Lung edema increases transvascular filtration rate but not filtration coefficient

1989 ◽  
Vol 66 (4) ◽  
pp. 1553-1560 ◽  
Author(s):  
J. C. Parker ◽  
M. I. Townsley ◽  
J. T. Cartledge
Keyword(s):  
Weight Gain ◽  
Filtration Rate ◽  
Autologous Blood ◽  
Filtration Coefficient ◽  
Lung Edema ◽  
Base Line ◽  
Edema Formation ◽  
Independent Variables ◽  
Highly Correlated ◽  
Severe Pulmonary Edema

To determine whether the accelerated rate of lobe weight gain during severe pulmonary edema is attributed to increased permeability of the microvascular barrier or a loss of tissue forces opposing filtration, the effect of edema on capillary filtration coefficient (Kf,C), interstitial compliance (Ci), and the volume of fluid filtered after a step increase in microvascular pressure (delta Vi) were determined in eight isolated left lower lobes of dog lungs perfused at 37 degrees C with autologous blood. After attaining a base-line isogravimetric state, the capillary pressure (Pc) was increased in successive steps of 2, 5, and 10 cmH2O. This sequence of vascular pressure increases was repeated three times. Edema accumulation was expressed as weight gained as a percent of initial lobe weight (% delta Wt), and Kf,C was measured by time 0 extrapolation of the weight gain curve. An exponential rate constant for the decrease in the rate of weight gain with time (K) was calculated for each curve. Ci was then calculated by assuming that the capillary wall and interstitium constitute a resistance-capacitance network. Kf,C was not increased by edema formation in any group. Between mild (% delta Wt less than 30%) and severe edema states (% delta Wt greater than 50%) respective mean Ci increased significantly from 3.54 to 9.12 ml.cmH2O-1.100 g-1, K decreased from 0.089 to 0.036 min-1, and delta Vi increased from 1.28 to 2.4 ml.cmH2O-1.100 g-1. The delta Vi during each Pc increase was highly correlated with Kf,C and Ci when used together as independent variables (r = 0.99) but less well correlated when used separately.(ABSTRACT TRUNCATED AT 250 WORDS)

Indirect estimate of perimicrovascular pressure rise in edema in isolated zone 1 lung

1988 ◽  
Vol 65 (1) ◽  
pp. 337-342 ◽  
Author(s):  
T. Tanita ◽  
M. Onizuka ◽  
N. C. Staub
Keyword(s):  
Reflection Coefficient ◽  
Filtration Rate ◽  
Time Course ◽  
Pressure Rise ◽  
Filtration Coefficient ◽  
Base Line ◽  
Autologous Plasma ◽  
Lung Weight ◽  
Edema Formation ◽  
Low Protein

To determine how liquid accumulation affects extra-alveolar perimicrovascular interstitial pressure, we measured filtration rate under zone 1 conditions (25 cmH2O alveolar pressure, 20 or 10 cmH2O vascular pressure) in isolated dog lung lobes in which all vessels were filled with autologous plasma. In the base-line condition, starting with normal extra-alveolar water content, filtration rate decreased by about one-half over 1 h as edema liquid slowly accumulated. We repeated each experiment after inducing edema (up to 100% lung weight gain). The absolute values and time course of filtration in the edema condition did not differ from base-line, i.e., the edema did not affect the time course of filtration. To compute the maximal initial and maximal change in extra-alveolar perimicrovascular pressure that occurred over each 1-h filtration study, we first assumed that the reflection coefficient is 0 in the Starling equation, then calculated perimicrovascular pressure and filtration coefficient from two equations with two unknowns. The mean filtration coefficient in 10 lobes is 0.063 g/(min X cmH2O X 100 g wet wt), and the initial perimicrovascular pressure is 3.9 cmH2O, rising by 4-7 cmH2O at 1 h. Finally we tested low protein perfusates and found the filtration rate was higher. We calculated an overall reflection coefficient = 0.44, a decrease in the initial perimicrovascular pressure to 1.9 cmH2O and a slightly lower increase after 1 h of edema formation, 2.2-6.6 cmH2O.

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.

Filtration coefficient obtained by stepwise pressure elevation in isolated dog lung

1984 ◽  
Vol 56 (4) ◽  
pp. 862-867 ◽  
Author(s):  
I. C. Ehrhart ◽  
W. M. Granger ◽  
W. F. Hofman
Keyword(s):  
Oleic Acid ◽  
Weight Gain ◽  
Lung Injury ◽  
Filtration Coefficient ◽  
Base Line ◽  
Lung Lobe ◽  
Pressure Elevation ◽  
Isolated Lung ◽  
Capillary Filtration Coefficient ◽  
Lower Lung

The base-line capillary filtration coefficient (Kf) obtained from rates of lobe weight gain during stepwise vascular pressure elevation is reported to be threefold greater in isolated than in intact dog lung. To further evaluate the stepwise pressure elevation technique, we obtained Kf in control and oleic acid-injured isolated lung. The left lower lung lobe was removed, placed on a balance, ventilated, and pump perfused with autogenous blood. Saline (n = 6) or oleic acid (n = 6) was infused, and rate of lobe weight gain was obtained during stepwise pressure elevation. Kf averaged 0.071 +/- 0.012 and 0.243 +/- 0.027 ml X min-1 X Torr-1 X 100 g-1 in the control and injured lobes, respectively. Stepwise pressure elevation can yield a base-line Kf in isolated lung similar to Kf's obtained from this and other gravimetric methods in intact and isolated lung. Furthermore, Kf increased severalfold following lung injury with oleic acid. The stepwise pressure elevation technique for Kf determination in isolated lung can be a useful tool for quantitating changes in vascular permeability.

