Studies of Arterial Endothelial Integrity with the Dye Exclusion Test — A Review

1981 ◽  
pp. 211-238 ◽  
Author(s):  
S. Björkerud ◽  
G. Bondjers ◽  
A. Bylock ◽  
G. Hansson
Keyword(s):  
Endothelial Integrity

How to preserve endothelial integrity of internal thoracic arteries

2005 ◽  
Vol 53 (S 3) ◽  
Author(s):  
M Grapow ◽  
MA Konerding ◽  
P Matt ◽  
F Bernet ◽  
DC Reineke ◽  
...  
Keyword(s):  
Endothelial Integrity

scholarly journals Preservation of renal endothelial integrity and reduction of renal edema by aprotinin does not preserve renal perfusion and function following experimental cardiopulmonary bypass

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Nicole A. M. Dekker ◽  
Anoek L. I. van Leeuwen ◽  
Matijs van Meurs ◽  
Jill Moser ◽  
Jeannette E. Pankras ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Renal Injury ◽  
Weight Ratio ◽  
Kidney Injury ◽  
Dry Weight ◽  
Renal Perfusion ◽  
Plasma Creatinine ◽  
Microcirculatory Perfusion ◽  
Neutrophil Influx ◽  
Endothelial Integrity

Abstract Background Acute kidney injury is a severe complication following cardiopulmonary bypass (CPB) and is associated with capillary leakage and microcirculatory perfusion disturbances. CPB-induced thrombin release results in capillary hyperpermeability via activation of protease-activated receptor 1 (PAR1). We investigated whether aprotinin, which is thought to prevent thrombin from activating PAR1, preserves renal endothelial structure, reduces renal edema and preserves renal perfusion and reduces renal injury following CPB. Methods Rats were subjected to CPB after treatment with 33.000 KIU/kg aprotinin (n = 15) or PBS (n = 15) as control. A secondary dose of 33.000 KIU/kg aprotinin was given 60 min after initiation of CPB. Cremaster and renal microcirculatory perfusion were assessed using intravital microscopy and contrast echography before CPB and 10 and 60 min after weaning from CPB. Renal edema was determined by wet/dry weight ratio and renal endothelial structure by electron microscopy. Renal PAR1 gene and protein expression and markers of renal injury were determined. Results CPB reduced cremaster microcirculatory perfusion by 2.5-fold (15 (10–16) to 6 (2–10) perfused microvessels, p < 0.0001) and renal perfusion by 1.6-fold (202 (67–599) to 129 (31–292) au/sec, p = 0.03) in control animals. Both did not restore 60 min post-CPB. This was paralleled by increased plasma creatinine (p < 0.01), neutrophil gelatinase-associated lipocalin (NGAL; p = 0.003) and kidney injury molecule-1 (KIM-1; p < 0.01). Aprotinin treatment preserved cremaster microcirculatory perfusion following CPB (12 (7–15) vs. 6 (2–10) perfused microvessels, p = 0.002), but not renal perfusion (96 (35–313) vs. 129 (31–292) au/s, p > 0.9) compared to untreated rats. Aprotinin treatment reduced endothelial gap formation (0.5 ± 0.5 vs. 3.1 ± 1.4 gaps, p < 0.0001), kidney wet/dry weight ratio (4.6 ± 0.2 vs. 4.4 ± 0.2, p = 0.046), and fluid requirements (3.9 ± 3.3 vs. 7.5 ± 3.0 ml, p = 0.006) compared to untreated rats. In addition, aprotinin treatment reduced tubulointerstitial neutrophil influx by 1.7-fold compared to untreated rats (30.7 ± 22.1 vs. 53.2 ± 17.2 neutrophil influx/section, p = 0.009). No differences were observed in renal PAR1 expression and plasma creatinine, NGAL or KIM-1 between groups. Conclusions Aprotinin did not improve renal perfusion nor reduce renal injury during the first hour following experimental CPB despite preservation of renal endothelial integrity and reduction of renal edema.

