Arteriolar Cnv
Arteriolar Cnv - Related Videos
02:38
Analysis of Calcium Dynamics and Membrane Potential Changes in a Mouse Arteriolar Endothelium
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2025
Source: Hakim, M. A. et al., Isolation and Functional Analysis of Arteriolar Endothelium of Mouse Brain Parenchyma. J. Vis. Exp. (2022).This video demonstrates the functional analysis of an arteriolar endothelial tube isolated from a mouse brain. It outlines the steps for measuring intracellular calcium levels and membrane potential, both at baseline and in response to pharmacological stimulation.
06:40
Isolation and Functional Analysis of Arteriolar Endothelium of Mouse Brain Parenchyma
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Cited by 2 •
2022
Intensive preparation of intact mouse cerebral endothelial "tubes" from cerebral parenchymal arterioles is illustrated for studying cerebral blood flow regulation. Further, we demonstrate the experimental strengths of this endothelial study model for fluorescence imaging and electrophysiology measurement of key cellular signaling pathways, including changes in intracellular [Ca2+] and membrane potential.
16:43
Murine Spinotrapezius Model to Assess the Impact of Arteriolar Ligation on Microvascular Function and Remodeling
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Cited by 7 •
2013
We demonstrate a novel arterial ligation model in murine spinotrapezius muscle, including a step-by-step procedure and description of required instrumentation. We describe the surgery and relevant outcome measurements relating to vascular network remodeling and functional vasodilation using intravital and confocal microscopy.
09:56
In Vivo Multimodal Imaging and Analysis of Mouse Laser-Induced Choroidal Neovascularization Model
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Cited by 7 •
2018
Here, we present the usefulness of longitudinal in vivo imaging in the follow-up of morphological changes of laser-induced choroidal neovascularization in mice.
07:08
A Mouse Model for Laser-induced Choroidal Neovascularization
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Cited by 87 •
2015
Here, we present the mouse laser-induced choroidal neovascularization (CNV) protocol, an experimental model that re-creates the vascular hallmarks of neovascular age-related macular degeneration (AMD). Once mastered, it can reliably and effectively induce CNV as a model system to test various experimental measures.
FAQs
Tissue injury or reduced oxygen availability can activate angiogenic signaling within the affected retinal environment. Vascular endothelial growth factor, or VEGF, is identified in the overview as a key signal in this response. Its activity encourages vessel growth across weakened vascular boundaries, linking local tissue stress to the development of exudative lesions and subsequent visual disruption.
Vascular endothelial growth factor promotes the extension of new vessels from the choroid toward or beneath the retina after injury or ischemic stress. In arteriolar CNV, this signaling contributes not only to vessel growth but also to the formation of vessels prone to leakage. That leakage can produce fluid or blood accumulation and impair retinal organization.
The newly formed vessels are fragile and develop through weakened vascular boundaries, making them poorly suited to contain their contents. Fluid or blood can therefore escape into retinal tissues and create exudative lesions. These changes disturb retinal structure, which helps explain why visual symptoms may appear or worsen rapidly rather than progressing only gradually.
Leakage can impair vision by disturbing the retinal structure needed for normal visual function. Because the process may involve both fluid and blood, the resulting exudative changes can vary in extent and produce rapid visual changes. Monitoring the lesions is important because ongoing leakage signals continued activity that may threaten preservation of vision.
Clinical evaluation focuses on recognizing neovascular retinal disease and following changes in exudative lesions, leakage, and vision. Diagnosis establishes whether the retinal findings are consistent with this abnormal vascular response, while monitoring helps determine whether activity persists or changes. This information supports decisions about treatment and the need to preserve retinal function.
Intravitreal anti-VEGF therapy targets the angiogenic signaling that supports abnormal vessel growth and leakage. By inhibiting VEGF activity, treatment can reduce leakage from the affected vessels and help preserve vision. Its role is therefore directed at the active biological driver of the lesion rather than simply addressing the visible fluid or blood after it appears.