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Related Concept Videos

Inflammation01:38

Inflammation

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Overview
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Inflammatory Response I: Vascular and Cellular01:30

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Inflammatory Response01:28

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Extrinsic and Intrinsic Pathways of Hemostasis01:20

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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Vascular Spasm01:16

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The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
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Introduction to Hemostasis01:05

Introduction to Hemostasis

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Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
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Related Experiment Video

Updated: Jan 2, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
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Inflammatory Pathways Following Subarachnoid Hemorrhage.

Kevin Min Wei Khey1, Alec Huard1, Sherif Hanafy Mahmoud2

  • 1Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada.

Cellular and Molecular Neurobiology
|December 7, 2019
PubMed
Summary

Aneurysmal subarachnoid hemorrhage (SAH) triggers neuroinflammation, leading to delayed cerebral ischemia (DCI) and disability. Understanding these complex inflammatory pathways is crucial for preventing SAH complications.

Keywords:
Delayed cerebral ischemiaInflammationRuptured aneurysmSubarachnoid hemorrhageVasospasm

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Area of Science:

  • Neuroscience
  • Cerebrovascular Medicine
  • Inflammation Research

Background:

  • Aneurysmal subarachnoid hemorrhage (SAH) is a critical cerebrovascular event with significant disability, often caused by delayed cerebral ischemia (DCI).
  • Neuroinflammation is a suspected contributor to SAH complications, but clinical trials on anti-inflammatory agents have yielded inconsistent results.
  • The complexity of multiple activated inflammatory pathways in SAH hinders effective treatment strategies.

Purpose of the Study:

  • To review the molecular pathways involved in inflammation following SAH.
  • To explore the link between these inflammatory pathways and the development of SAH complications.
  • To provide insights for better understanding and prevention of SAH-induced DCI and disability.

Main Methods:

  • Literature review of studies investigating molecular and inflammatory pathways in SAH.
  • Analysis of evidence linking neuroinflammation to DCI and other SAH complications.
  • Synthesis of current understanding of overlapping inflammatory mechanisms in SAH.

Main Results:

  • SAH activates a complex network of inflammatory pathways in the brain.
  • These pathways contribute to the cascade of events leading to DCI and long-term neurological deficits.
  • Interactions between different inflammatory mediators play a critical role in disease progression.

Conclusions:

  • Elucidating the intricate inflammatory pathways in SAH is essential for developing targeted therapies.
  • Understanding pathway interactions may reveal novel strategies to prevent DCI and improve outcomes for SAH survivors.
  • Further research into the molecular mechanisms of neuroinflammation post-SAH is warranted.