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.

Increased left atrial pressure inhibits hypoxic pulmonary vasoconstriction

1994 ◽  
Vol 76 (4) ◽  
pp. 1502-1506 ◽  
Author(s):  
D. De Canniere ◽  
C. Stefanidis ◽  
R. Hallemans ◽  
M. Delcroix ◽  
P. Lejeune ◽  
...  
Keyword(s):  
Left Atrial ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Vena Cava ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Experimental Conditions ◽  
Balloon Catheters ◽  
Mean Pulmonary Arterial Pressure ◽  
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.

Longitudinal distribution of pulmonary vascular resistance with very high pulmonary blood flow

1987 ◽  
Vol 62 (1) ◽  
pp. 344-358 ◽  
Author(s):  
M. Younes ◽  
Z. Bshouty ◽  
J. Ali
Keyword(s):  
Blood Flow ◽  
Weight Gain ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Longitudinal Distribution ◽  
Flow Rates ◽  
Flow Threshold

Dog left upper lobes (LUL) were perfused in situ via the left lower lobe artery. Lobe weight was continuously monitored. Increasing lobar flow from normal to 10 times normal had little effect on left atrial pressure, which ranged from 1 to 5 mmHg. There was a flow threshold (Qth) below which lobar weight was stable. Qth ranged from 1.1 to 1.55 l/min (mean 1.27) corresponding to four times normal LUL blood flow. Above Qth, step increases in lobar flow resulted in progressive weight gain at a constant rate that was proportional to flow. The effective pressure at the filtration site (EFP) at different flow rates was estimated from the static vascular pressure that resulted in the same rate of weight gain. From this value and from mean pulmonary arterial (PA) and left atrial (LA) pressures, we calculated resistance upstream (Rus) and downstream (Rds) from filtration site. At Qth, Rds accounted for 60% of total resistance. This fraction increased progressively with flow, reaching 83% at Q of 10 times normal. We conclude that during high pulmonary blood flow EFP is closer to PA pressure than it is to LA pressure, and that this becomes progressively more so as a function of flow. As a result, the lung accumulates water at flow rates in excess of four times normal despite a normal left atrial pressure.

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

1990 ◽  
Vol 259 (1) ◽  
pp. H93-H100 ◽  
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.

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.

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.

Effect of blood flow rate and blood flow history on newborn pulmonary microcirculation

1991 ◽  
Vol 261 (2) ◽  
pp. H271-H279 ◽  
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Left Atrial ◽  
Total Pressure ◽  
Pulmonary Blood Flow ◽  
Blood Flow Rate ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Flow Rates ◽  
Pulmonary Arterial

The purpose of this study was to determine whether increased pulmonary blood flow and/or the history of pulmonary blood flow alters microvascular pressures in lungs of newborns. Using the direct micropuncture technique, we measured pressures in 20- to 60-microns-diameter arterioles and venules in isolated lungs of newborn rabbits at consecutive blood flow rates of 50 (baseline), 100, and/or 200 ml.min-1.kg-1. Then in some lungs we returned blood flow rate to baseline and repeated microvascular pressure measurements. We kept left atrial pressure the same at all blood flow rates. When blood flow rate increased and left atrial pressure was maintained constant, pulmonary arterial, 20- to 60-microns-diameter arteriolar, and 20- to 60-microns-diameter venular pressures increased such that the percentage of total pressure drop that occurred across veins increased. When we returned blood flow to baseline, venular pressure returned to baseline, but arteriolar and pulmonary arterial pressures returned to values less than baseline so that the percentage of the total pressure drop that occurred across microvessels decreased. Thus both blood flow rate and blood flow history are important determinants of the longitudinal distribution of pulmonary vascular pressures across newborn lungs. These findings also suggest that in newborn lungs venules greater than 60 microns diameter are poorly distensible such that higher blood flow rates result in increased microvascular pressures. Hence, under conditions of increased pulmonary blood flow, such as occurs with left to right shunts, the tendency for edema formation will increase in newborn lungs even if left atrial pressure does not increase.

