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.

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.

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.

Lymph flow during increases in pulmonary blood flow and microvascular pressure in dogs

1988 ◽  
Vol 255 (5) ◽  
pp. H1149-H1155 ◽  
Author(s):  
F. A. Grimbert ◽  
D. Martin ◽  
J. C. Parker ◽  
A. E. Taylor
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Protein Concentration ◽  
Balloon Catheter ◽  
Arterial Occlusion ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
The Relationship

We studied the effects of an increase in pulmonary blood flow (PBF) on steady-state lung lymph flow (QL) and protein transport in anesthetized dogs (n = 7) to estimate the effect of vascular recruitment in zone 3 on transvascular filtration. At the end of each experiment, we increased left atrial pressure to 25-30 mmHg using a balloon catheter and obtained a washdown of the lymph protein concentration. PBF was increased with an extracorporeal circuit, which pumped blood from the left to the right atrium, and increases in pulmonary capillary pressure (Pc) were minimized by lowering left atrial pressure. PBF was measured by thermodilution, and Pc was measured by transient analysis of arterial occlusion pressure with a Swan-Ganz catheter. PBF increases averaged 78% with increases ranging from 36 to 118%. Pc increases ranged from 0.5 to 6.3 mmHg, and QL increases averaged 31% with changes ranging from -2 to +138%. We observed a 16% increase in QL for each 1-mmHg increase in Pc during increased PBF, which was comparable to the relationship previously observed after an increased left atrial pressure. Lymph-to-plasma total protein concentration ratios (CL/CP) decreased from 0.71 +/- 0.04 to 0.625 +/- 0.06 during increased PBF. The relationship between CL/CP, QL, and Pc for both increased blood flow and increased left atrial pressure were within the expected range for increased pressure alone. These data suggest that there was minimal vascular recruitment for transvascular filtration in zone 3 when pulmonary blood flow was increased. Microvascular filtration pressure was the main determinant of fluid and protein transvascular filtration under these conditions.

Changes in microvascular permeability with acceleration of edema in dog lungs

1990 ◽  
Vol 258 (2) ◽  
pp. H395-H399 ◽  
Author(s):  
B. D. Butler ◽  
R. E. Drake ◽  
W. D. Sneider ◽  
S. J. Allen ◽  
J. C. Gabel
Keyword(s):  
Weight Gain ◽  
Pulmonary Edema ◽  
Membrane Permeability ◽  
Left Atrial ◽  
Membrane Filtration ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Edema Formation ◽  
Before And After

Elevation of left atrial pressure to 25–40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5–120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

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.

Positive end-expiratory pressure decreases bronchial blood flow in the dog

1984 ◽  
Vol 56 (5) ◽  
pp. 1289-1293 ◽  
Author(s):  
E. M. Baile ◽  
R. K. Albert ◽  
W. Kirk ◽  
S. Lakshaminarayan ◽  
B. J. Wiggs ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Left Atrium ◽  
Pulmonary Vascular Resistance ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Venous Pressure ◽  
Lower Lobe ◽  
Positive End Expiratory Pressure ◽  
The Right

Positive end-expiratory pressure (PEEP) increases pulmonary vascular resistance, but its effect on the bronchial circulation is unknown. We have compared two techniques for measuring bronchial blood flow in anesthetized, open-chest, ventilated dogs at varying levels of PEEP. Bronchial blood flow ( Qbr ) to the left lower lobe (LLL) and trachea was measured with radiolabeled microspheres. Total Qbr was partitioned into tracheal, bronchial, and parenchymal fractions. We also measured the bronchopulmonary anastomotic flow ( Qbra ) by attaching cannulas from the lobar pulmonary artery and vein to reservoirs, interrupting the LLL pulmonary blood flow and collecting the flow going into the reservoirs. We measured Qbr and Qbra in 10 animals ventilated with varying levels of PEEP (3, 10, and 15 cmH2O) applied randomly. Pulmonary venous pressure was kept at 0 cmH2O. There was no difference observed between Qbr and Qbra at PEEP 3 and 10 cmH2O, but at PEEP 15 cmH2O, Qbr was greater than Qbra , suggesting that at low left atrial pressures bronchial blood flow drains mainly to the left atrium, whereas at elevated alveolar pressures a larger fraction empties into the right side of the heart. PEEP decreased LLL Qbr and Qbra (P less than 0.01). That fraction of Qbr going to the trachea did not change with PEEP. However, the bronchial and parenchymal fractions decreased.

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.

