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Circulation, Vol 76, 884-890, Copyright © 1987 by American Heart Association

ARTICLES

Hormonal responses to cardiac tamponade: inhibition of release of atrial natriuretic factor despite elevation of atrial pressures

GB Mancini, MJ McGillem, ER Bates, AB Weder, SF DeBoe and RJ Grekin
Department of Internal Medicine, Veterans Administration Medical Center, Ann Arbor, MI 48105.

Atrial distension, rather than change in intra-atrial pressure, has been suggested as a principal mediator of release of atrial natriuretic factor (ANF). During cardiac tamponade, atrial pressures rise whereas transmural pressures and atrial stretch may not be affected. The roles of atrial pressure and atrial distension were investigated in six open- chest dogs subjected to cardiac tamponade and rapid volume expansion as disparate means of affecting intra-atrial pressures and atrial stretch. Hemodynamic measurements, immunoreactive ANF (ir-ANF), plasma renin activity, antidiuretic hormone, epinephrine, and norepinephrine were monitored before, during, and after three interventions: (1) tamponade, (2) rapid volume loading followed by tamponade, and (3) volume loading during tamponade. Volume expansion increased right atrial pressure and caused a significant rise in ir-ANF. Elevations of right atrial pressure caused by tamponade were comparable to those induced by volume infusion, but an increase in ir-ANF was not elicited during tamponade, and the ir-ANF response to volume loading was abolished when performed during tamponade. The relation between the change in ANF concentration and change in right atrial pressure were highly significant in the absence of tamponade, when atrial stretch was freely responsive to volume expansion (r = .73, p less than .0001), but not when stretch was inhibited (r = -.16, p = NS). These observations underscore the importance of considering the modulating effects of atrial compliance, transmural pressure, and atrial stretch on the relation between atrial pressures and ANF release.

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