Blood flow vs. venous pressure effects on filtration coefficient in oleic acid-injured lung

1998 ◽  
Vol 84 (3) ◽  
pp. 1011-1023 ◽  
Author(s):  
Daniel Anglade ◽  
Michel Corboz ◽  
Ahmed Menaouar ◽  
James C. Parker ◽  
Sagazaga Sanou ◽  
...  

On the basis of changes in capillary filtration coefficient ( K fc) in 24 rabbit lungs, we determined whether elevations in pulmonary venous pressure (Ppv) or blood flow (BF) produced differences in filtration surface area in oleic acid-injured (OA) or control (Con) lungs. Lungs were cyclically ventilated and perfused under zone 3 conditions by using blood and 5% albumin with no pharmacological modulation of vascular tone. Pulmonary arterial, venous, and capillary pressures were measured by using arterial, venous, and double occlusion. Before and during each K fc-measurement maneuver, microvascular/total vascular compliance was measured by using venous occlusion. K fc was measured before and 30 min after injury, by using a Ppv elevation of 7 cmH2O or a BF elevation from 1 to 2 l ⋅ min−1 ⋅ 100 g−1 to obtain a similar double occlusion pressure. Pulmonary arterial pressure increased more with BF than with Ppv in both Con and OA lungs [29 ± 2 vs. 19 ± 0.7 (means ± SE) cmH2O; P < 0.001]. In OA lungs compared with Con lungs, values of K fc (200 ± 40 vs. 83 ± 14%, respectively; P < 0.01) and microvascular/total vascular compliance ratio (86 ± 4 vs. 68 ± 5%, respectively; P < 0.01) increased more with BF than with Ppv. In conclusion, for a given OA-induced increase in hydraulic conductivity, BF elevation increased filtration surface area more than did Ppv elevation. The steep pulmonary pressure profile induced by increased BF could result in the recruitment of injured capillaries and could also shift downstream the compression point of blind (zone 1) and open injured vessels (zone 2).

1990 ◽  
Vol 69 (6) ◽  
pp. 2183-2189 ◽  
Author(s):  
J. U. Raj ◽  
R. Hillyard ◽  
P. Kaapa ◽  
M. Gropper ◽  
J. Anderson

We have determined the sites of hypoxic vasoconstriction in ferret lungs. Lungs of five 3- to 5-wk-old and five adult ferrets were isolated and perfused with blood. Blood flow was adjusted initially to keep pulmonary arterial pressure at 20 cmH2O and left atrial and airway pressures at 6 and 8 cmH2O, respectively (zone 3). Once adjusted, flow was kept constant throughout the experiment. In each lung, pressures were measured in subpleural 20- to 50-microns-diam arterioles and venules with the micropipette servo-nulling method during normoxia (PO2 approximately 100 Torr) and hypoxia (PO2 less than 50 Torr). In normoxic adult ferret lungs, approximately 40% of total vascular resistance was in arteries, approximately 40% was in microvessels, and approximately 20% was in veins. With hypoxia, the total arteriovenous pressure drop increased by 68%. Arterial and venous pressure drops increased by 92 and 132%, respectively, with no change in microvascular pressure drop. In 3- to 5-wk-old ferret lungs, the vascular pressure profile during normoxia and the response to hypoxia were similar to those in adult lungs. We conclude that, in ferret lungs, arterial and venous resistances increase equally during hypoxia, resulting in increased microvascular pressures for fluid filtration.


1984 ◽  
Vol 247 (5) ◽  
pp. R800-R805 ◽  
Author(s):  
R. A. Brace ◽  
P. S. Gold

Fluid movements across the capillary wall were studied in chronically catheterized, near-term fetal sheep. We hemorrhaged 15 fetuses and infused isotonic saline in seven fetuses. The average experimental changes in arterial pressure, venous pressure, and blood volume were then analyzed by using mathematical modeling and parameter optimization techniques to estimate mean values for the average whole-body interstitial and vascular compliances of the fetus and for the average whole-body fetal capillary filtration coefficient. After fetal hemorrhage, interstitial compliance averaged 45 ml X mmHg-1 X kg-1 of fetal weight and vascular compliance averaged 3.0 ml X mmHg-1 X kg-1, whereas the capillary filtration coefficient averaged 0.4 ml X min-1 X mmHg-1 X kg-1. For intravenous saline infusions, interstitial compliance averaged 45 ml X mmHg-1 X kg-1, and vascular compliance averaged 3.5 ml X mmHg-1 X kg-1, whereas the capillary filtration coefficient averaged 0.8 ml X min-1 X mmHg-1 X kg-1. These data suggest that the fetus has a high whole-body interstitial compliance and a high capillary filtration coefficient compared with the adult. In addition, it appears that the fetus has the ability to decrease its vascular compliance and capillary surface area after a fetal hemorrhage.


