pituitrin and Cardiac-Tamponade

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.

Topics: Animals; Atrial Function; Atrial Natriuretic Factor; Cardiac Tamponade; Dogs; Epinephrine; Female; Male; Norepinephrine; Pressure; Renin; Stroke Volume; Vasopressins

We have described a case of presumed excessive antidiuretic hormone (ADH) secretion due to pericardial effusion and tamponade. Pericardiotomy and drainage produced dramatic resolution of the antidiuresis. In the setting of pericardial tamponade, increased antidiuretic hormone secretion may be "appropriate" in response to overriding stimuli from the left atrial stretch receptors and carotid sinus baroreceptors.

Topics: Blood Volume; Cardiac Tamponade; Humans; Male; Middle Aged; Osmolar Concentration; Pericardial Effusion; Vasopressins

The hypothesis that receptors in the heart or pulmonary vasculature initiate a reflex that influences urine flow was derived from experiments designed to evaluate the effect of mechanical ventilation on renal function. These experiments indicated that urine flow usually decreases during positive-pressure breathing and usually increases during negative-pressure breathing. It was surmised that impulses from certain cardiopulmonary receptors affect the secretion of ADH, which in turn influences urine flow. A subsequent investigation appeared to localize the pertinent receptors to the left atrium, but the results of this particular investigation were influenced by several complication factors that have not been widely appreciated. The apparent localization of volume-regulating recpetors to the left atrium and the accumulating evidence that atrial receptors do respond to changes in atrial pressure or atrial volume triggered a myriad of further studies on the function of left receptors. Nearly all these studies employed indirect techniques that produced changes in systemic and pulmonary hemodynamics in addition to changes in left atrial pressure. Nevertheless, it often was assumed that if changes in left pressure were produced, any concomitant changes in circulating ADH or in urine flow were attributable to a reflex elicited from atrial receptors. Mush of the data obtained were interpreted as being compatible with the elft atrial volume-receptor hypothesis, but very liggle of the data pertained to left atrial receptors specifically.

Topics: Animals; Atrial Function; Biological Assay; Blood Pressure; Blood Volume; Cardiac Surgical Procedures; Cardiac Tamponade; Denervation; Diuresis; Dogs; Extracellular Space; Heart Failure; Hemorrhage; Hypothalamus; Immersion; Kidney; Mechanoreceptors; Natriuresis; Nerve Fibers, Myelinated; Positive-Pressure Respiration; Posture; Radioimmunoassay; Regional Blood Flow; Sensory Receptor Cells; Tachycardia; Vagotomy; Vagus Nerve; Vasopressins; Veratridine