Myocardial Lactate Release Research Articles

Myocardial extraction of cyclic AMP during pacing-induced angina

The application of cyclic AMP as a marker of myocardial ischemia in humans with coronary artery disease has been investigated during pacing-induced angina. Cyclic AMP was determined by a radioimmunoassay. In 15 patients myocardial lactate extraction at rest (20 +/- 12%) converted to production levels (-30 +/- 23%) during angina (p less than 0.0005). Insignificant changes occurred in coronary venous plasma cyclic-AMP levels. The mean myocardial cyclic-AMP extraction at rest (0.3 +/- 8.7%) converted to small release values (-6.0 +/-11%) during angina (= n.s.). No significant correlation was found between myocardial lactate and cyclic-AMP uptake or release. Therefore, cyclic AMP is an insensitive marker in the evaluation of myocardial ischemia.

Myocardial release of lactate, inosine and hypoxanthine during atrial pacing and exercise-induced angina.

The coronary venous efflux of lactate, inosine and hypoxanthine during pacing-induced angina has been compared with myocardial extraction of the catabolites during exercise-induced angina. Inosine and hypoxanthine were analyzed by enzyme assay after separation by column chromatography. Myocardial lactate extraction at rest (15 +/- 9%, mean +/- SD) was converted to production levels (-34 +/- 26%) during pacing-induced angina (p less than 0.0005) and increased (24 +/- 13%) during exercise (p less than 0.05). The arterial values at rest (850 +/- 330 mumol/1) were unchanged during pacing and increased five-fold during exercise (4380 +/- 1860 mumol/1). The mean myocardial inosine extraction at rest (33 +/- 10%) was transformed to release values (-41 +/- 30%) during pacing (p less than 0.0005) as well as during exercise (-20 +/- 27%) (p less than 0.0005). The hypoxanthine extraction at rest (25 +/- 11%) decreased during pacing (-7.8 +/- 29%) (p less than 0.0025) and exercise (10 +/- 25%) (NS). The slight increase of arterial inosine and hypoxanthine values was not significant. Myocardially produced lactate, a sensitive marker of pacing-induced ischemia, was obscured by elevated arterial concentrations during exercise. However, inosine significantly correlated with lactate during pacing, and was useful in detecting ischemic myocardial energy deficiency during exercise-induced angina.

The effect of nitroglycerin on myocardial release of inosine, hypoxanthine and lactate during pacing-induced angina.

The efficacy of nitroglycerin as an antianginal drug has been evaluated by calculation of myocardial extraction and production values of lactate and the adenosine triphosphate (ATP) catabolites inosine and hypoxanthine. Coronary venous and arterial blood was sampled at rest, during pacing-induced angina and 4--6 min after nitroglycerin at identical paced heart rates for enzymatic assay of inosine and hypoxanthine after separation by column chromatography and for determination of lactate. Sublingual nitroglycerin given to 10 patients with coronary artery disease decreased coronary venous lactate values from 1175 +/- 320 mumol/l during pacing-induced angina to 950 +/- 240 mumol/l (p less than 0.05). The calculated myocardial lactate production during angina (-31 +/- 19%) diminished after nitroglycerin (-1.7 +/- 22%) (p less than 0.0025). Coronary venous inosine values during angina (1275 +/- 865 nmol/l) decreased after nitroglycerin (795 +/- 555 nmol/l) (p = n.s.), the arterial values (885 +/- 610 nmol/l) increased (960 +/- 580 nmol/l) (p = n.s.), the myocardial inosine release (-26 +/- 20%) changed to extraction values (19 +/- 19%) (p less than 0.0005). Coronary venous hypoxanthine values during angina (1540 +/- 1035 nmol/l) were reduced (1110 +/- 675 nmol/l) (p = n.s.); the arterial values (1625 +/- 1050 nmol/l) decreased (1510 +/- 935 nmol/l) (p = n.s.), the myocardial hypoxanthine extraction (0.3 +/- 29%) with a wide individual variability increased after nitroglycerin (24 +/- 13%) (p less than 0.025). The myocardial release of inosine and lactate during severe angina with significant positive correlation (r = 0.66, p less than 0.0025) demonstrates that anaerobic glycolysis is accompanied by ATP breakdown. The unchanged myocardial inosine and hypoxanthine extraction after nitroglycerin indicates that nitroglycerin is capable of attenuating this effect. In spite of reduced mean myocardial lactate production after nitroglycerin ischemic myocardial energy deficiency may be less marked. Thus, the enhanced myocardial inosine uptake may be one factor contributing the beneficial effects of nitroglycerin including the improvement of myocardial oxygen balance.

The influence of nitroglycerine on myocardial release of inosine, hypoxanthine and lactate during pacing induced angina in humans with coronary artery disease

The influence of nitroglycerine on myocardial release of inosine, hypoxanthine and lactate during pacing induced angina in humans with coronary artery disease

Myocardial lactate oxidation and release in the dog in vivo.

Myocardial metabolism of lactate was studied in eight, anesthetized, non-heparinized, open-chest dogs maintained on positive pressure breathing with room air. Arterial and coronary sinus (CS) samples were obtained during a constant intravenous infusion of 2-C14-l-lactate, and were analyzed for chemical and radiochemical content of lactate, pyruvate, glucose and CO2, as well as chemical content of oxygen. The specific activity (dpm/μM) of lactate in CS blood was lower than that in the arterial samples. These differences are consistent with the addition of cold, unlabelled lactate to the CS blood by the myocardium. This lactate release amounted to 35.0±6.1% of the A-CS lactate uptake. Oxidation of lactate by the heart, which was measured from C14O2 production amounted to 45.9% of the myocardial oxygen uptake, after a correction was made for secondary labelling of pyruvate and glucose.

Evaluation of Myocardial Metabolism in Ischemic Heart Disease

Metabolism of the human heart during myocardial infarction may be studied by means of arterial and coronary sinus catheterization at little risk, but definite inconvenience. Ischemia has been readily detected through myocardial production or release of lactate, potassium, hydrogen, and certain enzymes. These findings may be of help in identifying the presence of acute myocardial injury or infarction and in evaluation of applied therapy. Other studies, particularly of metabolized substrates, including oxygen, have been less rewarding. The patchy nature of coronary atherosclerosis and its partial compensation by collateral vessels renders coronary venous inflow nonuniform. This makes interpretation of the meaning of the concentration of substances contained within the coronary venous effluent extremely difficult. Multiple-site venous sampling is particularly helpful in overcoming this inherent defect in the method.

Release of adenosine in reactive hyperemia of the dog heart.

Release of adenosine in reactive hyperemia of the dog heart.