Persistent fetal pulmonary hypoperfusion after acute hypoxia

1987 ◽  
Vol 253 (4) ◽  
pp. H941-H948 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso ◽  
R. B. Wilkening ◽  
G. Meschia
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Blood Flow ◽  
Adrenergic Blockade ◽  
Flow Transducer ◽  
Arterial Blood ◽  
Pulmonary Arterial

To determine the effects of duration of hypoxia on fetal pulmonary blood flow and vasoreactivity, we studied the response of the fetal pulmonary vascular bed before, during, and after prolonged (2-h) and more brief (30-min) exposures to acute hypoxia in 19 chronically instrumented unanesthetized fetal lambs. Left pulmonary arterial blood flow was measured by an electromagnetic flow transducer. Fetal PO2 was lowered by delivering 10-12% O2 to the ewe. During 2-h periods of hypoxia left pulmonary arterial blood flow decreased, and main pulmonary arterial and pulmonary vascular resistance increased. The increase in pulmonary vascular resistance was sustained throughout the 2-h period of hypoxia. After the return of the ewe to room air breathing, pulmonary vascular resistance remained elevated for at least 1 h despite the rapid correction of hypoxemia and in the absence of acidemia. In contrast, after 30 min of hypoxia, left pulmonary arterial blood flow, pulmonary arterial pressure, and pulmonary vascular resistance returned to base-line values rapidly with the termination of hypoxia. The persistent pulmonary hypoperfusion after 2 h of hypoxia was attenuated by alpha-adrenergic blockade and was characterized by a blunted vasodilatory response to increases in fetal PO2. When fetal PO2 was elevated during the posthypoxia period in the presence of alpha-blockade, pulmonary blood flow still remained unresponsive to increases in fetal PO2. We conclude that 2-h periods of acute hypoxia can decrease fetal pulmonary vasoreactivity, and we speculate that related mechanisms may contribute to the failure of the normal adaptation of the pulmonary circulation at birth.

Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

1961 ◽  
Vol 200 (2) ◽  
pp. 287-291 ◽  
Author(s):  
M. Harasawa ◽  
S. Rodbard
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Arterial Blood Flow ◽  
Tetraethylammonium Chloride ◽  
Blood Flows ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Flow Pressure

The effects of tetraethylammonium chloride (TEAC) and aminophylline on the pulmonary vascular resistance were studied in thoracotomized dogs. Pulmonary arterial blood flow and pressure, and systemic blood pressure were measured simultaneously. Both drugs showed marked hypotensive effects on the systemic vessels. In every instance pulmonary arterial pressures and blood flows were reduced by TEAC given via the pulmonary artery and increased by aminophylline. However, the calculated pulmonary vascular resistance remained essentially unchanged in all experiments. These data challenge the concept that the pulmonary vessels respond to these drugs by active vasodilatation

Platelet-activating factor modulates pulmonary vasomotor tone in the perinatal lamb

1998 ◽  
Vol 85 (3) ◽  
pp. 1079-1085 ◽  
Author(s):  
Basil O. Ibe ◽  
Sue Hibler ◽  
J. Usha Raj
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Platelet Activating Factor ◽  
Perinatal Period ◽  
Arterial Blood Flow ◽  
Vasomotor Tone ◽  
Arterial Blood ◽  
Determine Role ◽  
Pulmonary Arterial ◽  
Near Term

Eight near-term fetal lambs were studied acutely in utero to determine role of platelet-activating factor (PAF) in the regulation of vasomotor tone in systemic and pulmonary circulations in the immediate perinatal period. Four fetal lambs were studied predelivery and 2 h postdelivery to determine circulating PAF levels. Aortic and pulmonary arterial pressures and cardiac output were measured continuously, and systemic and pulmonary vascular resistances were calculated. Left pulmonary arterial blood flow was also measured in four fetal lambs. After delivery and oxygenation, circulating PAF levels fell significantly. When WEB-2170, a specific PAF-receptor antagonist, was infused to block effect of endogenous PAF in the eight near-term fetal lambs, systemic vascular resistance fell 30% but pulmonary vascular resistance fell dramatically by 68%. Specificity of WEB-2170 was tested in juvenile lambs and was found to be very specific in lowering vasomotor tone only when tone was elevated by action of PAF. Our data show that endogenous PAF levels in the fetus contribute to maintain a high basal systemic and pulmonary vasomotor tone and that a normal fall in circulating PAF levels after birth and oxygenation may facilitate fall in pulmonary vascular resistance at birth.

