Protective effects of preconditioning of the ischaemic myocardium involve cyclo-oxygenase products

A. Végh, Laszlo Szekeres, J. Parratt

Research output: Contribution to journalReview article

142 Citations (Scopus)

Abstract

Study objective - The aim was to determine whether short (preconditioning) occlusions of a coronary artery protect against the arrhythmias occurring during a subsequent more prolonged occlusion and to examine whether the observed protection is mediated by the release of a product of the cyclo-oxygenase pathway of arachidonic acid metabolism.Design - The effects were examined of two short (5 min) coronary artery occlusions, in chloraloseurethane anaesthetised dogs, on a subsequent prolonged (25 min) occlusion; analysis of ischaemia and reperfusion induced arrhythmias and of epicardial ST segment changes was performed.Experimental material - 46 anaesthetised mongrel dogs in a restricted body weight range were used.Measurements and main results - Preconditioning reduced the incidence and severity of ischaemic arrhythmias during a 25 min occlusion. Ventricular premature beats (VPB) reduced from 445 (SEM 140) to 96(22) (p<0.0l), ventricular fibrillation (VF) from 4/10 to 0/20 (p<0.05), and ventricular tachycardia from 9/10 to 6/20 (p<0.05). VF following reperfusion was reduced from 6/6 to 6/10 (p<0.05). Preconditioning thus increased survival from the prolonged ischaemia-reperfusion insult from 0% to 40%. The protective effect of preconditioning was lost in the presence of the cyclo-oxygenase inhibitor sodium meclofenamate (2 mg·kg-1), eg, VPBs 367(95), VF during occlusion 1/9 and during reperfusion 8/8, survival 0%.Conclusions - Short, preconditioning periods of myocardial ischaemia protect the myocardium against the arrhythmogenic effects of a more prolonged occlusion. That this protection is lost if the cyclo-oxygenase pathway is blocked suggests a protective role for prostanoids, most likely prostacyclin, as endogenous myocardial protective substances.

Original languageEnglish
Pages (from-to)1020-1023
Number of pages4
JournalCardiovascular Research
Volume24
Issue number12
DOIs
Publication statusPublished - Jan 1 1990

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Ischemic Preconditioning
Prostaglandin-Endoperoxide Synthases
Reperfusion
Myocardium
Ventricular Fibrillation
Cardiac Arrhythmias
Coronary Vessels
Ischemia
Meclofenamic Acid
Dogs
Ventricular Premature Complexes
Cyclooxygenase Inhibitors
Coronary Occlusion
Epoprostenol
Ventricular Tachycardia
Arachidonic Acid
Prostaglandins
Myocardial Ischemia
Body Weight
Incidence

Keywords

  • Arrhythmias
  • Cyclo-oxygenase products
  • Dog
  • Myocardial ischaemia
  • Preconditioning
  • Prostacyclin

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Protective effects of preconditioning of the ischaemic myocardium involve cyclo-oxygenase products. / Végh, A.; Szekeres, Laszlo; Parratt, J.

In: Cardiovascular Research, Vol. 24, No. 12, 01.01.1990, p. 1020-1023.

