Increased left atrial pressure inhibits hypoxic pulmonary vasoconstriction

An increase in left atrial pressure (Pla) has been reported to either inhibit or not affect hypoxic pulmonary vasoconstriction in intact dogs. We investigated mean pulmonary arterial pressure (Ppa)-flow (Q) relationships at low and high fixed Pla and Ppa-Pla relationships at fixed Q in piglets, which are known to present with a stronger hypoxic pulmonary pressor response than dogs. Seven piglets were anesthetized; equipped with balloon catheters in inferior vena cava and left atrium to control Q and Pla, respectively; and ventilated alternatively in hyperoxia [fractional concn of O2 in inspired air (FIO2) 0.4] and hypoxia (FIO2 0.12). In all experimental conditions, Ppa-Q plots were best described by a linear approximation with extrapolated pressure intercepts (Pi) not different from Pla. Hypoxia increased slope but not Pi of Ppa-Q plots. An increase in Pla from 8 to 17 mmHg induced a parallel shift of Ppa-Q plots to higher Ppa in hyperoxia but did not affect Ppa-Q plots in hypoxia. In hyperoxia, an increase in Pla at constant Q induced an approximately equal increase in Ppa, whereas in hypoxia there was no effect. The hypoxia-induced increase in Ppa was blunted by increased Pla at all levels of Q studied. We conclude that in anesthetized piglets at fixed Pla hypoxia increases the slope of Ppa-Q plots without affecting Pi and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. The results suggest that no closing pressure higher than normal Pla contributes to hyperoxic or hypoxic Ppa in the intact porcine pulmonary circulation.

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Inhibition of hypoxic pulmonary vasoconstriction by increased left atrial pressure in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.259.1.h93 ◽

1990 ◽

Vol 259 (1) ◽

pp. H93-H100 ◽

Cited By ~ 2

Author(s):

P. Lejeune ◽

J. M. De Smet ◽

P. de Francquen ◽

M. Leeman ◽

S. Brimioulle ◽

...

Keyword(s):

Left Atrial ◽

Hypoxic Pulmonary Vasoconstriction ◽

Atrial Pressure ◽

Left Atrial Pressure ◽

Experimental Conditions ◽

Mean Pulmonary Arterial Pressure ◽

Pulmonary Vasoconstriction ◽

Anesthetized Dogs ◽

Pulmonary Arterial ◽

The Mean

To further explore the mechanism of hypoxic pulmonary vasoconstriction, we studied the mean pulmonary arterial pressure (Ppa)/left atrial pressure (Pla) relationship at fixed cardiac index (Q) and the Ppa/Q relationship at several levels of fixed Pla in pentobarbital sodium-anesthetized dogs ventilated alternately in hyperoxia [fraction of inspired O2 (FIO2) 0.4 or 1.0] and in hypoxia (FIO2 0.1). In all experimental conditions, Ppa/Q plots were linear with extrapolated pressure intercepts (Pi) not significantly different from Pla. Hypoxia increased the slope of Ppa/Q plots and did not affect Pi. In hyperoxia, increasing Pla (3 to 26 mmHg) induced approximately equal increases in Ppa at fixed Q and shifted Ppa/Q plots toward higher pressures in a parallel manner. In hypoxia, increasing Pla (4 to 25 mmHg) did not affect Ppa at fixed Q until Pla exceeded 16 mmHg and shifted Ppa/Q plots toward higher pressures with a decrease in slope. Consequently, the hypoxia-induced increases in Ppa at constant Q and constant Pla were attenuated at higher Pla. Thus, in anesthetized dogs, hypoxia increases the slope of Ppa/Q plots without affecting Pi at fixed Pla, and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. These results can be explained without invoking a hypoxia-induced Starling resistor mechanism in the pulmonary circulation.

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Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures

Journal of Applied Physiology ◽

10.1152/jappl.1975.38.5.846 ◽

1975 ◽

Vol 38 (5) ◽

pp. 846-850 ◽

Cited By ~ 117

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.

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PEEP inhibits hypoxic pulmonary vasoconstriction in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.4.1867 ◽

1991 ◽

Vol 70 (4) ◽

pp. 1867-1873 ◽

Cited By ~ 13

Author(s):

P. Lejeune ◽

J. L. Vachiery ◽

J. M. De Smet ◽

M. Leeman ◽

S. Brimioulle ◽

...

Keyword(s):

Inferior Vena ◽

Intact Animal ◽

Hypoxic Pulmonary Vasoconstriction ◽

Balloon Catheter ◽

Vena Cava ◽

Pulmonary Hemodynamics ◽

Mean Pulmonary Arterial Pressure ◽

Pulmonary Vasoconstriction ◽

Anesthetized Dogs ◽

Pulmonary Arterial

The effects of an increase in alveolar pressure on hypoxic pulmonary vasoconstriction (HPV) have been reported variably. We therefore studied the effects of positive end-expiratory pressure (PEEP) on pulmonary hemodynamics in 13 pentobarbital-anesthetized dogs ventilated alternately in hyperoxia [inspired O2 fraction (FIO2) 0.4] and in hypoxia (FIO2 0.1). In this intact animal model, HPV was defined as the gradient between hypoxic and hyperoxic transmural (tm) mean pulmonary arterial pressure [Ppa(tm)] at any level of cardiac index (Q). Ppa(tm)/Q plots were constructed with mean transmural left atrial pressure [Pla(tm)] kept constant at approximately 6 mmHg (n = 5 dogs), and Ppa(tm)/PEEP plots were constructed with Q kept constant approximately 2.8 l.min-1.m-2 and Pla(tm) kept constant approximately 8 mmHg (n = 8 dogs). Q was manipulated using a femoral arteriovenous bypass and a balloon catheter in the inferior vena cava. Pla(tm) was held constant by a balloon catheter placed by left thoracotomy in the left atrium. Increasing PEEP, from 0 to 12 Torr by 2-Torr increments, at constant Q and Pla(tm), increased Ppa(tm) from 14 +/- 1 (SE) to 19 +/- 1 mmHg in hyperoxia but did not affect Ppa(tm) (from 22 +/- 2 to 23 +/- 1 mmHg) in hypoxia. Both hypoxia and PEEP, at constant Pla(tm), increased Ppa(tm) over the whole range of Q studied, from 1 to 5 l/min, but more at the highest than at the lowest Q and without change in extrapolated pressure intercepts. Adding PEEP to hypoxia did not affect Ppa(tm) at all levels of Q.(ABSTRACT TRUNCATED AT 250 WORDS)

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Left atrial pressure elevation recreates the altered lung lymph flow of seizures

Journal of Applied Physiology ◽

10.1152/jappl.1982.53.2.432 ◽

1982 ◽

Vol 53 (2) ◽

pp. 432-435 ◽

Cited By ~ 14

Author(s):

R. P. Simon ◽

L. L. Bayne ◽

M. P. Naughton

Keyword(s):

Left Atrial ◽

Pressor Response ◽

Lymph Flow ◽

Atrial Pressure ◽

Left Atrial Pressure ◽

Pressure Elevation ◽

Generalized Seizures ◽

Neural Interactions ◽

Lung Lymph ◽

Lung Lymph Flow

We compared the effects of elevated left atrial pressure of central nervous system origin (bicuculline-induced seizures) with an identical pulmonary vascular pressure elevation induced in six sheep by inflation of a balloon in the left atrium. The degree and duration of the consequent elevation in pulmonary lymph flow and the alteration in protein movement in the two groups was identical. Alterations in pulmonary fluid and protein flux resulting from generalized seizures can be explained by the pressor response alone; specific brain-lung neural interactions need not be postulated.

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