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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

Pharmacological modulation of the ATP sensitive potassium channels during repeated coronary occlusions: no effect on

T B Lindhardt1, N Gadsbøll, H Kelbaek

  • 1The Heart Centre, Cardiac Catheterisation Laboratory, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. lindhardt@dadlnet.dk

Heart (British Cardiac Society)
|March 17, 2004
PubMed

Insights

This study found that repeated episodes of myocardial ischemia did not trigger a protective preconditioning effect in the human heart, even when targeting ATP-sensitive potassium channels. Pharmacological interventions with pinacidil or glibenclamide did not alter the ischemic response.

Area of Science:

  • Cardiology
  • Cardiovascular Physiology
  • Pharmacology

Background:

  • Repeated myocardial ischemia may induce ischemic preconditioning.
  • ATP-sensitive potassium channels are implicated in mediating this protective effect.

Purpose of the Study:

  • To investigate the impact of pharmacologically modulating ATP-sensitive potassium channels during repeated coronary occlusions.
  • To determine if interventions targeting these channels can enhance myocardial protection against ischemia.

Main Methods:

  • A double-blind, double-dummy study involving 38 patients with coronary artery stenosis.
  • Patients underwent three identical coronary occlusions, randomized to pinacidil, glibenclamide, or placebo.
  • Myocardial ischemia assessed via ECG ST segment changes, left ventricular function, and angina scores.

Main Results:

  • All patients experienced significant ST elevation, reduced ejection fraction, and angina during the first occlusion.
  • These ischemic responses were not attenuated in subsequent occlusions.
  • Neither pinacidil nor glibenclamide pretreatment altered the severity of ischemia or ventricular dysfunction.

Conclusions:

  • The study did not find evidence of an intrinsic protective mechanism activated by short ischemic episodes in the human myocardium.
  • Pharmacological modulation of ATP-sensitive potassium channels did not confer protection under these experimental conditions.
Abstract

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