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.

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 lymphatic cannula outflow height on lung microvascular permeability estimations

1984 ◽  
Vol 57 (5) ◽  
pp. 1412-1416 ◽  
Author(s):  
G. A. Laine ◽  
R. E. Drake ◽  
F. G. Zavisca ◽  
J. C. Gabel
Keyword(s):  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lymph Vessel ◽  
Percent Change ◽  
Permeability Surface ◽  
Percent Increase ◽  
Anesthetized Dogs ◽  
Area Product ◽  
Lung Lymph

Estimates of the pulmonary microvascular membrane reflection coefficient (sigma) and permeability-surface area product (PS) are frequently made with the assumption that a percent change in transmicrovascular fluid flux (Jv) will be represented by an equal percent change in the lymph flow rate (QL) from a single cannulated lung lymph vessel. To test this, we measured QL in seven anesthetized dogs with the outflow end of the lymph cannula set at several heights (H) above and below the lung hilus. The left atrial pressure was then elevated to increase Jv, and QL was again measured at several H's. The percent increase in QL at elevated left atrial pressure depended on H. We used the QL data and lymph and plasma protein concentrations to estimate sigma and PS with a modified form of the Kedem and Katchalsky equations. The calculated values varied considerably with H. Our results indicate that changes in Jv are not represented by equal changes in QL. Therefore, techniques for estimating permeability that depend upon QL as an estimate of Jv may lead to erroneous estimates of sigma and PS.

Vasopressin-induced changes in cardiac vagal tone and oxygen consumption in dogs

1994 ◽  
Vol 266 (3) ◽  
pp. R838-R849
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Vagal Stimulation ◽  
Vagal Tone ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Beta Blockade ◽  
Cardiac Denervation ◽  
Anesthetized Dogs ◽  
Atropine Treatment

Experiments were conducted in 63 dogs to determine whether stimulation of vagal tone contributes to the decrease in O2 consumption (VO2) that results from arginine vasopressin (AVP) administration. Vagal stimulation with pilocarpine did not reduce VO2 in conscious dogs. In anesthetized dogs, bilateral electrical cervical efferent vagal stimulation lowered both cardiac output (CO; by 46%) and VO2 (by 22%) over the first 5 min. Between 7 and 11 min of stimulation, CO remained decreased, but VO2 returned to control. Significant increases in left atrial pressure, bradycardia, and a fall in mean arterial pressure accompanied vagal stimulation. All these effects of cervical vagal stimulation were abolished by cardiac denervation and also by pacing. Administration of a selective AVP V1 agonist led to significant reductions of CO and VO2. Cardiac denervation prevented the decrease in VO2 induced by AVP infusion, but not the decrease in CO. During AVP infusions, pacing at a rate slightly higher than control heart rate did not prevent the fall in CO or in VO2, whereas pacing at 150 beats/min prevented part of the fall in VO2. Sinoaortic denervation or atropine treatment prevented the decrease in VO2 resulting from AVP infusion. The combination of alpha- and beta-blockade did not affect the CO or the VO2 response to AVP infusion, nor did naloxone treatment. The administration of atrial or ventricular extracts, but not that of alpha-human atrial natriuretic peptide, led to a significant reduction in VO2. These results are compatible with the hypothesis that AVP infusion increases vagal tone to the heart, which, possibly as a result of increased left atrial pressure and reduced heart rate, may release a factor reducing VO2.

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.

Pulmonary neutrophil kinetics in sheep: effects of altered hemodynamics

1985 ◽  
Vol 59 (6) ◽  
pp. 1796-1801 ◽  
Author(s):  
J. A. Cooper ◽  
R. Bizios ◽  
A. B. Malik
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Left Atrial ◽  
Recovery Period ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Blood Volume ◽  
Neutrophil Kinetics

We investigated the effect of elevated left atrial pressure and reduced cardiac output on pulmonary neutrophil kinetics in the sheep. Sheep neutrophils were isolated, labeled with 111In-oxine, and reinfused. Erythrocytes were labeled with [99mTc]pertechnetate. A gamma camera measured the lung activities of the labeled neutrophils and erythrocytes. The results indicated that 38.5% of the total injected neutrophils marginated in the lung. Pulmonary hemodynamics were altered by inflating a left atrial balloon three times in each sheep for 15–30 min to achieve 5- to 25-mmHg increments in pulmonary arterial wedge pressure. At least a 30-min recovery period was allowed between inflations. After each left atrial balloon inflation, neutrophil uptake remained unchanged from base line, despite decreased mean cardiac output to 0.67 +/- 0.24 (+/- SD) 1/min and increased pulmonary blood volume. The absence of pulmonary neutrophil uptake was confirmed by arterial-venous measurements. Increased pulmonary blood volume had little effect on lung neutrophil uptake, suggesting that most of the pulmonary neutrophils are marginated. We conclude that the lungs have a large marginated neutrophil pool compared with the circulating pool and that reduced cardiac output and elevated left atrial pressure have no effect on pulmonary neutrophil kinetics in the sheep.

