Effect of histamine and alloxan on canine pulmonary vascular permeability

1980 ◽  
Vol 239 (1) ◽  
pp. H96-H100
Author(s):  
R. E. Drake ◽  
J. C. Gabel
Keyword(s):  
Membrane Permeability ◽  
Capillary Pressure ◽  
Vascular Permeability ◽  
Membrane Filtration ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Pulmonary Vascular Permeability ◽  
Constant Weight ◽  
Pulmonary Capillary ◽  
Capillary Membrane

We estimated the pulmonary capillary membrane filtration coefficient (Kf) and the maximum capillary pressure (PCcritical) at which the lung could maintain a constant weight in 1) 5 control experiments in anesthetized open-chested dogs, 2) 7 experiments in which the dogs were given 3.6-8.3 microgram . kg-1 . min-1 of histamine phosphate, and 3) in 6 experiments after 75-100 mg/kg of alloxan. In additional experiments, pulmonary lymph flow (QL) and protein concentration (CL) were measured during the infusion of histamine and alloxan. After histamine, Kf averaged 0.045 +/- 0,008 ml . min-1mmHg-1 (SE) and PCcritical was 22.1 +/- 1.1 mmHg. These values were not significantly different from the control Kf and PCcritical (0.036 +/- 0.006 and 22.5 +/- 2.3, respectively). After alloxan, Kf (1.43 +/- 0.69) was larger and PCcritical (12.4 +/- 1.3) was significantly less than control (P less than 0.05). Histamine caused no significant change in QL or CL; however, both were increased after alloxan. These results show that Kf, PCcritical, QL, and CL are all changed by an increase in capillary membrane permeability caused by alloxan. Because none of these factors as significantly affected by histamine, dog lung capillary membrane permeability may not be affected by histamine.

Granulocytes mediate the increase in pulmonary vascular permeability after thrombin embolism

1983 ◽  
Vol 54 (6) ◽  
pp. 1489-1495 ◽  
Author(s):  
M. V. Tahamont ◽  
A. B. Malik
Keyword(s):  
Vascular Permeability ◽  
Control Group ◽  
Base Line ◽  
Protein Ratio ◽  
Pulmonary Vascular Permeability ◽  
Pulmonary Capillary ◽  
Cellular Factors ◽  
Pulmonary Embolization ◽  
Lung Lymph

We examined the effect of pulmonary embolization with microthrombi on the lung vascular permeability to proteins and the role of platelets and granulocytes as putative cellular factors in mediating the alterations in permeability. Anesthetized artificially ventilated sheep were prepared with lung lymph fistulas. Pulmonary embolization was induced using thrombin. Pulmonary vascular resistance (PVR) was increased approximately threefold from baseline. Pulmonary lymph flow (Qlym) increased 2 h after thrombin, but the lymph-to-plasma protein ratio (L/P) did not change significantly from base line. Raising the pulmonary capillary pressure (Pc) by inflating a left atrial balloon produced a large increase in Qlym but no change in L/P, indicating a permeability-increasing effect of thrombin. Reduction of platelet count with antiplatelet serum before thrombin also produced an increase in Qlym without a change in L/P. Raising Pc in this group resulted in changes comparable with those in the control group, i.e., increased Qlym without a change in L/P. In contrast to both control and platelet-depleted groups, reduction of the granulocyte count with hydroxyurea did not affect Qlym or L/P after thrombin. Raising Pc in this group increased Qlym but decreased L/P, indicating normal capillary sieving of proteins. Therefore embolization of pulmonary vessels with microthrombi increases pulmonary vascular permeability, and the increase is mediated by granulocytes.