Pulmonary vasodilator drugs decrease lung liquid production in fetal sheep

1995 ◽  
Vol 79 (4) ◽  
pp. 1212-1218 ◽  
Author(s):  
J. J. Cummings
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Fetal Lung ◽  
Prostaglandin D2 ◽  
Fetal Sheep ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial ◽  
Lung Liquid

To examine a potential relationship between pulmonary vasodilatation and fetal lung liquid production, I measured lung liquid production in 20 fetal sheep at 130 +/- 4 days gestation while using several agents known to increase pulmonary blood flow. Thirty-two studies were done in which left pulmonary arterial flow (Qlpa) was measured by an ultrasonic Doppler flow probe and net lung luminal liquid production (Jv) was measured by plotting the change in lung luminal liquid concentration of radiolabeled albumin, an impermeant tracer that was mixed into the lung liquid at the start of each study. Qlpa and Jv were measured during a 1- to 2-h baseline period and then during a 1- to 2-h infusion period in which the fetuses received either an intravenous infusion of acetylcholine (n = 8), prostaglandin D2 (n = 10), or the leukotriene blocker FPL-55712 (n = 7). These vasodilators work by different mechanisms, each mechanism having been implicated in the decrease in pulmonary vascular resistance seen at birth. Control (saline) infusions (n = 7) caused no change in either Qlpa or Jv over 4 h. All vasodilator agents significantly increased pulmonary blood flow and decreased Jv. Pulmonary arterial pressure did not change significantly in either the control, acetylcholine, prostaglandin, or leukotriene-blocker studies, indicating that pulmonary vascular resistance decreased. Thus agents that increase pulmonary blood flow by mechanisms that occur at birth also decrease lung liquid production in fetal lambs.

Effect of high intra-alveolar O2 tensions on pulmonary circulation in perfused lungs of dogs

1965 ◽  
Vol 208 (1) ◽  
pp. 130-138 ◽  
Author(s):  
G. J. A. Cropp
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Time Course ◽  
Systemic Circulation ◽  
The Body ◽  
Arterial Blood ◽  
Pulmonary Parenchyma ◽  
Pulmonary Arterial

The resistance to blood flow in the pulmonary circulation of dogs (PVR) increased when their lungs were ventilated with 95–100% oxygen and were perfused with blood that recirculated only through the pulmonary circulation; the systemic circulation was perfused independently. This increase in PVR occurred even when nerves were cut or blocked but was abolished by inhaled isopropylarterenol aerosol. Elevation of intra-alveolar Po2 without increase in pulmonary arterial blood Po2 was sufficient to increase pulmonary vascular resistance. The pulmonary venules or veins were thought to be the likely site of the constriction. These reactions were qualitatively similar to those produced by injection of serotonin or histamine into the pulmonary circulation. The time course of the response and failure to obtain it when the blood was perfused through the remainder of the body before it re-entered the pulmonary circulation are compatible with a theory that high intra-alveolar O2 tension activates a vasoconstrictor material in the pulmonary parenchyma.

Leukotriene end organ antagonists increase pulmonary blood flow in fetal lambs

1985 ◽  
Vol 249 (3) ◽  
pp. H570-H576 ◽  
Author(s):  
S. J. Soifer ◽  
R. D. Loitz ◽  
C. Roman ◽  
M. A. Heymann
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Blood Gases ◽  
Physiological Control ◽  
Arterial Blood ◽  
High Pulmonary Vascular Resistance

The factors responsible for maintaining the normally low pulmonary blood flow and high pulmonary vascular resistance in the fetus are not well understood. Since leukotrienes are potent pulmonary vasoconstrictors in many adult animal species, we determined whether leukotrienes were perhaps involved in the control of the fetal pulmonary circulation by studying the effects of putative leukotriene end organ antagonists in two groups of fetal lambs. In six fetal lambs studied at 130-134 days gestation, FPL 55712 increased pulmonary blood flow by 61% (P less than 0.05) and reduced pulmonary vascular resistance by 45% (P less than 0.05). There was a small increase in heart rate but no changes in pulmonary and systemic arterial pressures and systemic arterial blood gases. In six other fetal lambs studied at 130-140 days gestation, FPL 57231 increased pulmonary blood flow by 580% (P less than 0.05) and decreased pulmonary vascular resistance by 87% (P less than 0.05). Pulmonary and systemic arterial pressures decreased (P less than 0.05), and heart rate increased (P less than 0.05). Leukotriene end organ antagonism significantly increases fetal pulmonary blood flow and decreases pulmonary vascular resistance. Leukotrienes may play a role in the physiological control of the fetal pulmonary circulation.

Nitric oxide inhibition varies with hemoglobin saturation

1993 ◽  
Vol 75 (5) ◽  
pp. 2332-2336 ◽  
Author(s):  
J. Iwamoto ◽  
F. C. Morin
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Left Pulmonary Artery ◽  
Flow Transducer ◽  
Arterial Blood

Endothelium-derived nitric oxide (NO) appears to be involved in the regulation of pulmonary vascular tone by O2. We hypothesized that the ability of blood to inhibit the vasodilation caused by NO would vary inversely with the saturation of hemoglobin by O2. To test this hypothesis, we used the pulmonary circulation of the unanesthetized fetal lamb as a bioassay for NO-induced vasodilation. Two to 3 days before the experiment, the main pulmonary artery, left atrium, carotid artery, and trachea of the fetus were catheterized and an ultrasonic blood flow transducer was placed around the proximal portion of the left pulmonary artery. On the day of the experiment, NO solution was prepared by bubbling 10% NO-90% N2 gas mixture in saline. This solution was injected into the fluid-filled potential air spaces of the fetal lungs via the trachea. At the highest dose (0.8 mumol), NO increased pulmonary blood flow fourfold and decreased pulmonary vascular resistance similarly. The dose-response curve for NO was similar to those obtained from isolated pulmonary blood vessels and gas-ventilated animals. Mixing NO solution with maternal arterial blood before injection decreased the effect of NO, and mixing it with venous blood virtually eliminated the effect. The decrease in fetal pulmonary vascular resistance caused by NO was inhibited by blood in inverse proportion to the saturation of hemoglobin with O2 in the blood (R2 = 0.93, P < or = 0.0001), confirming our hypothesis.