Effect of pulmonary blood flow on measurements of respiratory mechanics using the interrupter technique

1993 ◽  
Vol 74 (3) ◽  
pp. 1083-1088 ◽  
Author(s):  
N. J. Freezer ◽  
C. J. Lanteri ◽  
P. D. Sly
Keyword(s):  
Blood Flow ◽  
Chest Wall ◽  
Respiratory System ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Respiratory Mechanics ◽  
Dynamic Compliance ◽  
Left Atrial Pressure ◽  
Conducting Airways ◽  
The Relationship

The relationship between respiratory mechanics, changes in pulmonary blood flow (PBF), pulmonary arterial pressure, and left atrial pressure is unclear. Conventional methods for the measurement of respiratory mechanics model the respiratory system as a single compartment, which may not adequately represent the respiratory system in a diseased state. The interrupter technique models the respiratory system as two compartments, with the "flow resistance" of the conducting airways and chest wall (Raw) considered separately from Pdif, a measure of the viscoelastic properties of the lung and chest wall, together with any pendelluft present. The respiratory mechanics of 15 infants in the first year of life were studied during cardiac catheterization with the use of conventional methods and the interrupter technique. The infants had a PBF-to-systemic blood flow ratio ranging from 0.6 to 4.0:1. The specific dynamic compliance of the respiratory system was not related to the PBF; however, there was a significant relationship between PBF and the total resistance of the respiratory system (Rrs) [analysis of variance (ANOVA) F = 5.69, P < 0.05], Raw (ANOVA, F = 12.30, P < 0.01), and Pdif (ANOVA, F = 3.79, P < 0.05). Rrs increased significantly with an increase in mean left atrial pressure (ANOVA, F = 6.92, P < 0.05); however, dynamic compliance, Raw, and Pdif did not. These results suggest that the relationship between Rrs and PBF is due an increase in the resistive properties of the conducting airways and tissue components.

Effect of edema on pulmonary blood flow in the isolated perfused dog lung lobe

1980 ◽  
Vol 48 (3) ◽  
pp. 444-449 ◽  
Author(s):  
J. Bhattacharya ◽  
K. Nakahara ◽  
N. C. Staub
Keyword(s):  
Blood Flow ◽  
Weight Gain ◽  
Extravascular Lung Water ◽  
Pulmonary Blood Flow ◽  
Lower Lobe ◽  
Interstitial Edema ◽  
Lung Water ◽  
Lung Lobe ◽  
Low Levels ◽  
The Relationship

We determined the relationship between the amount of edema and changes in blood flow in the isolated, perfused, and ventilated lower lobe of dog lung. We held vascular pressure constant and measured lobe weight and flow continuously. Vascular pressures were set to produce minimal weight gain in four lobes (controls) and large weight gain in six lobes (edema). In all lobes, the outflow pressure exceeded alveolar pressure at end expiration (zone III conditions). The control lobes gained an average of 20% in weight over 4 h, but blood flow remained constant. They showed interstitial edema histologically and extravascular lung water was increased 38%. The edema lobes gained weight rapidly, ultimately tripling their weight. In these lobes, blood flow remained constant until lobe weight had doubled; then flow decreased progressively to low levels. These lobes showed extensive alveolar edema histologically and extravascular lung water was increased 238%. Pulmonary blood flow is not affected by interstitial edema, but is markedly reduced when alveolar flooding occurs.

Lung microvascular pressure profile measured by micropuncture in anesthetized dogs

1988 ◽  
Vol 64 (2) ◽  
pp. 874-879 ◽  
Author(s):  
J. M. Shepard ◽  
M. A. Gropper ◽  
G. Nicolaysen ◽  
N. C. Staub ◽  
J. Bhattacharya
Keyword(s):  
Left Atrial ◽  
Left Lung ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Alveolar Pressure ◽  
Pressure Zone ◽  
Isolated Lung ◽  
Anesthetized Dogs

We have micropunctured the lung in the open thorax of 17 anesthetized dogs to measure microvascular pressure. After intravenous pentobarbital sodium (25 mg/kg), we exposed the left lung through a wide left thoracotomy, which required rib excision. Through a double-lumen endotracheal tube, we ventilated the right lung to maintain normal blood gases and pH while we held the left lung motionless at an inflation pressure of 5 cmH2O. To reduce motion on the surface of the left lower lobe, we resected the left upper lobe, placed a Plexiglas baffle between the lobe and the heart, and held the lobe surface in a suction ring. In accordance with procedures we have previously described, we micropunctured subpleural vessels to measure microvascular pressure. At base line when alveolar pressure exceeded left atrial pressure (zone 2 conditions), 21, 38, and 41% of the total pressure drop occurred, respectively, in the arterial, microvascular, and venous segments. When we raised left atrial pressure above alveolar pressure (zone 3 conditions), the corresponding pressure drops were 30, 55, and 20% of total. The blood flow in the superficial layer of the lung averaged 15% less than the flow in the deeper layers as measured by distribution of 99mTc-albumin macroaggregates. We conclude that the intact and the isolated lung preparations in dog exhibit similar distributions of subpleural microvascular pressure.

Sign in / Sign up

Export Citation Format

Share Document