Mechanisms leading to lung edema in pulmonary embolization

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz
Keyword(s):  
Pulmonary Edema ◽  
Capillary Permeability ◽  
Lysergic Acid ◽  
Lung Edema ◽  
Pulmonary Infarction ◽  
Edema Formation ◽  
Lung Lobe ◽  
Pulmonary Embolization ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.

Growth and seasonal weight changes as they relate to spring and autumn set points in mule deer

1991 ◽  
Vol 69 (3) ◽  
pp. 744-747 ◽  
Author(s):  
Lyle A. Renecker ◽  
W. M. Samuel
Keyword(s):  
Growth Rate ◽  
Weight Loss ◽  
Weight Gain ◽  
Mule Deer ◽  
Odocoileus Hemionus ◽  
Weight Changes ◽  
Annual Cycles ◽  
Body Weights ◽  
Compensatory Gain ◽  
Highly Correlated

Growth rate and potential, 25 hand-reared mule deer (Odocoileus hemionus hemionus) were examined. When possible, body weights of all animals were recorded weekly. Female deer matured faster than males, but males attained a larger body size. Regressions of winter weight loss of both sexes on peak autumn weight were highly correlated. Similarly, spring and summer compensatory gain in females could be predicted from the minimum spring weight. Annual cycles of intake and weight gain may have adaptations that improve reproductive success and winter survival.

Complement activation in the brain after experimental intracerebral hemorrhage

2000 ◽  
Vol 92 (6) ◽  
pp. 1016-1022 ◽  
Author(s):  
Ya Hua ◽  
Guohua Xi ◽  
Richard F. Keep ◽  
Julian T. Hoff
Keyword(s):  
Brain Edema ◽  
Complement Activation ◽  
Autologous Blood ◽  
Complement Cascade ◽  
Edema Formation ◽  
Content Type ◽  
Erythrocyte Lysis ◽  
The Brain ◽  
Brain Edema Formation ◽  
Fine Print

Object. Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. Erythrocyte lysis may be mediated by the complement cascade, which then triggers parenchymal injury. In this study the authors examine whether the complement cascade is activated after ICH and whether inhibition of complement attenuates brain edema around the hematoma.Methods. This study was divided into three parts. In the first part, 100 µl of autologous blood was infused into the rats' right basal ganglia, and the animals were killed at 24 and 72 hours after intracerebral infusion. Their brains were tested for complement factors C9, C3d, and clusterin (a naturally occurring complement inhibitor) by using immunohistochemical analysis. In the second part of the study, the rats were killed at 24 or 72 hours after injection of 100 µl of blood. The C9 and clusterin proteins were quantitated using Western blot analysis. In the third part, the rats received either 100 µl of blood or 100 µl of blood plus 10 µg of N-acetylheparin (a complement activation inhibitor). Then they were killed 24 or 72 hours later for measurement of brain water and ion contents. It was demonstrated on Western blot analysis that there had been a sixfold increase in C9 around the hematoma 24 hours after the infusion of 100 µl of autologous blood. Marked perihematomal C9 immunoreactivity was detected at 72 hours. Clusterin also increased after ICH and was expressed in neurons 72 hours later. The addition of N-acetylheparin significantly reduced brain edema formation in the ipsilateral basal ganglia at 24 hours (78.5 ± 0.5% compared with 81.6 ± 0.8% in control animals, p < 0.001) and at 72 hours (80.9 ± 2.2% compared with 83.6 ± 0.9% in control animals, p < 0.05) after ICH.Conclusions. It was found that ICH causes complement activation in the brain. Activation of complement and the formation of membrane attack complex contributes to brain edema formation after ICH. Blocking the complement cascade could be an important step in the therapy for ICH.

alpha-Trinositol decreases lung edema formation after smoke inhalation in an ovine model

1994 ◽  
Vol 76 (1) ◽  
pp. 278-282 ◽  
Author(s):  
H. Nakazawa ◽  
T. O. Gustafsson ◽  
L. D. Traber ◽  
D. N. Herndon ◽  
D. L. Traber
Keyword(s):  
Thermal Injury ◽  
Sham Group ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
Lung Edema ◽  
Ovine Model ◽  
Edema Formation ◽  
Surgical Preparation ◽  
Lung Lymph ◽  
Lung Lymph Flow