Physical factors affecting normal and serotonin-constricted pulmonary vessels

1960 ◽  
Vol 198 (4) ◽  
pp. 864-872 ◽  
Author(s):  
Abraham M. Rudolph ◽  
Peter A. M. Auld
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Venous Pressure ◽  
Physical Factors ◽  
Factors Affecting ◽  
Pulmonary Vessels ◽  
High Flows ◽  
Pulmonary Arterial

The effects of changes of pulmonary blood flow, pulmonary venous and pulmonary arterial pressure on calculated pulmonary vascular resistance were evaluated in open-chest, intact dogs, in which the pulmonary and systemic circulations were separately perfused. Similar observations were made after constricting the pulmonary vessels by continuous infusion of serotonin. An increase in pulmonary blood flow produced a decrease in pulmonary vascular resistance. At high flows, the calculated resistance in the serotonin-constricted vessels could be reduced to levels considered normal at lower flows in normal vessels. An increase of pulmonary venous pressure resulted in a decrease of calculated resistance up to pulmonary venous pressure levels of 15–20 mm Hg in ‘normal’ vessels, but in serotonin-constricted vessels, resistance continued to be decreased by increase of pulmonary venous pressure up to 25–30 mm Hg. These findings confirm that the usual formula for calculating pulmonary vascular resistance assesses only resistance to flow, but does not provide information regarding vascular tone.

Systemic and pulmonary vasomotor waves

1965 ◽  
Vol 209 (1) ◽  
pp. 37-50 ◽  
Author(s):  
Ricardo Ferretti ◽  
Neil S. Cherniack ◽  
Guy Longobardo ◽  
O. Robert Levine ◽  
Eugene Morkin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Breathing Pattern ◽  
Pulmonary Arterial Pressure ◽  
Arterial Blood Flow ◽  
Mayer Waves ◽  
Arterial Blood ◽  
Vasomotor Activity ◽  
Pulmonary Arterial

Rhythmic oscillations in systemic arterial blood pressure (Mayer waves) were produced in the dog by metabolic acidosis; hypoxia generally augmented the amplitude of the Mayer waves. When the Mayer waves exceeded 20 mm Hg in amplitude, they were associated with rhythmic fluctuations in pulmonary arterial pressure. The pulmonary arterial waves resembled the Mayer waves with respect to frequency and independence of the breathing pattern but were generally smaller in amplitude Measurements of instantaneous pulmonary arterial blood flow indicate that the rhythmic fluctuations in pulmonary arterial pressure represent the passive effects of fluctuations in pulmonary blood flow rather than fluctuations in pulmonary vasomotor activity. In turn, the swings in pulmonary arterial blood flow appear to originate in rhythmic variations in systemic vasomotor activity.

Volume characteristics of extra- and intraparenchymal segments of the canine pulmonary artery

1977 ◽  
Vol 42 (4) ◽  
pp. 519-524 ◽  
Author(s):  
M. Friedman ◽  
A. Wanner
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Acute Hypoxia ◽  
Relative Volume ◽  
Volume Distribution ◽  
Arterial Tree ◽  
Lung Inflation ◽  
Air Breathing ◽  
Arterial Blood ◽  
Pulmonary Arterial

The volumes of the extraparenchymal segment (VpaEP) and intraparenchymal segment (VpaIP) of the pulmonary arterial tree were determined in intact anesthetized dogs during room air breathing and acute hypoxia. Total pulmonary arterial blood volume (Vpatotal) was calculated as the product of pulmonary blood flow and pulmonary arterial circulation time. An angiographic technique was used to estimate VpEP. VpaIP was calculated by subtracting VpaEP from Vpatotal. During room air breathing at functional residual capacity, mean +/- SD of VpaEP was 17.1 +/- 5.1 ml and of VpaIP was 31.7 +/- 20.8 ml, representing 40% and 60%, respectively, of Vpatotal. Vpatotal increased 22.2 +/- 10.5 ml during lung inflation, with proportional increases in VpaIP and VpaEP. VpaEP was found to be influenced equally by changes in transmural pulmonary arterial and transpulmonary pressures. Acute hypoxia was accompanied by an increase in pulmonary vascular resistance and a decrease in volume distensibility of the extraparenchymal segment. Vpatotal increased 76% without changes in the relative volume distribution of VpaEP and VpaIP. These findings can be best explained by active vasomotion with an increase in down-stream pulmonary vascular resistance.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

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