Effect of airway and left atrial pressures on microcirculation of newborn lungs

1990 ◽  
Vol 69 (3) ◽  
pp. 1063-1072
Author(s):  
C. D. Fike ◽  
S. J. Lai-Fook

To determine the effect of lung inflation and left atrial pressure on the hydrostatic pressure gradient for fluid flux across 20- to 60-microns-diam venules, we isolated and perfused the lungs from newborn rabbits, 7-14 days old. We used the micropuncture technique to measure venular pressures in some lungs and perivenular interstitial pressures in other lungs. For all lungs, we first measured venular or interstitial pressures at a constant airway pressure of 5 or 15 cmH2O with left atrial pressure greater than airway pressure (zone 3). For most lungs, we continued to measure venular or interstitial pressures as we lowered left atrial pressure below airway pressure (zone 2). Next, we inflated some lungs to whichever airway pressure had not been previously used, either 5 or 15 cmH2O, and repeated venular or interstitial pressures under one or both zonal conditions. We found that at constant blood flow a reduction of left atrial pressure below airway pressure always resulted in a reduction in venular pressure at both 5 and 15 cmH2O airway pressures. This suggests that the site of flow limitation in zone 2 was located upstream of venules. When left atrial pressure was constant relative to airway pressure, the transvascular gradient (venular-interstitial pressures) was greater at 15 cmH2O airway pressure than at 5 cmH2O airway pressure. These findings suggest that in newborn lungs edema formation would increase at high airway pressures only if left atrial pressure is elevated above airway pressure to maintain zone 3 conditions.

1993 ◽  
Vol 74 (5) ◽  
pp. 2112-2120
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz

The purpose of this study was to determine the effect of lung inflation and left atrial pressure on the hydrostatic pressure gradient for fluid flux across 20- to 80-microns-diam arterioles and venules in isolated perfused lungs of adult rabbits. We used the micropuncture technique and measured microvascular or interstitial pressures at constant airway pressures of 5 and 15 cmH2O with left atrial pressure adjusted above (zone 3 conditions) or below (zone 2 conditions) airway pressure. Only in lungs inflated to the higher airway pressure did a reduction in left atrial pressure below airway pressure result in concomitant reductions in venular pressure. This suggests that the site of flow limitation in zone 2 shifted from venules > 80 microns diam toward vessels <20 microns diam with inflation from 5 to 15 cmH2O. With the lungs under zone 3 conditions, both transarteriolar and transvenular gradients (microvascular-interstitial pressures) were greater at the higher compared with the lower airway pressure. In contrast, transarteriolar and transvenular gradients changed in opposite directions when compared at the two inflation pressures under zone 2 conditions. Counteracting changes in transmicrovascular gradients make it difficult to predict the effect on fluid filtration from lung inflation under zone 2 conditions. When zone 3 conditions are maintained during inflation, the tendency for edema formation should increase.


1990 ◽  
Vol 258 (2) ◽  
pp. H395-H399 ◽  
Author(s):  
B. D. Butler ◽  
R. E. Drake ◽  
W. D. Sneider ◽  
S. J. Allen ◽  
J. C. Gabel

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.


1977 ◽  
Vol 232 (1) ◽  
pp. H35-H43 ◽  
Author(s):  
S. M. Scharf ◽  
P. Caldini ◽  
R. H. Ingram

In paralyzed anesthetized dogs the cardiovascular effects of increasing positive end-expiratory pressure (PEEP) were explored under two conditions: a) end-expiratory lung volume increasing, b) end-expiratory lung volume kept nearly constant by matching pleural pressure rise to end-expiratory airway pressure rise. Two series of experiments were done: I) xenous return was allowed to fall, II) venous return was kept constant by infusion of volume. Right atrial pressure, pulmonary arterial pressure, and left atrial pressure increased under all conditions when measured relative to atmospheric pressure, but increased relative to pleural pressure only under condition a. The rise in left atrial relative to pleural pressure may indicate a degree of left ventricular dysfunction associated with increasing end-expiratory lung volume. Furthermore, when end-expiratory lung volume increased, inequality of the rise in pulmonary artery wedge pressure exceeded the rise in left atrial pressure in series I. From plots of cardiac output as a function of right atrial pressure it was possible to conclude that the decrease in venous return is partially offset by an increase in mean circulatory pressure.


1979 ◽  
Vol 46 (1) ◽  
pp. 74-78 ◽  
Author(s):  
R. S. Chang ◽  
P. Silverman ◽  
R. M. Effros

The vascular, interstitial, and cellular compartments of 15 isolated, perfused and ventilated rabbit lungs determined by a steady-state indicator-dilution procedure. Five lungs were perfused with constant pulmonary artery flow and zero left atrial pressure for more than 1 h. Edema formation was continuous and pulmonary vascular volume (PVV) decreased initially at a time when pulmonary vascular resistance (PVR) was falling. Increases in PVR were not seen until edema formation had become severe. In 10 other lungs, increases in pulmonary artery or left atrial pressure resulted in elevation of PVV and accelerated edema formation. The initially abrupt increase in PVV was followed by a more gradual increase over a 10-min period. Return of fluid to the vasculature was never observed in these studies. Labeled albumin readily entered the extravascular space but a relatively constant fraction of the interstitium remained inaccessible to albumin. No changes were found in the cellular volume during edema formation.


1988 ◽  
Vol 64 (2) ◽  
pp. 874-879 ◽  
Author(s):  
J. M. Shepard ◽  
M. A. Gropper ◽  
G. Nicolaysen ◽  
N. C. Staub ◽  
J. Bhattacharya

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.


2021 ◽  
Vol 77 (18) ◽  
pp. 1200
Author(s):  
Prince Sethi ◽  
Nikhil Parimi ◽  
Prakash Acharya ◽  
Amandeep Goyal ◽  
Emmanuel Daon ◽  
...  

2011 ◽  
Vol 25 (2) ◽  
pp. 244-250 ◽  
Author(s):  
S. Suzuki ◽  
T. Ishikawa ◽  
L. Hamabe ◽  
D. Aytemiz ◽  
H. Huai-Che ◽  
...  

Cardiology ◽  
1996 ◽  
Vol 87 (3) ◽  
pp. 224-229 ◽  
Author(s):  
Jer-Min Lin ◽  
Yi-Heng Li ◽  
Kwan-Lih Hsu ◽  
Juey-Jen Hwang ◽  
Yung-Zu Tseng

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