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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...
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Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Ischemic Stroke l: Introduction01:15

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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.
Cellular Injury II: Classification01:21

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Cellular injury is any process that disrupts a cell’s ability to maintain homeostasis, leading to structural or functional changes. It is broadly classified based on etiology (cause) and mechanism of damage.Classification by EtiologyCellular injury may result from several causes. Hypoxic injury happens due to reduced oxygen delivery, most commonly from inadequate blood supply, such as arterial obstruction; for example, coronary artery thrombosis can cause myocardial infarction. Chemical injury...
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Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...

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Related Experiment Video

Updated: Jun 5, 2026

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
11:42

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis

Published on: November 20, 2013

Calcium and ischemic injury.

W H Barry1

  • 1Cardiology Division, University of Utah Medical Center, Salt Lake City, UT 84132, USA.

Trends in Cardiovascular Medicine
|January 18, 2011
PubMed
Summary
This summary is machine-generated.

Ischemia elevates intracellular calcium ([Ca(2+)](i)) in heart cells, contributing to myocyte injury and potentially reperfusion damage. While calcium overload is a key factor, other injury pathways also play a role.

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Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
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Area of Science:

  • Cardiovascular Physiology
  • Cellular Biology
  • Biochemistry

Background:

  • Ischemia leads to increased intracellular calcium ([Ca(2+)](i)) in cardiac myocytes.
  • This calcium dysregulation contributes to myocyte injury through various mechanisms.

Purpose of the Study:

  • To investigate the role of intracellular calcium ([Ca(2+)](i)) in cardiac myocyte injury during ischemia and reperfusion.
  • To explore the mechanisms by which altered calcium homeostasis contributes to cell damage and affects recovery.

Main Methods:

  • Analysis of intracellular calcium ([Ca(2+)](i)) levels in cardiac myocytes under ischemic conditions.
  • Assessment of myocyte injury markers and functional changes post-reperfusion.
  • Evaluation of calcium handling pathways, including Na-Ca exchange and mitochondrial calcium uptake.

Main Results:

  • Ischemia causes a significant increase in intracellular calcium ([Ca(2+)](i)) despite initial force reduction.
  • Elevated [Ca(2+)](i) activates proteases, phospholipases, and damages mitochondria.
  • During reperfusion, increased [Ca(2+)](i) can lead to hypercontracture and altered organelle calcium loading.

Conclusions:

  • Altered calcium homeostasis is a significant contributor to ischemic and reperfusion injury in cardiac myocytes.
  • While elevated [Ca(2+)](i) is critical, other non-calcium-dependent injury pathways are also important.
  • Understanding calcium's role is crucial for developing therapeutic strategies for cardiac ischemia.