Effects of lung inflation and blood flow on capillary transit time in isolated rabbit lungs

1992 ◽  
Vol 72 (6) ◽  
pp. 2420-2427 ◽  
Author(s):  
P. M. Wang ◽  
C. D. Fike ◽  
M. R. Kaplowitz ◽  
L. V. Brown ◽  
I. Ayappa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Transit Time ◽  
Transpulmonary Pressure ◽  
Lung Inflation ◽  
Video Signals ◽  
Pulmonary Capillary ◽  
Direct Measurements ◽  
Video Microscope ◽  
The Difference ◽  
Group 2

In a previous study, direct measurements of pulmonary capillary transit time by fluorescence video microscopy in anesthetized rabbits showed that chest inflation increased capillary transit time and decreased cardiac output. In isolated perfused rabbit lungs we measured the effect of lung volume, left atrial pressure (Pla), and blood flow on capillary transit time. At constant blood flow and constant transpulmonary pressure, a bolus of fluorescent dye was injected into the pulmonary artery and the passage of the dye through the subpleural microcirculation was recorded via the video microscope on videotape. During playback of the video signals, the light emitted from an arteriole and adjacent venule was measured using a video photoanalyzer. Capillary transit time was the difference between the mean time values of the arteriolar and venular dye dilution curves. We measured capillary transit time in three groups of lungs. In group 1, with airway pressure (Paw) at 5 cmH2O, transit time was measured at blood flow of approximately 80, approximately 40, and approximately 20 ml.min-1.kg-1. At each blood flow level, Pla was varied from 0 (Pla less than Paw, zone 2) to 11 cmH2O (Pla greater than Paw, zone 3). In group 2, at constant Paw of 15 cmH2O, Pla was varied from 0 (zone 2) to 22 cmH2O (zone 3) at the same three blood flow levels. In group 3, at each of the three blood flow levels, Paw was varied from 5 to 15 cmH2O while Pla was maintained at 0 cmH2O (zone 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of pulmonary blood flow during exercise using nitrous oxide

1962 ◽  
Vol 17 (4) ◽  
pp. 579-586 ◽  
Author(s):  
Margaret R. Becklake ◽  
C. J. Varvis ◽  
L. D. Pengelly ◽  
S. Kenning ◽  
M. McGregor ◽  
...  
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Dilution Technique ◽  
Fick Principle ◽  
Pulmonary Capillary Blood Flow ◽  
Time Period ◽  
Pulmonary Capillary ◽  
Wide Range ◽  
Pulmonary Capillary Blood ◽  
The Difference

Pulmonary capillary blood flow (Qc) in the exercising subject was calculated from the rate of disappearance of N2O during steady state breathing of an N2O-He-O2 mixture. Measurements were made after alveolar rinsing (reciprocal of N2 washout) had occurred, and up to 30 sec, a time period accompanied by minimal recirculation, since FaNN2O during this period did not rise significantly. Repeatability of the method, judged as the difference of a second estimate from a first on the same subject, was comparable to that reported for the direct Fick technique in resting subjects (31 of 33 paired observations agreed within 20%). Results over a wide range agreed with almost simultaneous measurements by a dye dilution technique (24 of 26 paired observations agreed within 20%), and when related to pulse rate and to Vo2, were comparable to those of the other workers whose subjects were studied in a similar posture. Indeed, this technique (using the indirect Fick principle under “steady state” conditions) probably attains its greatest accuracy during exercise when other methods become less easily applicable. Submitted on December 18, 1961

Processing of pulmonary afferent input patterns by respiratory I-beta neurons

1989 ◽  
Vol 256 (2) ◽  
pp. R379-R393 ◽  
Author(s):  
J. Bajic ◽  
E. J. Zuperku ◽  
F. A. Hopp
Keyword(s):  
Transpulmonary Pressure ◽  
Afferent Input ◽  
Central Component ◽  
Beta Activity ◽  
Neuronal Responses ◽  
Lung Inflation ◽  
Inhibitory Component ◽  
The Difference ◽  
Discharge Patterns ◽  
Fixed Times

To characterize the dynamics of the control of respiratory I-beta neurons by slowly adapting pulmonary stretch receptors, the neuronal discharge responses to lung inflation and electrically induced vagal input patterns were analyzed. Unitary recordings from single medullary I-beta neurons and whole phrenic nerve activity were recorded in chloralose-urethan-anesthetized paralyzed cats. Neuronal discharge patterns were quantified in terms of cycle-triggered histograms. The net response to a test afferent input pattern generated during neural inspiration was expressed as the difference between the central component of I-beta activity and the total response. The central component was obtained during control respiratory cycles in which lung inflation occurred during neural expiration and no vagal feedback occurred during neural inspiration. For a set of test inflations with different ramp rates, the net responses, measured at fixed times with respect to the onset of neural inspiration, were linearly related to transpulmonary pressure. However, the slopes of these relationships increased as a function of time during neural inspiration. Neuronal responses to electrically induced ramp vagal input patterns were similar to those produced by ramp inflation. The net response due to electrically induced ipsilateral step patterns consisted of a rapid excitatory and a slow inhibitory component, whereas only the slow inhibitory component was observed for contralateral patterns. The implications of these findings with respect to the modes of neural processing and effects on phrenic output patterns are discussed.

Transit time dispersion in the pulmonary arterial tree

1998 ◽  
Vol 85 (2) ◽  
pp. 565-574 ◽  
Author(s):  
Anne V. Clough ◽  
Steven T. Haworth ◽  
Christopher C. Hanger ◽  
Jerri Wang ◽  
David L. Roerig ◽  
...  
Keyword(s):  
Transit Time ◽  
Mean Transit Time ◽  
Arterial Tree ◽  
Lung Lobe ◽  
Transit Times ◽  
Pulmonary Capillary ◽  
Time Dispersion ◽  
Pulmonary Arterial ◽  
The Difference ◽  
In Transit

Knowledge of the contributions of arterial and venous transit time dispersion to the pulmonary vascular transit time distribution is important for understanding lung function and for interpreting various kinds of data containing information about pulmonary function. Thus, to determine the dispersion of blood transit times occurring within the pulmonary arterial and venous trees, images of a bolus of contrast medium passing through the vasculature of pump-perfused dog lung lobes were acquired by using an X-ray microfocal angiography system. Time-absorbance curves from the lobar artery and vein and from selected locations within the intrapulmonary arterial tree were measured from the images. Overall dispersion within the lung lobe was determined from the difference in the first and second moments (mean transit time and variance, respectively) of the inlet arterial and outlet venous time-absorbance curves. Moments at selected locations within the arterial tree were also calculated and compared with those of the lobar artery curve. Transit times for the arterial pathways upstream from the smallest measured arteries (200-μm diameter) were less than ∼20% of the total lung lobe mean transit time. Transit time variance among these arterial pathways (interpathway dispersion) was less than ∼5% of the total variance imparted on the bolus as it passed through the lung lobe. On average, the dispersion that occurred along a given pathway (intrapathway dispersion) was negligible. Similar results were obtained for the venous tree. Taken together, the results suggest that most of the variation in transit time in the intrapulmonary vasculature occurs within the pulmonary capillary bed rather than in conducting arteries or veins.

Effect of lung inflation and hypoxia on pulmonary arterial blood volume

1977 ◽  
Vol 43 (1) ◽  
pp. 8-13 ◽  
Author(s):  
E. J. Quebbeman ◽  
C. A. Dawson
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Transpulmonary Pressure ◽  
The Other ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Arterial Blood Volume

Isolated cat lungs were perfused with constant blood flow. During control conditions (Pa02, 100 Torr), pulmonary artery pressure increased as the lungs were inflated. Hypoxia (Pa02, 22 Torr) increased arterial pressure. However, as the lungs were inflated arterial pressure fell. Thus, the magnitude of the hypoxic pressor response was reduced by inflation. During control conditions, arterial volume (ether bolus method) increased with increasing transpulmonary pressure. Hypoxia decreased arterial volume, and the increase in arterial volume with inflation was somewhat less than that during control conditions. When the influences of vascular and transpulmonary pressures were examined independently by changing one while holding the other constant, increasing transpulmonary pressure increased arterial volume beyond that which could be accounted for by changes in the differences between arterial and pleural pressure. However, this influence of transpulmonary pressure did not appear to be altered by hypoxia. Thus, while hypoxia decreased arterial volume at all levels of lung inflation, it had relatively little effect on the influence of interdependence between the pulmonary arterial bed and the surrounding lung tissue.

Effect of alveolar and pleural pressures on interstitial pressures in isolated dog lungs

1991 ◽  
Vol 70 (2) ◽  
pp. 914-918 ◽  
Author(s):  
M. R. Glucksberg ◽  
J. Bhattacharya
Keyword(s):  
Transpulmonary Pressure ◽  
Pleural Pressure ◽  
Alveolar Pressure ◽  
Lung Lobe ◽  
Direct Measurements ◽  
The Difference

We report the first direct measurements of perialveolar interstitial pressures in lungs inflated with negative pleural pressure. In eight experiments, we varied surrounding (pleural) pressure in a dog lung lobe to maintain constant inflation with either positive alveolar and ambient atmospheric pleural pressures (positive inflation) or ambient atmospheric alveolar and negative pleural pressures (negative inflation). Throughout, vascular pressure was approximately 4 cmH2O above pleural pressure. By the micropuncture servo-null technique we recorded interstitial pressures at alveolar junctions (Pjct) and in the perimicrovascular adventitia (Padv). At transpulmonary pressure of 7 cmH2O (n = 4), the difference of Pjct and Pady from pleural pressure of 0.9 +/- 0.4 and -1.1 +/- 0.2 cmH2O, respectively, during positive inflation did not significantly change (P less than 0.05) after negative inflation. After increase of transpulmonary pressure from 7 to 15 cmH2O (n = 4), the decrease of Pjct by 3.3 +/- 0.3 cmH2O and Pady by 2.0 +/- 0.4 cmH2O during positive inflation did not change during negative inflation. The Pjct-Pady gradient was not affected by the mode of inflation. Our measurements indicate that, in lung, when all pressures are referred to pleural or alveolar pressure, the mode of inflation does not affect perialveolar interstitial pressures.

Regional differences in alveolar density in the human lung are related to lung height

2015 ◽  
Vol 118 (11) ◽  
pp. 1429-1434 ◽  
Author(s):  
John E. McDonough ◽  
Lars Knudsen ◽  
Alexander C. Wright ◽  
W. Mark Elliott ◽  
Matthias Ochs ◽  
...  
Keyword(s):  
Pressure Gradient ◽  
Regional Differences ◽  
Volume Fraction ◽  
Transpulmonary Pressure ◽  
Pleural Pressure ◽  
Lung Inflation ◽  
Residual Capacity ◽  
Alveolar Duct ◽  
The Difference

The gravity-dependent pleural pressure gradient within the thorax produces regional differences in lung inflation that have a profound effect on the distribution of ventilation within the lung. This study examines the hypothesis that gravitationally induced differences in stress within the thorax also influence alveolar density in terms of the number of alveoli contained per unit volume of lung. To test this hypothesis, we measured the number of alveoli within known volumes of lung located at regular intervals between the apex and base of four normal adult human lungs that were rapidly frozen at a constant transpulmonary pressure, and used microcomputed tomographic imaging to measure alveolar density (number alveoli/mm3) at regular intervals between the lung apex and base. These results show that at total lung capacity, alveolar density in the lung apex is 31.6 ± 3.4 alveoli/mm3, with 15 ± 6% of parenchymal tissue consisting of alveolar duct. The base of the lung had an alveolar density of 21.2 ± 1.6 alveoli/mm3 and alveolar duct volume fraction of 29 ± 6%. The difference in alveolar density can be negated by factoring in the effects of alveolar compression due to the pleural pressure gradient at the base of the lung in vivo and at functional residual capacity.

