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Acute Myocardial Infarction in Rats
07:45

Acute Myocardial Infarction in Rats

Published on: February 16, 2011

The endothelin system and its role in acute myocardial infarction

Sheila A Doggrell1

  • 1Doggrell Biomedical Communications, 47 Caronia Crescent, Lynfield, Auckland, New Zealand. s.doggrell@xtra.co.nz

Expert Opinion on Therapeutic Targets
|May 27, 2004
PubMed

Insights

Endothelin-1 (ET-1) causes coronary artery constriction and may worsen heart attacks. Blocking ET-1 receptors (ET(A)) reduced damage and arrhythmias in animal models, suggesting a potential therapy for acute myocardial infarction (AMI).

Area of Science:

  • Cardiovascular Pharmacology
  • Ischemic Heart Disease Research

Background:

  • Endothelin (ET)-1 is a potent coronary vasoconstrictor and positive inotrope.
  • Elevated plasma ET-1 levels post-acute myocardial infarction (AMI) contribute to myocardial ischemia and ventricular dysfunction.
  • ET-1 may also be pro-arrhythmic, increasing the risk of heart rhythm disturbances.

Purpose of the Study:

  • To investigate the therapeutic potential of endothelin receptor antagonists in acute myocardial infarction (AMI).
  • To evaluate the effects of ET(A) receptor blockade on ventricular arrhythmias and infarct size in preclinical AMI models.
  • To assess the impact of ET(A) receptor blockade on coronary artery diameter in humans.

Main Methods:

  • Ventricular arrhythmias were assessed during coronary artery occlusion in rats treated with ET(A) receptor blockade.
  • Infarct size was measured in animal models of AMI (coronary occlusion/reperfusion) following short-term ET(A) receptor blockade.
  • Infarct size was also evaluated in rabbits using endothelin-converting enzyme inhibition (SM-19712).
  • Coronary artery dilation was assessed in humans receiving ET(A) receptor blockade.

Main Results:

  • ET(A) receptor blockade reduced ventricular arrhythmias during coronary artery occlusion in rats.
  • Short-term ET(A) receptor blockade decreased infarct size in animal models of AMI.
  • Inhibition of endothelin-converting enzyme also reduced infarct size in a rabbit AMI model.
  • ET(A) receptor blockade was associated with coronary artery dilation in human subjects.

Conclusions:

  • ET(A) receptor antagonists demonstrate protective effects in animal models of AMI, reducing infarct size and arrhythmias.
  • Coronary artery dilation observed in humans suggests a beneficial hemodynamic effect.
  • Short-term ET(A) receptor blockade warrants consideration for clinical trials in human AMI patients.

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