Nickel and Disrupted Endothelial Integrity: Implications to PM2.5-associated Cardiovascular Disorders

Epidemiology ◽  
2011 ◽  
Vol 22 ◽  
pp. S79 ◽  
Author(s):  
Jingping Niu ◽  
Song Qu ◽  
Xinbiao Guo ◽  
Xiaomei Li ◽  
Bin Luo ◽  
...  
Keyword(s):  
Cardiovascular Disorders ◽  
Endothelial Integrity

Pathogenesis of Pulmonary Hemorrhagic Syndrome in Human Leptospirosis

2021 ◽  
Author(s):  
Antonio C. Nicodemo ◽  
Amaro Nunes Duarte-Neto
Keyword(s):  
Intercellular Junctions ◽  
Human Leptospirosis ◽  
New Knowledge ◽  
Hemorrhagic Pneumonia ◽  
Severe Leptospirosis ◽  
Endothelial Integrity

Based on a previous study and by incorporating new knowledge, the goal of our study was to understand more fully the pathogenesis of hemorrhagic pneumonia of severe human leptospirosis, highlighting the onset of capillary lesions by Leptospira itself and/or its antigenic/toxic products acting on the endothelium and binding to cadherins. Both events lead to loss of endothelial integrity, alter permeability, cause rupture, and open intercellular junctions, contributing to the hemorrhagic phenomena associated with severe leptospirosis.

Gastric ulceration induced by nonsteroidal anti-inflammatory drugs is a neutrophil-dependent process

1990 ◽  
Vol 259 (3) ◽  
pp. G462-G467 ◽  
Author(s):  
J. L. Wallace ◽  
C. M. Keenan ◽  
D. N. Granger
Keyword(s):  
Platelet Activating Factor ◽  
Gastric Ulceration ◽  
Gastric Damage ◽  
Blue Staining ◽  
Vascular Endothelial ◽  
Cyclooxygenase Activity ◽  
Inhibit Prostaglandin Synthesis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Endothelial Integrity

The hypothesis that neutrophils play an important role in the pathogenesis of gastric ulceration induced by nonsteroidal anti-inflammatory drugs (NSAIDs) was tested in rats. Rats made neutropenic by prior treatment with an antibody to rat neutrophils raised in goat were found to be significantly more resistant to the gastric-damaging actions of indomethacin or naproxen than were control rats or rats pretreated with normal goat serum. The reduction of damage in neutropenic rats was not due to effects of the antineutrophil serum on either gastric acid secretion or the ability of indomethacin or naproxen to inhibit prostaglandin synthesis. Gastric cyclooxygenase activity was inhibited by greater than 95% in both normal and neutropenic rats that received indomethacin or naproxen. Reduction of circulating neutrophil numbers by treating rats with methotrexate also resulted in a significant reduction in the susceptibility to gastric damage induced by indomethacin. Since activation of circulating neutrophils appeared to be important in the development of gastric erosions after administration of indomethacin, and in the significant changes in vascular endothelial integrity (Monastral Blue staining) observed within 15 min of indomethacin administration, we investigated the possibility that leukotrienes (LTs) and platelet-activating factor (PAF) might be involved in the pathogenesis of indomethacin-induced ulceration. Changes in gastric LTB4 synthesis were not observed after indomethacin administration. Pretreatment with either an LTD4 antagonist or a PAF antagonist was without significant effect on the extent of gastric damage induced by indomethacin. These results suggest an important role for neutrophils in the pathogenesis of NSAID-induced gastric ulceration. Neutrophils may be important in the vascular injury that occurs early after administration of these compounds.

scholarly journals Bone Marrow Derived Mesenchymal Stem Cells Inhibit Inflammation and Preserve Vascular Endothelial Integrity in the Lungs after Hemorrhagic Shock

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e25171 ◽  
Author(s):  
Shibani Pati ◽  
Michael H. Gerber ◽  
Tyler D. Menge ◽  
Kathryn A. Wataha ◽  
Yuhai Zhao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Hemorrhagic Shock ◽  
Vascular Endothelial ◽  
Endothelial Integrity

PPACK attenuates plasmin-induced changes in endothelial integrity

1993 ◽  
Vol 70 (6) ◽  
pp. 425-436 ◽  
Author(s):  
Leroy E. Rabbani ◽  
Michael T. Johnstone ◽  
M.Audrey Rudd ◽  
Patricia Devine ◽  
Dorinda George ◽  
...  
Keyword(s):  
Endothelial Integrity ◽  
Induced Changes
Sign in / Sign up

Export Citation Format

Share Document