Research output: Contribution to journalReview article

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abstract = "Study objective - The aim was to determine whether short (preconditioning) occlusions of a coronary artery protect against the arrhythmias occurring during a subsequent more prolonged occlusion and to examine whether the observed protection is mediated by the release of a product of the cyclo-oxygenase pathway of arachidonic acid metabolism.Design - The effects were examined of two short (5 min) coronary artery occlusions, in chloraloseurethane anaesthetised dogs, on a subsequent prolonged (25 min) occlusion; analysis of ischaemia and reperfusion induced arrhythmias and of epicardial ST segment changes was performed.Experimental material - 46 anaesthetised mongrel dogs in a restricted body weight range were used.Measurements and main results - Preconditioning reduced the incidence and severity of ischaemic arrhythmias during a 25 min occlusion. Ventricular premature beats (VPB) reduced from 445 (SEM 140) to 96(22) (p<0.0l), ventricular fibrillation (VF) from 4/10 to 0/20 (p<0.05), and ventricular tachycardia from 9/10 to 6/20 (p<0.05). VF following reperfusion was reduced from 6/6 to 6/10 (p<0.05). Preconditioning thus increased survival from the prolonged ischaemia-reperfusion insult from 0{\%} to 40{\%}. The protective effect of preconditioning was lost in the presence of the cyclo-oxygenase inhibitor sodium meclofenamate (2 mg·kg-1), eg, VPBs 367(95), VF during occlusion 1/9 and during reperfusion 8/8, survival 0{\%}.Conclusions - Short, preconditioning periods of myocardial ischaemia protect the myocardium against the arrhythmogenic effects of a more prolonged occlusion. That this protection is lost if the cyclo-oxygenase pathway is blocked suggests a protective role for prostanoids, most likely prostacyclin, as endogenous myocardial protective substances.",
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N2 - Study objective - The aim was to determine whether short (preconditioning) occlusions of a coronary artery protect against the arrhythmias occurring during a subsequent more prolonged occlusion and to examine whether the observed protection is mediated by the release of a product of the cyclo-oxygenase pathway of arachidonic acid metabolism.Design - The effects were examined of two short (5 min) coronary artery occlusions, in chloraloseurethane anaesthetised dogs, on a subsequent prolonged (25 min) occlusion; analysis of ischaemia and reperfusion induced arrhythmias and of epicardial ST segment changes was performed.Experimental material - 46 anaesthetised mongrel dogs in a restricted body weight range were used.Measurements and main results - Preconditioning reduced the incidence and severity of ischaemic arrhythmias during a 25 min occlusion. Ventricular premature beats (VPB) reduced from 445 (SEM 140) to 96(22) (p<0.0l), ventricular fibrillation (VF) from 4/10 to 0/20 (p<0.05), and ventricular tachycardia from 9/10 to 6/20 (p<0.05). VF following reperfusion was reduced from 6/6 to 6/10 (p<0.05). Preconditioning thus increased survival from the prolonged ischaemia-reperfusion insult from 0% to 40%. The protective effect of preconditioning was lost in the presence of the cyclo-oxygenase inhibitor sodium meclofenamate (2 mg·kg-1), eg, VPBs 367(95), VF during occlusion 1/9 and during reperfusion 8/8, survival 0%.Conclusions - Short, preconditioning periods of myocardial ischaemia protect the myocardium against the arrhythmogenic effects of a more prolonged occlusion. That this protection is lost if the cyclo-oxygenase pathway is blocked suggests a protective role for prostanoids, most likely prostacyclin, as endogenous myocardial protective substances.

AB - Study objective - The aim was to determine whether short (preconditioning) occlusions of a coronary artery protect against the arrhythmias occurring during a subsequent more prolonged occlusion and to examine whether the observed protection is mediated by the release of a product of the cyclo-oxygenase pathway of arachidonic acid metabolism.Design - The effects were examined of two short (5 min) coronary artery occlusions, in chloraloseurethane anaesthetised dogs, on a subsequent prolonged (25 min) occlusion; analysis of ischaemia and reperfusion induced arrhythmias and of epicardial ST segment changes was performed.Experimental material - 46 anaesthetised mongrel dogs in a restricted body weight range were used.Measurements and main results - Preconditioning reduced the incidence and severity of ischaemic arrhythmias during a 25 min occlusion. Ventricular premature beats (VPB) reduced from 445 (SEM 140) to 96(22) (p<0.0l), ventricular fibrillation (VF) from 4/10 to 0/20 (p<0.05), and ventricular tachycardia from 9/10 to 6/20 (p<0.05). VF following reperfusion was reduced from 6/6 to 6/10 (p<0.05). Preconditioning thus increased survival from the prolonged ischaemia-reperfusion insult from 0% to 40%. The protective effect of preconditioning was lost in the presence of the cyclo-oxygenase inhibitor sodium meclofenamate (2 mg·kg-1), eg, VPBs 367(95), VF during occlusion 1/9 and during reperfusion 8/8, survival 0%.Conclusions - Short, preconditioning periods of myocardial ischaemia protect the myocardium against the arrhythmogenic effects of a more prolonged occlusion. That this protection is lost if the cyclo-oxygenase pathway is blocked suggests a protective role for prostanoids, most likely prostacyclin, as endogenous myocardial protective substances.

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