1990 ◽  
Vol 68 (4) ◽  
pp. 1581-1589 ◽  
Author(s):  
T. Shibamoto ◽  
J. C. Parker ◽  
A. E. Taylor ◽  
M. I. Townsley

The capillary filtration coefficient (Kf,c) is a sensitive and specific index of vascular permeability if surface area remains constant, but derecruitment might affect Kf,c in severely damaged lungs with high vascular resistance. We studied the effect of high and low blood flow rates on Kf,c in papaverine-pretreated blood-perfused isolated dog lungs perfused under zone 3 conditions with and without paraquat (PQ, 10(-2) M). Three Kf,cs were measured successively at hourly intervals for 5 h. These progressed sequentially from isogravimetric blood flow with low vascular pressure (I/L) to high flow with low vascular pressure (H/L) to high flow with high vascular pressure (H/H). The blood flows of H/L and H/H were greater than or equal to 1.5 times that of I/L. There were no significant changes in Kf,c in lungs without paraquat over a 50-fold range of blood flow rates. At 3 h after PQ, I/L-Kf,c was significantly increased and both isogravimetric capillary pressure and total protein reflection coefficient were decreased from base line. At 4 and 5 h, H/L-Kf,c was significantly greater than the corresponding I/L-Kf,c (1.01 +/- 0.22 vs. 0.69 +/- 0.09 and 1.26 +/- 0.19 vs. 0.79 +/- 0.10 ml.min-1.cmH2O-1.100 g-1, respectively) and isogravimetric blood flow decreased to 32.0 and 12.0% of base line, respectively. Pulmonary vascular resistance increased to 12 times base line at 5 h after PQ. We conclude that Kf,c is independent of blood flow in uninjured lungs. However, Kf,c measured at isogravimetric blood flow underestimated the degree of increase in Kf,c in severely damaged and edematous lungs because of a high vascular resistance and derecruitment of filtering surface area.


1975 ◽  
Vol 39 (4) ◽  
pp. 672-679 ◽  
Author(s):  
P. Caldini ◽  
J. D. Leith ◽  
M. J. Brennan

The effect of CPPV on edema formation in lungs perfused at constant blood flow was studied in whole dogs and in isolated dog lungs. In intact animals, subjected to an increase in left atrial pressure relative to pleural pressure of 40 Torr, pulmonary shunts correlate inversely (r = -0.82) with the level of end-expiratory pressure (PEE). CPPV had no significant effect on total extravasation of liquid even though PEE higher than 20 Torr was effective in preventing liquid from accumulating in the airways. In isolated lobes, perfused at constant blood flow and at a venous pressure of zero, accumulation of liquid occurred when PEE was increased above 8–10 Torr. At comparable levels of pulmonary arterial pressure, an increase in PEE resulted in lesser accumulation of liquid than when pulmonary venous pressure was elevated. Morphometric measurements revealed no significant difference in the distribution of accumulated liquid within the lung parenchyma between lobes made edematous either by raising venous pressuure or by raising PEE. It would appear that CPPV, while beneficial in improving arterial oxygen tension in pulmonary edema, does not prevent extravasation of liquid in lungs perfused at constant blood flow. High levels of PEE appear to damage the lung by favoring accumulation of liquid in the extravascular spaces of the lung.


