Epicardial Vasospasm
Epicardial Vasospasm - Related Videos
07:44
Epicardial Outgrowth Culture Assay and Ex Vivo Assessment of Epicardial-derived Cell Migration
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Cited by 9 •
2016
Here, we describe methods for isolating primary mouse epicardial cells by an outgrowth culture assay and assessing the functional migration of epicardial-derived cells (EPDC) using an ex vivo heart culture system. These protocols are suitable for identifying genetic and chemical modulators of epicardial epithelial-to-mesenchymal transition (EMT) and motility.
06:31
In Vitro Culture of Epicardial Cells From Mouse Embryonic Heart
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Cited by 13 •
2016
The epicardium is an essential source of multipotent cardiovascular progenitor cells and paracrine factors that are required for cardiovascular development and regeneration. We describe here a method to culture mouse embryonic epicardial cells.
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...
09:17
High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation
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Cited by 20 •
2011
This report provides a detailed description of the methodology and results of simultaneous endocardial and epicardial optical mapping of electrical excitation in the intact left atrium of a Langendorff-perfused sheep heart during stretch-induced atrial fibrillation.
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.
FAQs
Excessive contraction of coronary vascular smooth muscle is the immediate functional event in Epicardial Vasospasm. Endothelial dysfunction and altered vasomotor signaling can disturb the normal balance controlling coronary tone, making the artery more prone to constrict intensely. This mechanism links vascular biology to transient reductions in myocardial blood flow and helps explain why pharmacologic vasodilators are studied.
Because the narrowing is temporary rather than caused by fixed obstructive disease, symptoms and ischemic effects may occur without a persistent anatomical blockage. This distinction makes Epicardial Vasospasm useful for examining coronary tone separately from fixed obstruction. It also directs attention toward vasomotor signaling and endothelial function when interpreting transient episodes.
ST-segment elevation can accompany an episode because intense arterial constriction reduces myocardial blood flow. In this setting, the electrical change provides a clinically relevant indicator of transient ischemia rather than evidence that fixed obstructive disease must be present. Its association with vasospasm supports using the condition to connect coronary hemodynamics with observed cardiac findings.
Endothelial dysfunction may contribute by impairing the vasomotor signals that normally help regulate coronary tone. When this regulatory environment is altered, vascular smooth muscle can contract excessively, intensifying arterial narrowing and flow reduction. This relationship makes endothelial function an important pharmacologic context for studying drugs that influence vascular tone.
Nitrates and calcium channel blockers are identified as vasodilator therapies relevant to Epicardial Vasospasm. The source context supports evaluating them in relation to recurrent episodes and coronary tone, rather than treating the condition only as a fixed blockage. Studying these agents helps pharmacologists assess how drug-induced vasodilation may affect transient ischemic events.
Assessment focuses on correlating transient ischemic symptoms with evidence of altered coronary blood flow or vasomotor narrowing. Clinicians may consider ischemic chest pain, possible ST-segment elevation, and the absence of fixed obstructive disease as parts of the clinical context. This framework helps distinguish episodic vasospasm from persistent obstruction and informs preventive planning.
Because it links a controllable change in coronary tone with ischemic consequences, Epicardial Vasospasm serves as a model for pharmacology research. Investigators can use it to examine vascular smooth muscle contraction, endothelial function, and responses to vasodilator therapy. The model therefore connects signaling questions with clinically relevant changes in coronary perfusion and ischemia.
Drug assessment should account for effects on vascular smooth muscle and endothelial function, since altered activity in either area can influence coronary tone. Epicardial Vasospasm provides a relevant context for asking whether a compound could modify vasomotor behavior, coronary blood flow, or recurrent ischemic episodes. This perspective supports safer evaluation of drugs affecting the vasculature.