Assessment of alveolar-capillary membrane permeability of dogs by aerosolization

1981 ◽  
Vol 51 (4) ◽  
pp. 955-962 ◽  
Author(s):  
G. J. Huchon ◽  
J. W. Little ◽  
J. F. Murray
Keyword(s):  
Membrane Permeability ◽  
Left Atrial ◽  
Volume Of Distribution ◽  
The Body ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pressure Groups ◽  
Capillary Membrane ◽  
Anesthetized Dogs ◽  
Alveolar Capillary

We developed a method for measuring an index of alveolar-capillary membrane permeability (PI) by aerosolizing a mixture of 99mTc-diethylenetriaminepentaacetic acid (Tc-DTPA) and 125I-antipyrine (I-AP) and injecting 111In-DTPA (In-DTPA). The I-AP was used to compute the quantity of Tc-DTPA delivered and the In-DTPA the quantity of Tc-DTPA in the body. The PI was the ratio of the uptake of Tc-DTPA per minute to the amount deposited at the end of aerosolization. In 14 anesthetized dogs we measured the volume of distribution of I-AP (0.54 +/- 0.034 l/kg body wt) and/or showed that the volumes of distribution of Tc-DTPA and In-DTPA were similar. We measured PI in four groups of dogs: control (n = 5), oleic acid (n = 5), hydrochloric acid (n = 6), and high left atrial pressure (n = 5). The PI increased significantly in both groups with acid-induced increased permeability compared with the control and high left atrial pressure groups, which did not differ from each other. We conclude that the aerosolization method is suitable for differentiating increased from normal permeability.

Effects of coronary flow reduction on lung vascular tissue transport in sheep

1983 ◽  
Vol 55 (6) ◽  
pp. 1906-1915 ◽  
Author(s):  
T. R. Harris ◽  
J. C. Collins ◽  
R. J. Roselli
Keyword(s):  
Left Atrial ◽  
Coronary Flow ◽  
Vascular Tissue ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Flow Reduction ◽  
Second Period ◽  
Increased Pressure

This study was performed to measure the effects of a sustained reduction in coronary flow on lung lymph flow and protein content. Ten halothane-anesthetized sheep with cannulated lymphatic vessels were provided with a carotid-to-left anterior descending coronary artery cannula containing an electromagnetic flowmeter. One group of five animals was observed at base line and after coronary flow was reduced to 38% of base line. A second group of five animals acted as controls and was observed at base line, for 111 min of increased left atrial pressure, and a second period of normal pressures. Sustained coronary flow reduction led to significant increases in pulmonary arterial pressure, left atrial pressure, lymph flow, total protein lymph-to-plasma concentration ratio (L/P), and protein lymph clearance (L/P X lymph flow). Analysis of the pressure, lymph, protein, and indicator data with a two-pore model of the microvascular barrier showed that the observations were consistent with the concept that coronary flow reduction decreased functioning lung capillary surface but increased the size of the large pore and the number of small pores relative to the number of larger pores. Control studies showed increases in lymph flow and decreases in L/P with increased pressure but no significant changes in any variable between the first and second period of normal pressures. We conclude that coronary flow reduction increases lung vascular-tissue transport by decreasing the resistance of the microvascular barrier to protein and fluid movement. However, increased pressure secondary to left ventricular dysfunction plays a role in the magnitude of this response.

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.

Mechanism of diuretic response associated with atrial tachycardia

1975 ◽  
Vol 229 (6) ◽  
pp. 1486-1491 ◽  
Author(s):  
J Boykin ◽  
P Cadnapaphornchai ◽  
KM McDonald ◽  
RW Schrier
Keyword(s):  
Left Atrial ◽  
Atrial Tachycardia ◽  
Free Water ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Atrial Pacing ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs

Left atrial pacing was performed in three groups of anesthetized dogs. In the first group of eight intact dogs a mean increase in atrial rate (AR) from 140 +/- 7 to 244 +/- 6 was associated with a decrease in urinary osmolality (U osmol) from 631 +/- 72 to 264 +/- 43 mosmol/kg (P less than .001), and free-water clearance (CH20) increased from -.325 +/- .06 to +.355 +/- .15 ml/min (P less than .001). At the same time left atrial pressure (LAP) increased from 6 +/- 1 to 15 +/- 1 mmHg (P less than .001). A second group of studies was performed in six hypophysectomized, steroid-replaced animals receiving 40-50 muU/kg per min of antidiuretic hormone (ADH). In these animals AR was increased from 148 +/- 17 to 250 +/- 17 but diuresis did not occur. In these studies Uosmol was 690 +/- 55 before and 704 +/- 49 mosmol/kg after atrial pacing and CH20 also did not change. Left atrial pressure increased from 10 +/- 2 to 19 +/- 2 mmHg during atrial pacing. A third group of studies was performed in five animals with bilateral cervical vagotomy. In these animals AR was increased from 159 +/- 6 to 258 +/- 17 and LAP increased from 7 +/- 1 to 16 +/- 2 mmHg. Osmolality increased from 808 +/- 72 to 1,049 +/- 65 musmol/kg (P less than .005) and CH20 was unchanged. These results, therefore, indicate that atrial tachycardia primarily increases renal water excretion by suppressing ADH release. This reflex is dependent on the integrity of cervical vagal pathways.

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.

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