The effect of atrial stretching on the genesis of atrial arrhythmias was studied in 26 dogs. Left atrial dilatation was produced by inflation of a balloon catheter. Electrophysiological studies were performed by programmed electrical stimulation of the atrium and ventricle. The irritability of the atrium markedly increased when it was distended and atrial arrhythmias (sustained or non-sustained atrial tachyarrhythmias) could regularly be induced by administration of an early extrastimulus or--more rarely--by atrial burst pacing. In 10 cases spontaneous atrial tachycardia appeared during atrial balloon dilatation. The atrial effective refractory period shortened and the atrial conduction time lengthened on atrial stretching, while other electrical variables (cycle length, sinus node recovery time, atrioventricular conduction time, intraventricular conduction, ventricular refractory period, QT interval) remained unchanged. Atrial balloon dilatation was not accompanied by marked haemodynamic changes, and the left ventricular pressure curve, the contractility of the left ventricle and the central venous pressure did not change significantly on atrial stretching. The experimental data suggest that the atrial dilatation plays an important part in the pathogenesis of atrial arrhythmias.

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It has been shown that the adenosine concentration in the pericardial fluid of the normal heart is higher by one order of magnitude than that of the venous plasma. A further increase in the pericardial adenosine concentration was also demonstrated in myocardial ischaemia or hypoxia. It was proposed that pericardial nucleoside levels may represent the interstitial concentrations of the adenine nucleosides. An experimental model was designed to determine the intrapericardial concentrations of adenosine, inosine and hypoxanthine during coronary spasm provoked by intracoronary administration of endothelin-1 (ET-1; 0.08+/-0.02 nmol/g of myocardial tissue). In the in situ dog heart (n=10), adenosine, inosine and hypoxanthine concentrations were determined by HPLC in fluid samples collected from the closed pericardial sac before and after ET-1 administration, and from the systemic arterial blood. Systemic blood pressure, heart rate and standard ECG were registered continuously. We found that the nucleoside concentrations in the infusate samples increased significantly during coronary spasm [adenosine, 1.49+/-0.44 compared with 0.37+/-0.07 microM (P<0.05); inosine, 27.43+/-11.51 compared with 0.47+/-0.11 microM (P<0.05); hypoxanthine, 21.17+/-6.49 compared with 4.91+/-1.24 microM (P<0.05)], while a significant decrease in blood pressure and an elevation in ECG ST segments were observed. The levels of the purine metabolites did not change in the systemic blood. The data indicate that changes in adenine nucleoside levels measured in pericardial infusate samples reflect activation of coronary metabolic adaptation in this model of spastic ischaemia, and that pericardial nucleoside levels may characterize alterations in interstitial adenine nucleoside concentrations.

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Poly-ADP-ribose synthetase inhibition improves the recovery of myocardial and endothelial function after cardiopulmonary bypass with hypothermic cardiac arrest.

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