vasoconstriction is demonstrated by both diversion of blood flow away from hypoxic test segments and by increased perfusion pressure. Flow diversion (FD%) decreases with the size of the hypoxic test segment (%QSN) from a maximum of 75% for very small segments to zero when the whole lung is hypoxic. FD% increases linearly as alveolar oxygen tension (PAO2) of the test segment is decreased in the range of 130--28 Torr. When mixed venous oxygen tension (PVO2) is less than 45 Torr FD% is reduced. These relationships are described by FD% = [74.99 - 0.0778 (%QSN) - 0.00661 (%QSN)2] [1.268 - 0.0096 (PAO2)] [0.47 + 0.012 (PVO2)], with r = 0.92 and standard error for prediction of 8.4%. Pulmonary perfusion pressure changes (PPH/PPN) increase with the size of the hypoxic test segments from 0 with very small segments to approximately 2.2 for the hypoxic whole lung. For all test segments PPH/PPN increases linearly with PAO2. These relationships are described by PPH/PPN = 1 + [0.0043 (%QSN) + 0.000072 (%QSN)2] [1.234 - 0.0096 (PAO2)], with r = 0.91 and standard error for prediction of 0.3 units. Responses to hypoxic pulmonary vasoconstriction in dogs are therefore shown to be predictable and continuous, and the physiological basis for action of each of the variables is discussed.

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.

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