GLUCOSE IS ARRHYTHMOGENIC IN THE ANOXIC-REOXYGENATED EMBRYONIC CHICK HEART

Unlike in adult heart, embryonic myocardium works at low Po-2 and depe nds preferentially on glucose. Therefore, activity of the embryonic he art during anoxia and reoxygenation should be particularly affected by changes in glucose availability. Hearts excised from 4-d-old chick em bryos were submitted in vitro to strictly controlled anoxia-reoxygenat ion transitions at glucose concentrations varying from 0 to 29 mmol/L. Spontaneous and regular heart contractions were detected optically as movements of the ventricle wall and instantaneous heart rate, amplitu de of contraction, and velocities of contraction and relaxation were d etermined. Anoxia induced transient tachycardia and rapidly depressed contractile activity, whereas reoxygenation provoked a temporary and c omplete cardioplegia (oxygen paradox). In the presence of glucose, atr ial rhythm became irregular during anoxia and chaotic-periodic during reoxygenation. The incidence of these arrhythmias depended on duration of anoxia, and no ventricular ectopic beats were observed. Removal of glucose or blockade of glycolysis suppressed arrhythmias. These resul ts show similarities but also differences with respect to the adult he art. Indeed, glucose 1) delayed the anoxic contractile failure, shorte ned the reoxygenation-induced cardiac arrest, and improved the recover y of contractile activity; 2) attenuated stunning at 20 mmol/L but wor sened it at 8 mmol/L; and 3) paradoxically, was arrhythmogenic during anoxia and reoxygenation, especially when present at the physiologic c oncentration of 8 mmol/L. The last named phenomenon seems to be charac teristic of the young embryonic heart, and our findings underscore tha t fluctuations of glycolytic activity may play a role in the reactivit y of the embryonic myocardium to anoxia-reoxygenation transitions.