Endothelin-1 Induced Mcao
Endothelin-1 Induced Mcao - Related Videos
07:43
Utilizing a Cranial Window to Visualize the Middle Cerebral Artery During Endothelin-1 Induced Middle Cerebral Artery Occlusion
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Cited by 4 •
2013
This article describes a method for visualizing rat cerebral arteries through a cranial window using temporal craniectomy in order to view proximal portions of the middle cerebral artery (Figure 1). This versatile method can be combined with various techniques of drug delivery to measure cerebral artery reactivity in vivo.
07:26
Endothelin-1 Induced Middle Cerebral Artery Occlusion Model for Ischemic Stroke with Laser Doppler Flowmetry Guidance in Rat
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Cited by 26 •
2013
Several animal models of cerebral ischemia have been developed to simulate the human condition of stroke. This protocol describes the endothelin-1 (ET-1) induced middle cerebral artery occlusion (MCAO) model for ischemic stroke in rats. In addition, important considerations, advantages, and shortcomings of this model are discussed.
06:38
The Stroke Preclinical Assessment Network Multi-Laboratory Model of Thromboembolic Stroke with Thrombolysis: TE-MCAo
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2025
To simulate thromboembolic stroke, emboli prepared from heterologous rat blood were injected into the middle cerebral artery, followed by administration of systemic thrombolysis for recanalization. This version of the model is optimized for use in a multi-laboratory network and supports testing multiple candidate therapeutics.
03:12
Visualizing Pathogen-Induced Oxidative Stress in C. elegans Using GFP-Tagged SKN-1
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2026
Source: Naji, A., et al. Studying Oxidative Stress Caused by the Mitis Group Streptococci in Caenorhabditis elegans. J. Vis. Exp. (2019)This video demonstrates the use of green fluorescent protein-tagged SKN-1 in C. elegans to monitor oxidative stress by tracking green fluorescence. Worms exposed to S. gordonii show strong nuclear fluorescence, confirming pathogen-induced stress, while those fed E. coli display diffuse green fluorescence in the cytoplasm, indicating minimal SKN-1 activation.
01:18
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
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2024
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists. ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
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The key event is potent constriction of the middle cerebral artery after endothelin-1 is applied nearby. This narrows the vessel and reduces blood delivery to downstream brain tissue, creating a localized ischemic region. Because the constriction can later diminish, the model also permits observation of how tissue and cellular responses develop as cerebral blood flow recovers.
Localized constriction concentrates ischemia in the vascular territory downstream from the middle cerebral artery rather than producing a generalized reduction in brain perfusion. Its sustained nature supports development of infarct-related changes and neurological deficits, while the controlled placement of endothelin-1 provides a defined experimental setting for examining cerebrovascular mechanisms and responses to injury.
As the vasoconstrictor effect diminishes, blood flow can recover after the ischemic period. This temporal feature allows investigators to examine not only infarct development during reduced perfusion but also processes associated with recovery. It therefore supports study of changing cellular responses and neurological outcomes across both ischemic injury and subsequent restoration of circulation.
The central workflow begins by applying endothelin-1 near the middle cerebral artery to produce the intended constriction. Researchers then examine the resulting ischemic consequences in vivo, including tissue injury, neurological deficits, and cellular responses. Because the vascular effect may later decline, assessments can also address changes associated with recovery of blood flow.
Key outcomes include the development of infarction, neurological deficits, and cellular responses within the ischemic brain. These readouts connect vascular constriction with tissue damage and functional consequences. Examining them together helps investigators characterize the severity and progression of the experimental injury rather than relying on a single indicator of cerebral ischemia.
This approach is useful for evaluating neuroprotective treatments, investigating mechanisms that regulate cerebral blood vessels, and studying recovery after ischemic injury. Its in vivo design links vascular events with brain and behavioral outcomes, while its controlled occlusion can support experiments that require a more defined ischemic challenge than some surgical approaches provide.