Altered Lung Vascular Permeability During Intermittent Haemodialysis

1988 ◽  
Vol 3 (4) ◽  
pp. 426-431 ◽  
Author(s):  
D. Bell ◽  
J. Nicoll ◽  
Melanie Jackson ◽  
A. Millar ◽  
R. J. Winney ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Intermittent Haemodialysis ◽  
Lung Vascular Permeability

scholarly journals The G protein βγ subunit mediates reannealing of adherens junctions to reverse endothelial permeability increase by thrombin

2009 ◽  
Vol 206 (12) ◽  
pp. 2761-2777 ◽  
Author(s):  
Nebojsa Knezevic ◽  
Mohammad Tauseef ◽  
Tracy Thennes ◽  
Dolly Mehta
Keyword(s):  
Vascular Permeability ◽  
Focal Adhesion ◽  
Inflammatory Mediator ◽  
Adherens Junctions ◽  
Endothelial Permeability ◽  
Endothelial Barrier ◽  
Dependent Manner ◽  
Permeability Increase ◽  
Lung Vascular Permeability

The inflammatory mediator thrombin proteolytically activates protease-activated receptor (PAR1) eliciting a transient, but reversible increase in vascular permeability. PAR1-induced dissociation of Gα subunit from heterotrimeric Gq and G12/G13 proteins is known to signal the increase in endothelial permeability. However, the role of released Gβγ is unknown. We now show that impairment of Gβγ function does not affect the permeability increase induced by PAR1, but prevents reannealing of adherens junctions (AJ), thereby persistently elevating endothelial permeability. We observed that in the naive endothelium Gβ1, the predominant Gβ isoform is sequestered by receptor for activated C kinase 1 (RACK1). Thrombin induced dissociation of Gβ1 from RACK1, resulting in Gβ1 interaction with Fyn and focal adhesion kinase (FAK) required for FAK activation. RACK1 depletion triggered Gβ1 activation of FAK and endothelial barrier recovery, whereas Fyn knockdown interrupted with Gβ1-induced barrier recovery indicating RACK1 negatively regulates Gβ1-Fyn signaling. Activated FAK associated with AJ and stimulated AJ reassembly in a Fyn-dependent manner. Fyn deletion prevented FAK activation and augmented lung vascular permeability increase induced by PAR1 agonist. Rescuing FAK activation in fyn−/− mice attenuated the rise in lung vascular permeability. Our results demonstrate that Gβ1-mediated Fyn activation integrates FAK with AJ, preventing persistent endothelial barrier leakiness.

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.

Effects of neuropeptide Y on lung vascular permeability in the pulmonary circulation of rats

1994 ◽  
Vol 256 (2) ◽  
pp. 227-230 ◽  
Author(s):  
Akiko Hirabayashi ◽  
Kimitoshi Nishiwaki ◽  
Kazumi Taki ◽  
Yasuhiro Shimada ◽  
Naohisa Ishikawa
Keyword(s):  
Neuropeptide Y ◽  
Vascular Permeability ◽  
Pulmonary Circulation ◽  
Lung Vascular Permeability

scholarly journals Participation of neuropeptide Y Y3-receptor subtype in the increase in lung vascular permeability---for therapy of respiratory failure

1999 ◽  
Vol 114 (supplement) ◽  
pp. 168-172
Author(s):  
Naohisa Ishikawa ◽  
Ossama Hamdy ◽  
Hiroshi Maekawa ◽  
Hidetsugu O. Murakami ◽  
Kimitoshi Nishiwaki ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Neuropeptide Y ◽  
Vascular Permeability ◽  
Receptor Subtype ◽  
Lung Vascular Permeability

scholarly journals Expression of urocortin in rat lung and its effect on pulmonary vascular permeability

2006 ◽  
Vol 189 (1) ◽  
pp. 167-178 ◽  
Author(s):  
Yuqing Wu ◽  
Yinyan Xu ◽  
Hong Zhou ◽  
Jin Tao ◽  
Shengnan Li
Keyword(s):  
Receptor Antagonist ◽  
Vascular Permeability ◽  
Alveolar Epithelium ◽  
Bronchial Epithelium ◽  
Rat Lung ◽  
Pulmonary Vascular Permeability ◽  
Peripheral Tissues ◽  
The Central Nervous System ◽  
Hematoxylin And Eosin ◽  
Lung Vascular Permeability

Urocortin (UCN), a newly identified, 40-amino-acid, corticotropin-releasing hormone (CRH) structurally related peptide, has been demonstrated to be expressed in the central nervous system and many peripheral tissues of rats and man. This study aimed to investigate the expression profile of UCN in rat lung and the effect of UCN on lung vascular permeability. The expression of UCN mRNA was detected by reverse transcriptase PCR (RT–PCR). UCN peptide was measured by immunohistochemistry and Western blot analysis. We found that both UCN mRNA and peptide were obviously expressed in rat lung. Immunohistochemistry results showed that UCN peptide is mainly expressed in bronchial epithelium mucosa and alveolar epithelium. We also found that rats receiving inhalation aerosol of UCN had a significant elevation of lung vascular permeability compared with rats receiving vehicle and ovalbumin (OVA) by the Evans blue (EB) technique. UCN aerosol inhalation resulted in obvious pulmonary congestion and edema observed under light microscope by hematoxylin and eosin (HE) staining. The nonselective peptide CRH receptor antagonist astressin markedly reduced lung vascular permeability triggered by UCN. Enhanced pulmonary vascular permeability induced by UCN was markedly inhibited by pretreatment with the mast-cell stabilizer cromolyn and histamine-1 (H1) receptor antagonist azelastine respectively, but not by the leukotriene receptor antagonist montelukast. In summary, in the present study, we demonstrated for the first time that UCN is expressed in rat lung and contributes to an increase in lung vascular permeability through activation of CRH receptors. Mast cells and histamine may be involved in this effect of UCN. Peripherally produced UCN in lung may act as an autocrine and paracrine proinflammatory factor.

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