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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Ischemic Heart Disease: Overview01:17

Ischemic Heart Disease: Overview

Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...

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Analysis of Oxidative Stress in Zebrafish Embryos
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Oxidative stress in ischaemic stroke.

Laura Nanetti1, Francesca Raffaelli, Arianna Vignini

  • 1Department of Biology, Università Politecnica delle Marche, Ancona, Italy. l_nanetti@hotmail.com

European Journal of Clinical Investigation
|June 1, 2011
PubMed
Summary

Biomarkers for acute ischemic stroke were identified. Increased oxidative stress markers and decreased antioxidant capacity correlate with stroke severity, aiding in assessing cerebral ischemia.

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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
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Published on: August 18, 2015

Area of Science:

  • Biochemistry
  • Neurology
  • Oxidative Stress Research

Background:

  • Ischemic stroke triggers reactive oxygen species (ROS), exacerbating tissue damage via multiple molecular pathways.
  • Understanding the role of oxidative stress in acute ischemic stroke pathogenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To evaluate serum levels of lipoperoxide, hydroperoxide, conjugated dienes, and total antioxidant capacity as specific biochemical markers for cerebral ischemia.
  • To correlate changes in these markers with clinical evolution in acute ischemic stroke patients.

Main Methods:

  • Serum samples from 50 acute ischemic stroke patients were analyzed at stroke onset (T0) and one month later (T1).
  • Assays included measurements of lipoperoxide, hydroperoxide, conjugated dienes, and total antioxidant capacity.
  • Clinical severity was assessed using the National Institutes of Health Stroke Scale (NIHSS).

Main Results:

  • Significantly higher levels of lipoperoxide, hydroperoxide, and conjugated dienes were observed in the early stages (T0) compared to later evaluation (T1).
  • Total antioxidant capacity significantly increased at T1 compared to T0.
  • A significant negative correlation was found between total antioxidant capacity and NIHSS scores, while positive correlations existed between oxidative stress markers and NIHSS scores.

Conclusions:

  • Elevated free radical generation and oxidative stress play a role in acute ischemic lesion pathogenesis.
  • The activation of defense mechanisms, such as total antioxidant capacity, may limit ischemic damage progression.
  • These oxidative stress markers show potential for use in assessing cerebral ischemia and patient outcomes.