Vasospasm
Vasospasm - Related Videos
07:03
A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
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Cited by 22 •
2013
Aneurysmal subarachnoid hemorrhage (SAH) is bleeding that occurs into the subarachnoid space when an aneurysm ruptures. While the morbidity and mortality from this event has been on a decline due to improved treatment approaches, the risk of vasospasm after subarachnoid hemorrhage continues to be the same as it was several years ago. The importance of establishing a comprehensive and reproducible animal model to identify initiating events of cerebral vasospasm has been the focus of research...
08:12
A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
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Cited by 4 •
2018
The goal of this article is to present a method that allows a 3-dimensional reconstruction of the cerebrovascular tree in mice after micro computed tomography and determination of volumes of entire vessel segments that can be used to quantify cerebral vasospasm in murine models of subarachnoid hemorrhage.
10:41
Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
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2021
The aim of this manuscript is to present a sonography-based method that allows in vivo imaging of blood flow in cerebral arteries in mice. We demonstrate its application to determine changes in blood flow velocities associated with vasospasm in murine models of subarachnoid hemorrhage (SAH).
11:47
Heterotopic Renal Autotransplantation in a Porcine Model: A Step-by-Step Protocol
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Cited by 24 •
2016
Porcine models of organ transplantation provide an important platform to study mechanisms of organ preservation. This article describes a heterotopic porcine renal autotransplantation model, which allows investigating new approaches to improve the outcome of transplantation using marginal kidney grafts.
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.
FAQs
Calcium-dependent signaling increases the activity of vascular smooth-muscle contraction, allowing the vessel wall to remain narrowed for longer. This matters because reduced downstream flow can deprive tissues of oxygen and nutrients, linking a cellular signaling change with ischemia. Studying this pathway helps explain how abnormal contraction can become a sustained vascular event.
Normal vessel tone depends partly on balanced nitric oxide and endothelin regulation. When that balance is disrupted, signals favoring contraction may outweigh signals supporting relaxation, making blood flow more vulnerable to prolonged narrowing. Examining these regulators gives researchers a way to connect biochemical signaling with changes in circulation and to evaluate strategies intended to restore vessel relaxation.
Irritation of a vessel can act as an additional trigger for abnormal smooth-muscle behavior, rather than being only a consequence of reduced flow. Its importance is that vasospasm may reflect both intracellular calcium-linked contraction and altered conditions at the vessel wall. Including irritation in experimental interpretations helps distinguish a signaling disturbance from a response associated with local vessel irritation.
These vascular beds are examined because the consequences of impaired flow differ by the tissue supplied. In cerebral vessels, vasospasm is relevant to neurological injury; in coronary vessels, it can contribute to cardiac complications; and in peripheral vessels, it can limit circulation to downstream tissues. Comparing these settings connects one vascular response with distinct biological and clinical outcomes.
Mechanistic studies can support the identification of diagnostic indicators by relating vessel narrowing to calcium-dependent contraction and disrupted nitric oxide or endothelin regulation. The goal is not simply to note reduced flow, but to connect an observable vascular change with underlying signaling. Such information can help characterize vasospasm across cerebral, coronary, and peripheral settings.
Treatment-oriented research focuses on restoring vascular smooth-muscle relaxation rather than addressing reduced flow alone. If relaxation returns, the vessel can widen and circulation to downstream tissues can improve. This framework makes vasospasm relevant to studies that connect molecular regulation, vessel behavior, and tissue outcome, while recognizing that affected vascular beds can produce different complications.