Key result
Isoproterenol accelerates ATP depletion and energy charge reduction during regional myocardial ischemia.
Why the study?
Beta-adrenergic agonists cause extension of ischaemic lesions in myocardium, but their effects on adenine nucleotide metabolism in acute regional ischaemia were unclear.
Isoproterenol may worsen energetics in ischemic myocardium; leaves open translation to human acute coronary syndromes.
Previous studies have demonstrated that beta-adrenergic agonists cause extension of ischaemic lesions in the myocardium. In the present study the effects of isoproterenol on adenine nucleotide metabolism were investigated in cat hearts with regional ischaemia following permanent coronary occlusion for 45 min. Adenine nucleotides and their metabolites were measured by high performance liquid chromatography and regional myocardial blood flow was measured by 15-microns radiolabelled microspheres in a total of 255 paired tissue samples. Compared with untreated control cats, ATP and the energy charge were more reduced in ischaemic myocardium of isoproterenol-treated cats. Increased amounts of the degradation products inosine and hypoxanthine/xanthine were also found in these regions. These results could be ascribed to increased cardiac performance caused by isoproterenol, which augments the imbalance between energy production and oxygen supply in ischaemic myocardium.
No takes yet. Share an insight, caveat, or question.
Stangeland et al. (1985) studied acute regional ischaemia. Isoproterenol vs. Untreated control cats was evaluated on Adenine nucleotide metabolism (ATP, energy charge, and degradation products). Isoproterenol treatment in cat hearts with regional ischaemia led to a greater reduction in ATP and energy charge and increased degradation products compared with untreated controls.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: