Distribution of Pulmonary Blood Flow and Extravascular Lung Water in Chronic Pulmonary Disease

1970 ◽  
Vol 5 (4) ◽  
pp. 284
Author(s):  
Eric N.C. Milne
1996 ◽  
Vol 80 (5) ◽  
pp. 1513-1519 ◽  
Author(s):  
J. Tsang ◽  
B. Brush

Previous reports have shown that neutrophils are retained in the lung after acute embolization and that these neutrophils play an important role in the subsequent formation of permeability pulmonary edema. The present study was designed to test the hypothesis that acute embolic injury results in microvascular damage in lung regions with the greater retention of neutrophils. Seventeen pigs (20 +/- 2 kg) were embolized by injecting polystyrene beads (250 microns; labeled with 131I) into the right atrium over 5 min. Five pigs, which received no embolic beads, served as controls. Neutrophils (89 +/- 5% pure), isolated on Ficoll-Histopaque gradient, were radiolabeled with 111In-oxine. Twenty minutes after embolization, the radiolabeled neutrophils were injected into the right atrium along with 85Sr-labeled microspheres to mark the initial neutrophil distribution within the lung as well as the regional pulmonary blood flow at the time of their delivery. The animals were killed 50 min after embolization, and the lungs were removed, frozen over liquid nitrogen, and cut into 60 samples. The data show that after embolization regional neutrophil retention was inversely related to the regional blood flow but was not affected by the embolic load in the same region. Regional extravascular lung water was increased in regions of higher neutrophil retention, but the regions with increased edema did not receive a greater embolic load. These results show that microvascular injury occurs in the lung regions with the greatest neutrophil retention and that this increased retention of neutrophils is unrelated to the extent of embolization.


1980 ◽  
Vol 48 (3) ◽  
pp. 444-449 ◽  
Author(s):  
J. Bhattacharya ◽  
K. Nakahara ◽  
N. C. Staub

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.


1990 ◽  
Vol 22 (3) ◽  
pp. 136-142 ◽  
Author(s):  
K. Nakahara ◽  
S. Nanjo ◽  
A. Matsumura ◽  
Y. Kawashima

1980 ◽  
Vol 49 (5) ◽  
pp. 834-840 ◽  
Author(s):  
A. B. Malik ◽  
H. van der Zee ◽  
P. H. Neumann ◽  
N. B. Gertzberg

Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.


1992 ◽  
Vol 72 (3) ◽  
pp. 944-953 ◽  
Author(s):  
V. B. Serikov ◽  
M. S. Rumm ◽  
K. Kambara ◽  
M. I. Bootomo ◽  
A. R. Osmack ◽  
...  

A noninvasive method for measuring pulmonary blood flow and lung mass (called airway thermal volume), based on the measurements of lung heat exchange with environment, is described. The lungs function as a steady-state heat exchange system, having an inner heat source (pulmonary blood flow) and an external heat sink (ventilation). Sudden changes in the steady-state condition, such as caused by hyperventilation of dry air, lead to a new steady state after a few minutes. The expired air temperature difference between the initial and final steady states is proportional to pulmonary blood flow, whereas the rate at which the new steady state is achieved is proportional to airway thermal volume. The method was tested in 20 isolated dogs lungs, 9 perfused goat lungs, and 27 anesthetized sheep. The expired air temperature fall during hyperventilation was inversely proportional to the perfusion rate of the isolated lungs, and half-time of the temperature fall was proportional to the lung tissue mass. Experiments in anesthetized sheep showed that the measured airway thermal volume is close to the total mass of the excised lungs, including its residual blood (r = 0.98). Pulmonary edema and fluid instillation into the bronchial tree increased in the measured lung mass.


2006 ◽  
Vol 101 (2) ◽  
pp. 583-589 ◽  
Author(s):  
A. Cortney Henderson ◽  
David L. Levin ◽  
Susan R. Hopkins ◽  
I. Mark Olfert ◽  
Richard B. Buxton ◽  
...  

Head-down tilt has been shown to increase lung water content in animals and alter the distribution of ventilation in humans; however, its effects on the distribution of pulmonary blood flow in humans are unknown. We hypothesized that head-down tilt would increase the heterogeneity of pulmonary blood flow in humans, an effect analogous to the changes seen in the distribution of ventilation, by increasing capillary hydrostatic pressure and fluid efflux in the lung. To test this, we evaluated changes in the distribution of pulmonary blood flow in seven normal subjects before and after 1 h of 30° head-down tilt using the magnetic resonance imaging technique of arterial spin labeling. Data were acquired in triplicate before tilt and at 10-min intervals for 1 h after tilt. Pulmonary blood flow heterogeneity was quantified by the relative dispersion (standard deviation/mean) of signal intensity for all voxels within the right lung. Relative dispersion was significantly increased by 29% after tilt and remained elevated during the 1 h of measurements after tilt (0.84 ± 0.06 pretilt, 1.09 ± 0.09 calculated for all time points posttilt, P < 0.05). We speculate that the mechanism most likely responsible for our findings is that increased pulmonary capillary pressures and fluid efflux in the lung resulting from head-down tilt alters regional blood flow distribution.


Surgery ◽  
1997 ◽  
Vol 122 (2) ◽  
pp. 313-323 ◽  
Author(s):  
Paul G Gauger ◽  
Michael C Overbeck ◽  
Robert A Koeppe ◽  
Barry L Shulkin ◽  
Julia N Hrycko ◽  
...  

1961 ◽  
Vol 39 (2) ◽  
pp. 193-206 ◽  
Author(s):  
TAKASHI NAKAMURA ◽  
RYO KATORI ◽  
KOZUI MIYAZAWA ◽  
SHO OHTOMO ◽  
TATSUZO WATANABE ◽  
...  

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