1990 ◽  
Vol 258 (5) ◽  
pp. H1550-H1558
Author(s):  
R. K. Minkes ◽  
P. J. Kadowitz

Cardiovascular responses to endothelin 2 (ET-2) and sarafotoxin 6b (S6b) were investigated in the cat. ET-2 (0.1-1 nmol/kg iv) decreased or elicited biphasic changes in arterial pressure (AP), whereas S6b (0.1-1 nmol/kg iv) only decreased AP. Central venous pressure (CVP), cardiac output (CO), and pulmonary arterial pressure (PAP) were increased. ET-2 produced biphasic changes in systemic vascular resistance (SVR), whereas S6b decreased SVR at the two lower doses and caused a biphasic change at the 1 nmol/kg dose. The effects of ET-1 and ET-2 were similar, whereas the effects of S6b were similar to ET-3. ET-2 and S6b had small effects on right ventricular contractile force and caused transient increases in heart rate. Distal aortic blood flow was increased in response to all doses of both peptides, whereas increases in carotid blood flow were observed only in response to the higher doses of ET-2 and S6b. ET-2 produced dose-dependent decreases in superior mesenteric artery (SMA) blood flow, whereas decreases in SMA flow in response to S6b were observed only at the 1 nmol/kg dose. Renal blood flow was decreased significantly only at the higher doses of ET-2 and S6b. The present data show that ET-2 and S6b can produce both vasodilation and vasoconstriction in the systemic and regional vascular beds of the cat and demonstrate previously unrecognized vasodilator activity in response to S6b. It is concluded that ET-2 and S6b produce complex cardiovascular responses in the anesthetized cat.


1987 ◽  
Vol 62 (5) ◽  
pp. 1982-1988 ◽  
Author(s):  
S. L. Soohoo ◽  
H. S. Goldberg ◽  
R. Graham ◽  
A. C. Jasper

In the West model of zonal distribution of pulmonary blood flow, increases in flow down zone 2 are attributed to an increase in driving pressure and a decrease in resistance resulting from recruitment and distension. The increase in flow down zone 3 is attributed to a decrease in resistance only. Recent studies indicate that, besides the pressure required to maintain flow through a vessel, there is an added pressure cost that must be overcome in order to initiate flow. These additional pressure costs are designated critical pressures (Pcrit). Because Pcrit exceed alveolar pressure, the distinction between zones in the West model becomes less secure, and the explanation for the increase in flow even in West zone 3 requires reexamination. We used two methods to test the hypothesis that the Pcrit is the pertinent backpressure to flow even in zone 3, when the pulmonary venous pressure (Ppv) exceeds alveolar pressure (PA) but is less than Pcrit in the isolated canine left caudal lobe. First, PA was maintained at 5 cmH2O, and pressure flow (P-Q) characteristics were obtained in zone 2 and zone 3. Next, with PA still at 5 cmH2O, we maintained a constant flow and measured the change in pulmonary arterial pressure as Ppv was varied. Both techniques indicated that the pertinent backpressure to flow was the greater of either Pcrit or Ppv and that PA was never the pertinent backpressure to flow. Also, our results indicate no significant change in the geometry of the flow channels between zone 2 and zone 3. These findings refine the zonal model of the pulmonary circulation.


2019 ◽  
pp. 901-908
Author(s):  
C.C. Bravo-Reyna ◽  
G. Torres-Villalobos ◽  
N. Aguilar-Blas ◽  
J. Frías-Guillén ◽  
J.R. Guerra-Mora

The purpose of calculating the capillary filtration coefficient is to experimentally evaluate edema formation in models of pulmonary ischemia-reperfusion injury. For many years, the obtaining of this coefficient implies a series of manual maneuvers during ex-vivo reperfusion of pulmonary arterial pressure, venous pressure and weight, as well as the calculation of the Kfc formula. Through automation, the calculation of capillary filtration coefficient could be easier and more efficient. To describe an automatic method designed in our laboratory to calculating the capillary filtration coefficient and compare with traditional determination of capillary filtration coefficient as gold standard method. An automatic three valve perfusion system was constructed, commanded by a mastery module connected to a graphical user interface. To test its accuracy, cardiopulmonary blocks of Wistar rats were harvested and distributed in manual (n=8) and automated (n=8) capillary filtration coefficient determination groups. Physiological parameters as pulmonary arterial pressure, pulmonary venous pressure, weight and capillary filtration coefficient were obtained. Results: Capillary filtration coefficient, pulmonary arterial pressure, venous arterial pressure shown no statistical significance difference between the groups. The automated perfusion system for obtaining Kfc was standardized and validated, giving reliable results without biases and making the process more efficient in terms of time and personal staff.


