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The ability of the atrial wall to secrete atrial natriuretic peptide was studied in eight dogs during 2 h of cardiac tamponade and for 2 h after decompression of the pericardium. Cardiac tamponade was induced by instillation of 5% dextrose in water into the pericardial cavity until aortic systolic pressure was reduced by 30% to 35%. Heart rate, cardiac output and atrial, pericardial and aortic pressures were measured at 60 and 120 min of tamponade and at 5, 30, 60, 90 and 120 min after decompression. Blood samples were withdrawn at the same time for the determination of atrial natriuretic peptide and aldosterone levels. Aortic pressure decreased significantly during tamponade and increased after decompression to near control levels. Right and left atrial pressures as well as intrapericardial pressure increased significantly during tamponade and returned to control levels after decompression. The effective transmural pressure, which was reduced during tamponade, was increased significantly at 5 min after decompression. Cardiac output was significantly reduced during tamponade and returned to pretamponade levels after decompression. Over the total experimental period, no significant changes in the levels of atrial natriuretic peptide were observed, whereas aldosterone increased significantly. It is concluded that the increased atrial pressure observed during cardiac tamponade did not stimulate the secretion of atrial natriuretic peptide. Furthermore, atrial distension observed immediately after decompression was not sufficient or of long enough duration to induce measurable increases in atrial natriuretic peptide levels. Finally, the secondary hyperaldosteronism did not activate atrial natriuretic peptide secretion either during cardiac tamponade or after decompression.

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