Fibronectin deficiency and intestinal transvascular fluid balance during bacteremia

1982 ◽  
Vol 242 (4) ◽  
pp. H557-H564
Author(s):  
B. C. Dillon ◽  
T. M. Saba
Keyword(s):  
Vascular Permeability ◽  
Fluid Balance ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Fluid Flux ◽  
Fluid Filtration ◽  
Coated Particles ◽  
P Protein ◽  
Small Intestinal

Reticuloendothelial (RE) clearance dysfunction, which can be induced by opsonic fibronectin deficiency, has been correlated with organ failure during sepsis. We investigate the role of opsonic fibronectin deficiency and RE blockade in modulating alterations in intestinal transvascular fluid balance induced by Pseudomonas bacteremia using an isolated, innervated, and autoperfused canine small intestinal segment. Intravenous infusion of gelatin-coated particles was used to induce fibronectin deficiency and RE blockade. Lymph flow and lymph/plasma (L/P) protein concentration ratios were stable following intravenous challenge with bacteria or gelatin-coated particles. In contrast, lymph flow increased and L/P ratio decreased significantly when bacteremia coexisted with particle-induced opsonic fibronectin deficiency and RE blockade. This elevation in lymph flow and decline in L/P ratio was associated with normal vascular permeability to albumin, IgG, and IgM. The increase in intestinal fluid flux during bacteremia with RE blockade appears to be due to an increase in microvascular hydrostatic pressure and not to an increase in vascular permeability. These findings emphasize a potentially important role for fibronectin and associated RE system function as determinants of fluid filtration during sepsis.

Effects of transient pulmonary hypertension on pulmonary vascular permeability

1983 ◽  
Vol 55 (3) ◽  
pp. 983-989 ◽  
Author(s):  
F. L. Minnear ◽  
P. S. Barie ◽  
A. B. Malik
Keyword(s):  
Pulmonary Edema ◽  
Vascular Permeability ◽  
Left Atrial ◽  
Lymph Flow ◽  
Balloon Inflation ◽  
Lung Water ◽  
Lung Weight ◽  
Pulmonary Vascular Permeability ◽  
Airway Edema ◽  
Vascular Surface

The effects of a transient increase in pulmonary microvascular pressure (Pmv) on pulmonary fluid and protein exchange were studied in anesthetized sheep in which pulmonary lymph was collected. Pmv was increased to 30-40 mmHg for 15-30 min in 18 sheep by either an intra-aortic injection of norepinephrine (NE) or a rapid inflation of a left atrial balloon. NE injection produced sustained two- to threefold increases in pulmonary lymph flow and protein flux, whereas rapid balloon inflation transiently elevated lymph flow even though Pmv increased to similar levels with both methods. The sustained increases with NE were not due to an increase in vascular permeability but probably the result of a persistent increase in vascular surface area. In three additional animals, Pmv was increased to over 50 mmHg for 15-30 min. In these animals, lymph flow increased only by 49%, but airway edema fluid was present. The ratio of extravascular lung water to bloodless dry lung weight was 5.77 +/- 0.13 as compared with 4.30 +/- 0.11 in sheep subjected to Pmv less than 50 mmHg and to 4.08 +/- 0.19 for controls. These findings indicate that high pressure-induced pulmonary edema depends on a threshold Pmv around 50 mmHg. A combination of high capillary pressure and impaired lymphatic flow may be the bases for the development of neurogenic and catecholamine-induced pulmonary edema.

TNF-alpha release in endotoxemia contributes to neutrophil-dependent pulmonary edema

1993 ◽  
Vol 264 (4) ◽  
pp. H1161-H1165 ◽  
Author(s):  
M. J. Horgan ◽  
G. P. Palace ◽  
J. E. Everitt ◽  
A. B. Malik
Keyword(s):  
Water Content ◽  
Vascular Permeability ◽  
Weight Ratio ◽  
Tnf Alpha ◽  
Human Neutrophils ◽  
Dependent Manner ◽  
Pulmonary Vascular Permeability ◽  
Lps Challenge ◽  
Pulmonary Capillary ◽  
Wet Weight

