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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Intracerebral hemorrhage elicits aberration in cardiomyocyte contractile function and intracellular Ca2+ transients

Cindy X Fang1, Shan Wu, Jun Ren

  • 1Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie 82071, USA.

Stroke
|June 10, 2006
PubMed

Insights

Intracerebral hemorrhage impairs cardiomyocyte function and calcium handling, leading to myocardial damage. These effects improve over 48 hours but some deficits persist, linked to protein changes and inflammation.

Area of Science:

  • Cardiology
  • Neuroscience
  • Cell Biology

Background:

  • Intracerebral hemorrhage (ICH) causes multi-organ damage, including cardiac dysfunction.
  • The precise mechanisms of ICH-induced myocardial dysfunction remain unclear.

Purpose of the Study:

  • To investigate the effects of ICH on cardiomyocyte contractile function.
  • To analyze intracellular calcium handling and related protein expression post-ICH.
  • To assess I kappa B beta protein (IkappaB) phosphorylation, hypoxia-inducible factor 1alpha (HIF-1alpha), and nitrosative damage within 48 hours of ICH.

Main Methods:

  • Evaluated mechanical and intracellular calcium properties of cardiomyocytes.
  • Measured peak shortening (PS), velocity of shortening/relengthening (+/-dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR90), and fura-2 fluorescence intensity (FFI).
  • Assessed intracellular calcium decay and cardiac protein expression, including IkappaB phosphorylation and HIF-1alpha.

Main Results:

  • ICH led to depressed cardiomyocyte contractility (PS, +/-dL/dt) and prolonged relaxation (TPS, TR90) at 12-24 hours.
  • Most contractile and calcium handling abnormalities normalized by 48 hours, except for -dL/dt and TR90.
  • Observed altered expression of calcium cycling proteins, enhanced IkappaB phosphorylation, HIF-1alpha, and nitrosative damage markers.

Conclusions:

  • ICH induces cardiomyocyte contractile and calcium dysregulation.
  • These alterations are potentially linked to modified calcium cycling protein expression, nitrosative damage, and myocardial IkappaB phosphorylation.
Abstract

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