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Pericytes constrict blood vessels after myocardial ischemia

Matheus A Costa1, Ana E Paiva1, Julia P Andreotti1

  • 1Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.

Journal of Molecular and Cellular Cardiology
|January 27, 2018
PubMed

Insights

Pericytes contribute to the no-reflow phenomenon after heart ischemia. Adenosine treatment may offer a novel therapeutic target to improve blood flow and reduce myocardial damage.

Area of Science:

  • Cardiovascular Biology
  • Cell Biology
  • Ischemia Research

Background:

  • The no-reflow phenomenon, characterized by reduced blood flow post-myocardial ischemia, causes significant heart damage.
  • Limited understanding of the cellular mechanisms underlying no-reflow hinders the development of effective therapeutic strategies.

Purpose of the Study:

  • To investigate the cellular mediators of the no-reflow phenomenon in the heart following ischemia.
  • To identify potential therapeutic targets for mitigating no-reflow and subsequent myocardial injury.

Main Methods:

  • Utilized a myocardial ischemia/reperfusion mouse model.
  • Employed high-resolution confocal imaging and advanced cellular analysis techniques.

Main Results:

  • Identified pericytes as key contributors to the no-reflow phenomenon in the post-ischemic heart.
  • Demonstrated that intravenous adenosine administration effectively increased vascular diameter at pericyte locations.

Conclusions:

  • Pericytes play a critical role in mediating cardiac no-reflow.
  • Adenosine presents a promising therapeutic target for inhibiting the no-reflow phenomenon and preserving myocardial tissue after ischemia.

Keywords:
HeartIschemiaPericytesVasoconstriction

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