We examined whether the generation of tumor necrosis factor (TNF-alpha) after lipopolysaccharide (LPS) challenge contributes to increases in lung vascular permeability and water content. Guinea pig lungs perfused at constant flow with Ringer-albumin solution (0.5 g/100 ml) were challenged for 120 min with LPS (Escherichia coli; final concentration 33 ng/ml; n = 5). Lung effluent samples were assayed for TNF-alpha activity using the modified L-929 fibroblast cytolytic assay. TNF-alpha concentrations increased in a time-dependent manner with a peak value of 100 +/- 20 pg/ml noted 90-120 min after LPS. Human neutrophils [polymorphonuclear leukocytes (PMN; 2 x 10(7)] added to the perfusion solution after endotoxin challenge (n = 5) produced a threefold increase in lung tissue myeloperoxidase (MPO) activity over control values. PMN, added after LPS and activated using phorbol 12-myristate 13-acetate (PMA; 5 x 10(-9) M; n = 6), produced three- to sixfold increases in mean pulmonary arterial pressure (Ppa) and pulmonary capillary pressure (Pcap), wet weight-to-dry weight ratio (W/D), and the pulmonary capillary filtration coefficient (Kf,c) over control values (P < 0.05). Activation of PMN with PMA in non-LPS-challenged lungs produced only threefold increases in Ppa and Pcap and did not change W/D and Kf,c. Infusion of an anti-TNF-alpha antibody before the LPS challenge reduced by approximately 50% the increases in Ppa, Pcap, MPO content, Kf,c, and lung wet weight gain (P < 0.05). Therefore, endotoxin-induced TNF-alpha generation in lungs significantly contributes to pulmonary sequestration of PMN. Activation of the sequestered PMN increases pulmonary vascular permeability and tissue water content.

Effect of complement activation with cobra venom factor on pulmonary vascular permeability

1986 ◽  
Vol 61 (6) ◽  
pp. 2202-2209 ◽  
Author(s):  
A. Johnson ◽  
J. A. Cooper ◽  
A. B. Malik
Keyword(s):  
Vascular Permeability ◽  
Plasma Protein ◽  
Complement Activation ◽  
Concentration Ratio ◽  
Protein Concentration ◽  
Cobra Venom ◽  
Plasma Protein Concentration ◽  
Cobra Venom Factor ◽  
Pulmonary Vascular Permeability ◽  
Protein Clearance

We examined the effect of acute complement activation on lung vascular permeability to proteins in awake sheep prepared with lung lymph fistulas. Complement was activated by cobra venom factor (CVF) infusion (400 U/kg for 1 h iv). Studies were made in two groups of sheep: 1) infusion of CVF containing the endogenous phospholipase A2 (PLA2) (n = 6); and 2) infusion of CVF pretreated with bromophenacyl bromide to inhibit PLA2 activity (n = 5). Intravascular complement activation transiently increased mean pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (PVR) in both groups. Pulmonary lymph flow (Qlym) and lymph protein clearance (Qlym X lymph-to-plasma protein concentration ratio) were also transiently increased in both groups. Pulmonary vascular permeability to proteins was assessed by raising left atrial pressure and determining the lymph-to-plasma protein concentration ratio (L/P) at maximal Qlym. In both groups the L/P at maximal Qlym was not different from normal. In a separate group (n = 4), CVF-induced complement activation was associated with 111In-oxine granulocyte sequestration in the lungs. In vitro plasma from CVF-treated animals aggregated neutrophils but did not stimulate neutrophils to produce superoxide anion generation. Therefore, CVF-induced complement activation results in pulmonary neutrophil sequestration and in increases in PVR and lymph protein clearance. The increase in lymph protein clearance is due to increased pulmonary microvascular pressure and not increased vascular permeability to proteins.

Increased pulmonary microvasuclar permeability induced by alpha-naphthylthiourea

1982 ◽  
Vol 52 (5) ◽  
pp. 1316-1323 ◽  
Author(s):  
G. Rutili ◽  
P. Kvietys ◽  
D. Martin ◽  
J. C. Parker ◽  
A. E. Taylor
Keyword(s):  
Vascular Permeability ◽  
Total Protein ◽  
Normal Lung ◽  
Base Line ◽  
Lung Water ◽  
Period 2 ◽  
Pulmonary Capillary ◽  
Capillary Membrane ◽  
Permeability Increase ◽  
Osmotic Reflection Coefficient

