Effect of prostaglandin E1 on leukotriene C4-induced increases in vascular permeability of hamster cheek pouch

Inflammation ◽  
1992 ◽  
Vol 16 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Tan Yong ◽  
William G. Mayhan
Keyword(s):  
Vascular Permeability ◽  
Prostaglandin E1 ◽  
Cheek Pouch ◽  
Leukotriene C4 ◽  
Hamster Cheek Pouch

scholarly journals Fibrin Degradation Products and Vascular Permeability

1977 ◽  
Author(s):  
Bengt Gerdin ◽  
Herman Högstorp ◽  
Olle Lindquist ◽  
Tom Saldeen ◽  
Erik Svensjö
Keyword(s):  
Molecular Weight ◽  
Vascular Permeability ◽  
High Molecular Weight ◽  
Degradation Products ◽  
Cheek Pouch ◽  
Low Molecular Weight ◽  
Hamster Cheek Pouch ◽  
Fibrin Degradation Products ◽  
Lymphatic Duct ◽  
Fibrin Clots

Increased vascular permeability plays an important role in the pathogenesis of the delayed microembolism syndrome. Fibrin degradation products (FDP) may play a role for this permeability disturbance. Fractions of lymph from the cannulated right lymphatic duct in dogs with induced microembolism syndrome and lysate from fibrin clots obtained by gel chromatography were used. The effect on vascular permeability was determined in the hamster cheek pouch and in the dorsal skin of the rat. Increased permeability was determined by leakage of fluorescein labelled dextran in the first model and by use of isotope labelled albumin in the second model. Lymph from the lymphatic duct and fractions of lysate from fibrin clots caused an increased vascular permeability of the same character in both models, the effect being partly due to high molecular weight products and partly due to low molecular weight products. The effect of high molecular weight products may possibly be due to their continous cleavage releasing low molecular weight vasoactive FDP. The effect of FDP on vascular permeability was enhanced by pretreatment with the β-adrenergic inhibitor propranolol and inhibited by the β2-adrenergie stimulator terbutaline. Bredykinin and PGE1 both increased macromolecular leakage in the hamster cheek pouch. This increase was also counteracted by terbutaline. The FDP effect on permeability might be due to contraction of the endothelial cells.

Effects of leukotriene C4 on the cerebral microvasculature

1986 ◽  
Vol 251 (2) ◽  
pp. H471-H474 ◽  
Author(s):  
W. G. Mayhan ◽  
G. Sahagun ◽  
R. Spector ◽  
D. D. Heistad
Keyword(s):  
Blood Brain Barrier ◽  
Fluorescent Microscopy ◽  
Brain Barrier ◽  
Cheek Pouch ◽  
Leukotriene C4 ◽  
Hamster Cheek Pouch ◽  
Cerebral Vasoconstriction ◽  
Blood Brain ◽  
Cerebral Arterioles ◽  
Potent Vasoconstrictor

Leukotriene C4, which is synthesized during cerebral ischemia, may contribute to disruption of the blood-brain barrier. The purpose of this study was to determine whether leukotriene C4 constricts cerebral arterioles and disrupts the blood-brain barrier. We used intravital fluorescent microscopy in hamsters and compared responses of vessels in the cerebrum with vessels in the cheek pouch. Increases in permeability of the cheek pouch and disruption of the blood-brain barrier were quantitated after superfusion with leukotriene C4 (0.3, 3.0, and 30 nM) by the formation of microvascular leaky sites. Changes in diameter of arterioles in the cheek pouch and cerebrum also were examined. In the cheek pouch, leukotriene C4 produced a dose-related decrease in diameter of arterioles (maximum = 40 +/- 8%; mean +/- SE) and an increase in microvascular permeability (maximum = 16 +/- 2 leaky sites). In contrast, in the cerebrum, leukotriene C4 produced only modest constriction of arterioles (maximum = 12 +/- 5%) and minimal disruption of the blood-brain barrier (maximum = 2 +/- 1 leaky sites). Thus the findings indicate that leukotriene C4, in contrast to its potent vasoconstrictor effects and increase in permeability in the hamster cheek pouch, produces only modest cerebral vasoconstriction and minimal disruption of the blood-brain barrier.

The influence of oxidative stress on permeability of capillary vessels in the cheek pouch of hamsters with alloxan-induced diabetes

VASA ◽  
2004 ◽  
Vol 33 (4) ◽  
pp. 211-214
Author(s):  
Ciechanowski ◽  
Kedzierska ◽  
Golembiewska ◽  
Miklaszewicz ◽  
Domanski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Protease Inhibitor ◽  
Protective Effect ◽  
Vascular Permeability ◽  
Diamine Oxidase ◽  
Superoxide Radical ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Radical Generation

Background: The aim of the study was to assess the influence of oxidative stress on the increase of permeability of capillary vessels in animals with alloxan-induced diabetes. Material and methods: The studies were performed in microcirculation system of hamster cheek pouch. After the blockade of histamine receptors and administration of diamine oxidase (DAO) and histamine into circulation fluorescein angiography was done. In addition, the influence of superoxide dismutase, aminoguanidine (DAO inhibitor) and trascolan (protease inhibitor) on vascular permeability caused by superoxide radical generation in DAO/histamine system was assessed. Results: The number of extravasal leakages in the group receiving HA and DAO was significantly higher (p < 0.001) than in the groups receiving potential vascular "sealers", e.g. SOD, aminoguanidine or trascolan. In the group receiving aminoguanidine the number of leakages was significantly lower (p < 0.05) compared to the group receiving SOD or trascolan. Conclusions: The protective effect of aminoguanidine, superoxide dismutase or trascolan decreasing the vascular permeability, suggests that the increased vascular permeability is a result of superoxide radical generation by diamine oxidase.

Role of nitric oxide in leukotriene C4-induced increases in microvascular transport

1993 ◽  
Vol 265 (1) ◽  
pp. H409-H414 ◽  
Author(s):  
W. G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Fluorescent Microscopy ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Leukotriene C4 ◽  
Hamster Cheek Pouch ◽  
Macromolecular Transport ◽  
Transport Of Macromolecules

The goal of this study was to determine the role of nitric oxide in alterations in macromolecular transport of the hamster cheek pouch in vivo in response to leukotriene C4. We used intravital fluorescent microscopy to examine the transport of macromolecules across the hamster cheek pouch in response to leukotriene C4 before and after application of an enzymatic inhibitor of nitric oxide, NG-monomethyl-L-arginine (L-NMMA; 1.0 microM). Increases in transport of macromolecules across the hamster cheek pouch were quantitated by the formation of venular leaky sites and clearance of fluorescein isothiocyanate-dextran (FITC-dextran; mol wt = 70 K). Leukotriene C4 (1.0 and 3.0 nM) produced an increase in the number of venular leaky sites and clearance of FITC-dextran-70K. Superfusion of L-NMMA (1.0 microM) significantly decreased leukotriene C4-induced increases in venular leaky sites and clearance of FITC-dextran-70K. In addition, superfusion of LY-83583 (10 microM) significantly decreased leukotriene C4-induced increases in venular leaky sites. In contrast, superfusion of NG-monomethyl-D-arginine (D-NMMA; 1.0 microM), indomethacin (10 mg/kg iv), or diphenhydramine hydrochloride; 15–20 mg/kg iv) did not significantly alter leukotriene C4-induced increases in venular leaky sites. Thus these findings suggest that production of nitric oxide and subsequent activation of guanylate cyclase play an important role in formation of venular leaky sites and clearance of FITC-dextran-70K in response to application of leukotriene C4.

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