Inhalation injury is a dominant cause of mortality in thermally injured individuals. After acute lung injury induced by smoke inhalation, lung lymph flow (QL) increased and pulmonary microvascular reflection coefficient to protein (sigma) decreased. alpha-Trinositol (PP56, 1D-myo-inositol 1,2,6-trisphosphate) can decrease edema formation after thermal injury. We therefore tested the hypothesis that alpha-trinositol could decrease the pulmonary edema noted with inhalation injury. Seven days after surgical preparation, sheep were insufflated with smoke from burning cotton towels. The alpha-trinositol group (n = 8) were treated with alpha-trinositol (2 mg/kg + 3.5 mg.kg-1 x h-1). The sham group (n = 7) received an equal volume of 0.9% NaCl. The sham group showed a large increase in QL (9.3 +/- 1.7 to 54.1 +/- 8.8 ml/h) and a decrease in sigma (0.79 +/- 0.03 to 0.48 +/- 0.03) 24 h after smoke inhalation. alpha-Trinositol attenuated the increase in QL (8.1 +/- 1.2 to 25.6 +/- 6.9 ml/h) and the decrease in sigma (0.76 +/- 0.03 to 0.60 +/- 0.03) noted with smoke inhalation. alpha-Trinositol thus decreased the changes in pulmonary microvascular permeability and transvascular fluid flux noted with inhalation injury.

Pressure-dependent increase in lung vascular permeability to water but not protein

1992 ◽  
Vol 72 (1) ◽  
pp. 211-218 ◽  
Author(s):  
I. C. Ehrhart ◽  
W. F. Hofman
Keyword(s):  
Vascular Permeability ◽  
Plasma Proteins ◽  
Autologous Blood ◽  
Relative Increase ◽  
Solvent Drag ◽  
Lung Weight ◽  
Fluid Filtration ◽  
Lung Lobe ◽  
Highly Correlated ◽  
Lung Vascular Permeability

Simultaneous measures of vascular permeability to fluid (capillary filtration coefficient, Kf) and to plasma proteins (solvent drag reflection coefficient, sigma) were obtained over venous pressures (Pv) from 14 to 105 Torr in the isolated ventilated canine lung lobe (n = 70) pump perfused with autologous blood. The sigma was obtained from the relative increase in the concentration of plasma proteins vs. erythrocytes during fluid filtration. Kf's were obtained from two gravimetric methods as well as from change in hematocrit. All Kf's increased (P less than 0.05) as Pv was increased. However, sigma averaged 0.59 +/- 0.01 (range 0.54–0.67) and was unchanged (P greater than 0.05) by elevation of Pv over 20–105 Torr. In 44 lobes where all three Kf measures were obtained, gravimetric measures of Kf did not differ (P greater than 0.05) and were highly correlated with Kf obtained from hematocrit change, Vf Kf (P less than 0.001). However, both weight-based Kf's exceeded Vf Kf (P less than 0.05), suggesting that fluid filtration was overestimated by rate of lung weight gain or underestimated by hematocrit change. Increased permeability to water but not to protein over Pv from 20 to 105 Torr indicates that permeability to both can change independently and is counter to the theory that elevated vascular pressure “stretches” vascular pores.

Alpha-thrombin-induced pulmonary vasoconstriction

1987 ◽  
Vol 63 (5) ◽  
pp. 1993-2000 ◽  
Author(s):  
M. J. Horgan ◽  
J. W. Fenton ◽  
A. B. Malik
Keyword(s):  
Pulmonary Edema ◽  
Base Line ◽  
Thrombin Injection ◽  
Weight Changes ◽  
Lung Weight ◽  
Edema Formation ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Hemodynamic ◽  
Proteolytic Site ◽  
Synthase Inhibitor

We examined the direct effects of thrombin on pulmonary vasomotor tone in isolated guinea pig lungs perfused with Ringer albumin (0.5% g/100 ml). The injection of alpha-thrombin (the native enzyme) resulted in rapid dose-dependent increases in pulmonary arterial pressure (Ppa) and pulmonary capillary pressure (Ppc), which were associated with an increase in the lung effluent thromboxane B2 concentration. The Ppa and Ppc responses decreased with time but then increased again within 40 min after thrombin injection. The increases in Ppc were primarily the result of postcapillary vasoconstriction. Pulmonary edema as evidenced by marked increases (60% from base line) in lung weight occurred within 90 min after thrombin injection. Injection of modified thrombins (i.e., gamma-thrombin lacking the fibrinogen recognition site or i-Pr2P-alpha-thrombin lacking the serine proteolytic site) was not associated with pulmonary hemodynamic or weight changes nor did they block the effects of alpha-thrombin. Indomethacin (a cyclooxygenase inhibitor), dazoxiben (a thromboxane synthase inhibitor), or hirudin (a thrombin antagonist) inhibited the thrombin-induced pulmonary vasoconstriction, as well as the pulmonary edema. We conclude that thrombin-induced pulmonary vasoconstriction is primarily the result of constriction of postcapillary vessels, and the response is mediated by generation of cyclooxygenase-derived metabolites. The edema formation is also dependent on activation of the cyclooxygenase pathway. The proteolytic site of alpha-thrombin is required for the pulmonary vasoconstrictor and edemogenic responses.

Sign in / Sign up

Export Citation Format

Share Document