1994 ◽  
Vol 76 (6) ◽  
pp. 2342-2347 ◽  
Author(s):  
I. C. Ehrhart ◽  
L. L. McCloud ◽  
S. E. Orfanos ◽  
J. D. Catravas ◽  
W. F. Hofman

The elevated cardiac output associated with exercise increases lung lymph flow and may increase extravascular lung water. However, it is not known if extremely elevated cardiac output alters pulmonary vascular permeability. The hematocrit-protein method was used to determine the solvent drag reflection coefficient, an index of vascular permeability to proteins, in the isolated blood-perfused canine lung lobe. Microvascular pressure was obtained by double vascular occlusion. Lobes filtered fluid during perfusion at normal flow, 0.451 +/- 0.005 l/min (LF; n = 8), or high flow, 2.319 +/- 0.080 l/min (HF; n = 7). In the LF, venous pressure was elevated to 19.0 +/- 0.5 Torr to induce filtration, whereas Pv was 3.3 +/- 0.1 Torr in the HF. In HF vs. LF, respectively, arterial pressure was 61.4 +/- 7.1 vs. 28.0 +/- 1.0 Torr (P < 0.05), microvascular pressure was 31.9 +/- 3.0 vs. 22.2 +/- 0.9 Torr (P < 0.05), and sigma was 0.52 +/- 0.07 vs. 0.51 +/- 0.02 (P > 0.05). The fivefold increase in blood flow did not alter pulmonary vascular permeability to proteins; however, the capillary filtration coefficient was fivefold greater in the HF vs. LF group (0.328 +/- 0.059 vs. 0.067 +/- 0.007; P < 0.002). These data are compatible with enzyme activity measures indicating a direct linear relationship between blood flow rate and perfused pulmonary microvascular surface area. Although the data do not rule out the possibility of increased pulmonary vascular permeability to water during very elevated blood flow rates, the greater filtration rate during elevated flow is more likely related to increases in both microvascular pressure and surface area.


1982 ◽  
Vol 242 (6) ◽  
pp. G596-G602
Author(s):  
P. R. Kvietys ◽  
J. M. McLendon ◽  
G. B. Bulkley ◽  
M. A. Perry ◽  
D. N. Granger

The purpose of the present study was to characterize the intrinsic mechanisms involved in the regulation of blood flow and oxygenation in the totally isolated, perfused canine pancreas. Arterial pressure, venous outflow pressure, blood flow, arteriovenous oxygen difference, and capillary filtration coefficient were measured during graded arterial pressure reductions and venous pressure elevation. Reductions in arterial pressure caused pancreatic blood flow and vascular resistance to decrease, whereas venous pressure elevation resulted in a decreased blood flow and increased vascular resistance. The reductions in blood flow produced by arterial and venous pressure alterations were associated with increases in oxygen extraction and capillary filtration coefficient. During the same pressure perturbations, oxygen uptake remained constant between blood flows of 40-100 ml.min-1.100 g-1, yet decreased progressively as blood flow was reduced below 40 ml.min-1.100 g-1. Arterial occlusion resulted in a postocclusive reactive hyperemia, the magnitude of which was related to the duration of occlusion. The findings of this study suggest that intrinsic regulation of pancreatic blood flow can be attributed to both metabolic and myogenic mechanisms. Resistance and exchange vessels both appear to play a role in the regulation of oxygen delivery to the pancreatic parenchyma.


1964 ◽  
Vol 19 (4) ◽  
pp. 713-724 ◽  
Author(s):  
J. B. West ◽  
C. T. Dollery ◽  
A. Naimark

The left lung from a dog was removed, ventilated with negative pressure, and perfused with venous blood. Pulmonary arterial, venous, and alveolar pressures could be varied over a large range. The distribution of blood flow in the lung was measured with Xe133. Under these conditions, there was no blood flow above the level at which alveolar equaled arterial pressure (measured at the arterial cannula). Below this level there was a linear increase in blood flow down the lung when the venous pressure was kept low. Raising the venous pressure made the distribution of flow more uniform below the level at which venous and alveolar pressures were equal although flow still increased down this zone. The flow distribution could be completely accounted for by the mechanical effects of the pressure inside and outside the blood vessels which each behaved like a Starling resistance. It was possible to simulate the flow distributions found in man in various physiological and diseased states. pulmonary; hydrostatic effect; Starling resistance Submitted on November 15, 1963


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