Influence of state of inflation of the lung on pulmonary vascular resistance

1960 ◽  
Vol 15 (5) ◽  
pp. 878-882 ◽  
Author(s):  
James L. Whittenberger ◽  
Maurice McGregor ◽  
Erik Berglund ◽  
Hans G. Borst
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Flow Resistance ◽  
Transpulmonary Pressure ◽  
Lung Inflation ◽  
Pulmonary Arterial ◽  
Low Levels ◽  
The Relationship ◽  
Complete Collapse

The relationship between the degree of pulmonary inflation and the pulmonary vascular resistance was studied in an open-chested dog preparation. It was possible to control the state of inflation and the blood flow to the lung under study. Vascular resistance could then be observed under controlled conditions. In most cases the resistance at complete collapse was very slightly higher than at moderate levels of inflation. In a few instances collapse was associated with a more marked elevation of resistance. Higher levels of inflation resulted in elevation of vascular resistance. At high levels of pulmonary blood flow and pulmonary arterial pressure, the flow resistance curve is lower than at low levels of blood flow. The resistance values obtained during deflation of the lung were consistently different at equal transpulmonary pressures from those obtained during inflation. The possible reasons for this hysteresis are discussed. Evidence is presented that the increased resistance at high levels of lung inflation is due to the effect of transpulmonary pressure on the vessels surrounding the alveoli. Submitted on January 11, 1960

Comparison of direct and indirect measurements of pulmonary capillary transit times

1987 ◽  
Vol 62 (3) ◽  
pp. 1150-1154 ◽  
Author(s):  
R. L. Capen ◽  
L. P. Latham ◽  
W. W. Wagner
Keyword(s):  
Transit Time ◽  
Diffusing Capacity ◽  
Indirect Measurements ◽  
Transit Times ◽  
Pulmonary Capillary ◽  
Direct Measurements ◽  
Capillary Blood Volume ◽  
Entire Lung ◽  
Time Required

Using in vivo microscopy, we made direct measurements of pulmonary capillary transit time by determining the time required for fluorescent dye to pass from an arteriole to a venule on the dependent surface of the dog lung. Concurrently, in the same animals, pulmonary capillary transit time was measured indirectly in the entire lung using the diffusing capacity method (capillary blood volume divided by cardiac output). Transit times by each method were the same in a group of five dogs [direct: 1.75 +/- 0.27 (SE) s; indirect: 1.85 +/- 0.33 s; P = 0.7]. The similarity of these transit times is important, because the widely used indirect determinations based on diffusing capacity are now shown to coincide with direct measurements and also because it demonstrates that measurements of capillary transit times on the surface of the dependent lung bear a useful relationship to measurements on the capillaries in the rest of the lung.

Correlation of γ-radioactivity and Scanning Electron Microscopy in measurement of retention of 111Indium-labeled canine endothelial cells on synthetic vascular grafts

1989 ◽  
Vol 47 ◽  
pp. 886-887
Author(s):  
E.J. Prendiville ◽  
S. Laliberté Verdon ◽  
K. E. Gould ◽  
K. Ramberg ◽  
R. J. Connolly ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ex Vivo ◽  
Vascular Grafts ◽  
Retention Data ◽  
Vascular Prostheses ◽  
Group 4 ◽  
Human Fibronectin ◽  
Insufficient Time ◽  
Group 3 ◽  
Group 2

Endothelial cell (EC) seeding is postulated as a mechanism of improving patency in small caliber vascular grafts. However the majority of seeded EC are lost within 24 hours of restoration of blood flow in previous canine studies . We postulate that the cells have insufficient time to fully develop their attachment to the graft surface prior to exposure to hemodynamic stress. We allowed EC to incubate on fibronectin-coated ePTFE grafts for four different time periods after seeding and measured EC retention after perfusion in a canine ex vivo shunt circuit.Autologous canine EC, were enzymatically harvested, grown to confluence, and labeled with 30 μCi 111 Indium-oxine/80 cm 2 flask. Four groups of 5 cm x 4 mm ID ePTFE vascular prostheses were coated with 1.5 μg/cm.2 human fibronectin, and seeded with 1.5 x 105 EC/ cm.2. After seeding grafts in Group 1 were incubated in complete growth medium for 90 minutes, Group 2 were incubated for 24 hours, Group 3 for 72 hours and Group 4 for 6 days. Grafts were then placed in the canine ex vivo circuit, constructed between femoral artery and vein, and subjected to blood flow of 75 ml per minute for 6 hours. Continuous counting of γ-activity was made possible by placing the seeded graft inside the γ-counter detection crystal for the duration of perfusion. EC retention data after 30 minutes, 2 hours and 6 hours of flow are shown in the table.

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