The effects of alpha-naphthylthiourea (ANTU) on lung microvascular permeability to plasma proteins were studied in anesthetized open-chest dogs. Lymph flow (Jv) was recorded, and total protein in plasma and lymph was analyzed after cannulating a small prenodal lung lymphatic. The protocol involved four experimental periods. Period 1. During this base-line period the preparation stabilized and steady states were reached in Jv, lymph total protein, pulmonary arterial pressure (Ppa), and left atrial pressure (Pla). Period 2. Pla was increased to approximately 20 cmH2O and maintained at that level until Jv and protein measurements attained a new steady state. Period 3. After Pla was lowered to control levels, ANTU (5 mg/kg body wt) was infused intravenously and parameters were measured for 3 h. Period 4 Pla was again raised to the pre-ANTU levels of period 2 and maintained for an additional 2–3 h. The lymphatic total protein clearance increased 8.6-fold for an equivalent increase in pulmonary capillary pressure after ANTU. Vascular permeability was assessed by estimating the osmotic reflection coefficient (sigma d) for total protein at the pulmonary capillary membrane. Sigma d decreased from 0.65 to 0.40 following ANTU. From plasma protein fractions in four experiments, equivalent pore radii for the capillary membrane of 95 and 280 A were calculated after ANTU compared with 80 and 200 A for normal lung capillaries. In addition, extravascular lung water increased from 3.8 +/- 0.16 to 5.87 +/- 0.25 following ANTU and to 7.55 +/- 0.55 (g/g blood-free dry wt) when Pla was elevated with ANTU. The experimental design allowed quantitative assessment of the vascular permeability increase after ANTU by use of lymph protein fluxes that had minimal errors due to changes in surface area or lymph contamination from nonpulmonary structures.

Increase in pulmonary capillary permeability in dogs exposed to 100% O2

1988 ◽  
Vol 65 (3) ◽  
pp. 1140-1146 ◽  
Author(s):  
F. Royer ◽  
D. J. Martin ◽  
G. Benchetrit ◽  
F. A. Grimbert
Keyword(s):  
Protein Concentration ◽  
Reference Data ◽  
Capillary Permeability ◽  
Lymph Flow ◽  
Plasma Protein Concentration ◽  
Capillary Filtration ◽  
Pulmonary Capillary ◽  
Hyperoxic Exposure ◽  
Two Stages ◽  
Minimal Estimate

Changes in pulmonary capillary filtration induced by hyperoxia were investigated in 15 dogs. After 12 h of normobaric hyperoxic exposure, animals were anesthetized and artificially ventilated with 100% O2. A pulmonary lymphatic vessel was cannulated, and lymph flow and protein content were measured together with pulmonary and systemic hemodynamics. An increase in pulmonary capillary filtration was found when compared with reference data (normoxic dogs in similar conditions) gathered from available literature: lymph flow increased from 21.8 +/- 13.4 to 125.2 +/- 131.6 microliter/min, and the lymph-to-plasma protein concentration ratio increased from 0.67 +/- 0.08 to 0.78 +/- 0.08. To characterize the mechanisms involved, left atrial pressure was increased in two stages (approximately 10 and approximately 25 mmHg). The results clearly indicated an increase in pulmonary capillary permeability as evidenced by a decrease of the minimal estimate of the protein reflection coefficient from 0.62 +/- 0.05 to 0.42 +/- 0.05.

Leukocyte repletion reverses protective effect of neutropenia in thrombin-induced increase in lung vascular permeability

1990 ◽  
Vol 259 (1) ◽  
pp. H149-H155 ◽  
Author(s):  
S. K. Lo ◽  
R. R. Garcia-Szabo ◽  
A. B. Malik
Keyword(s):  
Vascular Permeability ◽  
Lymph Flow ◽  
Control Group ◽  
Base Line ◽  
Pulmonary Vascular Permeability ◽  
Protein Clearance ◽  
Pulmonary Hemodynamic ◽  
Lung Lymph ◽  
Lung Vascular Permeability

