Vascular Endothelium Injury
Vascular Endothelium Injury - Related Videos
06:20
Imaging Leukocyte Adhesion to the Vascular Endothelium at High Intraluminal Pressure
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Cited by 22 •
2011
This is a method to visualise leukocyte adhesion to the endothelium in harvested pressurised vessels. The technique enables studying vascular adhesion under shear flow with differing intraluminal pressures up to 200 mmHg thus mimic-ing the pathophysiological conditions of high blood pressure.
11:18
Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
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Cited by 29 •
2013
Here we report an experimental technique of fluorescence intravital microscopy to visualize heterotypic platelet-neutrophil interactions on the activated endothelium during vascular inflammation and thrombus formation in live mice. This microscopic technology will be valuable to study the molecular mechanism of vascular disease and to test pharmacologic agents under pathophysiological conditions.
05:53
Intraluminal Drug Delivery to the Mouse Arteriovenous Fistula Endothelium
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Cited by 5 •
2016
After puncturing the aorta through the inferior vena cava (IVC) to create an aorto-caval fistula in the mouse, solution containing a drug is infused into the IVC via the same needle, followed by incubation. This method enables more robust drug delivery to the venous endothelium compared to the external route.
08:42
A Rat Carotid Balloon Injury Model to Test Anti-vascular Remodeling Therapeutics
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Cited by 8 •
2016
The rat carotid balloon injury model described below allows researchers to evaluate drugs or therapeutics that negate injury-induced arterial hyperplasia. Detailed pre-surgical preparation, surgical procedure, and post-surgical cares of the animal are described.
06:14
Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
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Cited by 2 •
2017
Restenosis following cardiovascular procedures (bypass surgery, angioplasty, or stenting) is a significant problem reducing the durability of these procedures. An ideal therapy would inhibit smooth muscle cell (VSMC) proliferation while promoting regeneration of the endothelium. We describe a model for simultaneous assessment of VSMC proliferation and endothelial function in vivo.
FAQs
Damage or dysfunction can impair nitric oxide signaling, reducing a pathway that supports normal vascular regulation. This shift favors vasoconstriction rather than appropriate vessel relaxation and contributes to loss of vascular homeostasis. Evaluating this change helps connect endothelial dysfunction with disease processes in which abnormal vessel tone is clinically important.
These conditions represent different sources of vascular stress that can disrupt endothelial performance. Their effects may converge on impaired nitric oxide signaling, increased permeability, and stronger leukocyte or platelet adhesion. This convergence explains why inflammation, oxidative stress, abnormal flow, and metabolic disturbances can each contribute to vascular inflammation, thrombosis, and cardiovascular disease.
Increased permeability indicates that the endothelial barrier no longer regulates movement across the vessel wall normally. Alongside enhanced leukocyte and platelet adhesion, this change can intensify vascular inflammation and support thrombus formation. Permeability therefore serves as an important mechanistic link between endothelial dysfunction and later vessel-wall complications.
The injured endothelium can become more adhesive to leukocytes and platelets while losing normal regulatory functions. Leukocyte adhesion supports inflammatory activity, whereas platelet adhesion creates conditions that favor clot formation. When these changes occur with impaired vessel relaxation and greater permeability, several harmful processes reinforce one another within the vessel wall.
Researchers examine the injury as a disease mechanism, a source of measurable biomarkers, and a target for therapeutic assessment. The relevant outcomes include altered nitric oxide signaling, permeability, leukocyte or platelet adhesion, vascular inflammation, thrombosis, and weakened repair. This framework supports investigation of endothelial changes in atherosclerosis, hypertension, and diabetes.
The topic is especially relevant to atherosclerosis, hypertension, and diabetes, where endothelial dysfunction can contribute to abnormal vascular behavior and disease progression. Studying the injury in these settings helps clarify how vascular inflammation, vasoconstriction, thrombosis, and impaired repair are connected, while also supporting efforts to identify biomarkers and evaluate protective therapies.