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Related Experiment Videos

ASIC3: a lactic acid sensor for cardiac pain.

D C Immke1, E W McCleskey

  • 1Vollum Institute, Oregon Health & Science University, Portland, OR 97201-3098, USA. immked@ohsu.edu

Thescientificworldjournal
|June 14, 2003
PubMed
Summary

Vasoocclusive pain, like angina, is triggered by insufficient blood flow causing ischemia. Sensory neurons in the heart possess an ion channel specifically activated by lactic acid, a byproduct of this ischemia.

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Area of Science:

  • Cardiology
  • Neuroscience
  • Pain Research

Background:

  • Vasoocclusive pain, exemplified by angina, arises from inadequate blood supply to tissues, leading to ischemia.
  • Conditions such as heart attack, sickle cell anemia, and peripheral artery disease involve vasoocclusive pain.
  • Ischemia forces cells into anaerobic metabolism, releasing lactic acid.

Purpose of the Study:

  • To investigate the role of specific ion channels in sensory neurons related to ischemia-induced pain.
  • To understand the molecular mechanisms underlying the detection of lactic acid by cardiac sensory neurons.

Main Methods:

  • Analysis of sensory neurons innervating the heart.
  • Investigation of ion channel function in response to ischemic conditions and lactic acid.

Main Results:

  • Sensory neurons in the heart are densely equipped with a specific ion channel.
  • This ion channel is activated by lactic acid, a key mediator of ischemic pain.
  • The channel is precisely tuned to detect the levels of lactic acid produced during muscle ischemia.

Conclusions:

  • Lactic acid released during muscle ischemia acts as a direct stimulus for sensory neurons in the heart.
  • This finding provides a novel molecular target for understanding and potentially treating vasoocclusive pain, including angina.

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