Effect of hypoxia on lung lymph flow in newborn lambs with left atrial hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. H487-H493
Author(s):  
J. U. Raj ◽  
T. A. Hazinski ◽  
R. D. Bland
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Control Period ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Fluid Filtration ◽  
Alveolar Hypoxia ◽  
Lung Lymph ◽  
Lung Lymph Flow

To determine the effect of left atrial hypertension on the vascular response to hypoxia in the newborn lung, we measured pulmonary artery and left atrial pressures, lung blood flow and lymph flow, and concentrations of protein in lymph and plasma of 13 lambs that spontaneously breathed air for 2-6 h (control period), followed by 8-11% O2 mixed with 3-5% CO2 and N2 for 2-4 h (experimental period). In eight studies, the lambs were made hypoxic first, after which we elevated their left atrial pressure by 10-12 Torr for 2-3 h. In 10 additional studies, we reversed the sequence by raising left atrial pressure first followed by addition of hypoxia. In lambs with normal left atrial pressure, alveolar hypoxia increased both pulmonary blood flow and lymph flow, with an associated reduction in lymph-to-plasma protein ratio (L/P). When left atrial pressure was increased in the presence of hypoxia, lymph flow increased by a small amount and L/P decreased further. In lambs with preexisting left atrial pressure elevation, addition of alveolar hypoxia increased both blood flow and lymph flow with no significant change in L/P. These results suggest that in newborn lambs with normal left atrial pressure, alveolar hypoxia increases lung lymph flow mainly by increasing microvascular filtration pressure, whereas in lambs with elevated left atrial pressure, hypoxia increases lymph flow by another mechanism, perhaps by increasing the perfused surface area for fluid filtration.

Hypoxic pulmonary vasoconstriction does not affect hydrostatic pulmonary edema formation

1987 ◽  
Vol 62 (2) ◽  
pp. 776-780 ◽  
Author(s):  
F. W. Cheney ◽  
M. J. Bishop ◽  
B. L. Eisenstein ◽  
L. D. Artman
Keyword(s):  
Pulmonary Edema ◽  
Left Atrial ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lower Lobe ◽  
Left Lower Lobe ◽  
Flow Diversion ◽  
Gas Mixture ◽  
Edema Formation ◽  
Pulmonary Vasoconstriction ◽  
Hypoxic Gas Mixture

We studied the effects of regional hypoxic pulmonary vasoconstriction (HPV) on lobar flow diversion in the presence of hydrostatic pulmonary edema. Ten anesthetized dogs with the left lower lobe (LLL) suspended in a net for continuous weighing were ventilated with a bronchial divider so the LLL could be ventilated with either 100% O2 or a hypoxic gas mixture (90% N2–5% CO2–5% O2). A balloon was inflated in the left atrium until hydrostatic pulmonary edema occurred, as evidenced by a continuous increase in LLL weight. Left lower lobe flow (QLLL) was measured by electromagnetic flow meter and cardiac output (QT) by thermal dilution. At a left atrial pressure of 30 +/- 5 mmHg, ventilation of the LLL with the hypoxic gas mixture caused QLLL/QT to decrease from 17 +/- 4 to 11 +/- 3% (P less than 0.05), pulmonary arterial pressure to increase from 35 +/- 5 to 37 +/- 6 mmHg (P less than 0.05), and no significant change in rate of LLL weight gain. Gravimetric confirmation of our results was provided by experiments in four animals where the LLL was ventilated with an hypoxic gas mixture for 2 h while the right lung was ventilated with 100% O2. In these animals there was no difference in bloodless lung water between the LLL and right lower lobe. We conclude that in the presence of left atrial pressures high enough to cause hydrostatic pulmonary edema, HPV causes significant flow diversion from an hypoxic lobe but the decrease in flow does not affect edema formation.

Effect of lung-inflating pressure on pulmonary blood pressure and flow

1963 ◽  
Vol 205 (6) ◽  
pp. 1178-1186 ◽  
Author(s):  
E. F. De Bono ◽  
C. G. Caro
Keyword(s):  
Left Atrial ◽  
Perfusion Pressure ◽  
Pressure Ratio ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Alveolar Pressure ◽  
Perfusion Flow ◽  
The Relationship ◽  
Perfusion Flow Rate

In ten dogs the widely exposed left lower lobe of the lung was inflated to different static pressures over the range 5–20 cm H2O while being perfused with blood from a constant-flow source over a range of flows up to 300 ml/min. Left atrial pressure was kept below 3–4 cm H2O. The relationship between perfusion pressure and inflating pressure was linear and the slope independent of perfusion flow rate except at very low rates of flow. The Δ perfusion pressure-to-Δ inflating pressure ratio, with one exception, varied from 0.6 to 1.0, indicating that the major part of alveolar pressure was transmitted to the capillaries. At normal rates of flow the relationship between perfusion pressure and flow was linear. The findings, together with results obtained on a model, suggest that: 1) Calculation of pulmonary vascular resistance from the pulmonary artery-left atrial pressure gradient is misleading where inflating pressure exceeds left atrial pressure. In such circumstances the precapillary resistance can be measured. 2) At normal rates of flow the dominant resistance in the pulmonary vascular bed is precapillary. Despite the distensibility of pulmonary vessels this resistance does not vary with perfusion pressure or flow.

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.

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