We examined the role of leukocytes in the pathogenesis of lung vascular injury induced by thrombin in awake sheep prepared with the lung lymph fistulas. Thrombin (80 U/kg) infusion in control sheep (n = 6) increased pulmonary arterial pressure (Ppa) twofold and pulmonary vascular resistance (PVR) three-fold for the 5-h experimental period. Thrombin also increased pulmonary vascular permeability to protein as assessed by decrease in the reflection coefficient (sigma) from 0.70 +/- 0.03 to 0.61 +/- 0.01. Thrombin caused similar initial pulmonary hemodynamic changes in sheep rendered neutropenic (n = 7; 2% neutrophil count of controls) by treatment with hydroxyurea; however, both Ppa and PVR returned toward base-line values within 120 min postthrombin challenge. The increases in pulmonary lymph flow and transvascular protein clearance also recovered rapidly beginning at 60 min after challenge with thrombin in neutropenic sheep. Neutropenia prevented the increase in lung vascular permeability as the sigma value of 0.71 +/- 0.02 was similar to the control value. Leukocytes isolated from control donor sheep were infused intra-arterially into recipient neutropenic sheep (n = 4) to assess the effects of neutrophil repletion on the pulmonary vascular responses. Thrombin (80 U/kg) challenge infused at 1-3 h after infusion of leukocytes increased lung lymph flow twofold and transvascular protein clearance fourfold and produced increases in Ppa and PVR comparable with the control group. The increases in these parameters were sustained for the 5-h experiment duration. The data indicate the essential pathogenetic role of neutrophils in mediating the thrombin-induced increase in lung vascular permeability.

Effects of bradykinin on intestinal transcapillary fluid exchange

1981 ◽  
Vol 59 (8) ◽  
pp. 786-789 ◽  
Author(s):  
J. A. Barrowman ◽  
M. A. Perry ◽  
P. R. Kvietys ◽  
M. Ulrich ◽  
D. N. Granger
Keyword(s):  
Pressure Gradient ◽  
Capillary Pressure ◽  
Protein Concentration ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Oncotic Pressure ◽  
Fluid Exchange ◽  
Intestinal Lymph ◽  
Pressure Exchange ◽  
Exchange Vessel

Bradykinin (50 μg∙L−1) increases intestinal lymph flow sixfold when infused intraarterially into the cat ileum. The capillary filtration coefficient and capillary pressure increase and interstitial fluid pressure rises from negative to positive values. A slight increase in lymph:plasma protein concentration occurs with a resulting fall in the transcapillary oncotic pressure gradient. These results indicate that the effect of bradykinin on intestinal lymph flow is attributable, at least in part, to increased capillary pressure, exchange vessel surface area, and a reduction in the effective transcapillary oncotic pressure gradient.

C-reactive protein inhibits increased pulmonary vascular permeability induced by fMLP in isolated rabbit lungs

1996 ◽  
Vol 271 (2) ◽  
pp. H507-H513 ◽  
Author(s):  
V. J. Abernathy ◽  
R. O. Webster ◽  
T. E. Dahms
Keyword(s):  
Vascular Permeability ◽  
Protein Concentration ◽  
Pressor Response ◽  
Serum Concentrations ◽  
C Reactive Protein ◽  
Pulmonary Vascular Permeability ◽  
Reactive Protein ◽  
Permeability Changes ◽  
Transient Rise ◽  
Pulmonary Arterial

Increased serum concentrations of C-reactive protein (CRP) have previously been shown to downregulate neutrophil (PMN) influx and vascular permeability changes in models of localized inflammation such as alveolitis [R. M. Heuertz, D. Xia, D. Samols, and R. O. Webster, Am. J. Physiol. 266 (Lung Cell. Mol. Physiol. 10): L649–L654, 1994]. Experiments in isolated, buffer-perfused rabbit lungs were used to determine whether CRP attenuates vascular lung injury induced by PMNs stimulated with the chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (fMLP). Peritoneal PMN were added to the perfusate of lungs from PMN-depleted rabbits. Stimulation with fMLP produced an immediate and transient rise in pulmonary artery pressure that peaked at 35–40 cmH2O. An increase in permeability occurred 60 min after fMLP, which was marked by a 70% increase (P < 0.05) in filtration coefficient and bronchoalveolar lavage (BAL) protein concentration. CRP pretreatment of PMNs prevented fMLP-induced increases in permeability and significantly reduced the BAL protein below levels in control lungs (P < 0.05). CRP pretreatment of PMNs did not alter the pulmonary arterial pressor response to fMLP and had no effect on the production of leukotrienes, thromboxane, prostacyclin, or superoxide anion induced by fMLP. The mechanism by which CRP protects lung tissue from vascular injury induced by activation of PMNs remains unclear.

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