Extracellular Volume Expansion Inhibits Antidiuretic Hormone Increase during Positive End-Expiratory Pressure in Conscious Dogs

Abstract

1. This study in conscious dogs examined the effects of extracellular volume expansion on plasma antidiuretic hormone, atrial natriuretic peptide and aldosterone concentrations, plasma renin activity, and haemodynamic and renal responses during controlled mechanical ventilation with 20 cmH2O positive end-expiratory pressure. 2. Twenty experiments (10 controls, 10 expansion experiments with 03 ml min−1 kg−1 body weight of a balanced electrolyte solution given intravenously throughout) were performed in five trained, conscious, tracheotomized dogs over 4 h: first and fourth hour, spontaneous breathing; second and third hour, 20 cmH2O positive end-expiratory pressure. 3. In the control experiments positive end-expiratory pressure increased plasma antidiuretic hormone concentration from 1.4 + 0.2 to 10.0 + 3.3 pg/ml, plasma aldosterone concentration from 113 + 19 to 258 + 58 pg/ml and heart rate from 77 + 5 to 94 + 5 beats/min. Positive end-expiratory pressure did not change plasma atrial natriuretic peptide concentration (55 + 5 pg/ml), plasma renin activity (2.6 + 0.4 pmol of angiotensin I h−1 ml−1) and mean arterial pressure 103 + 3 mmHg). 4. In the expansion experiments, positive end-expiratory pressure did not change plasma antidiuretic hormone concentration (1.1 + 0.1 pg/ml), plasma aldosterone concentration (25 + 2 pg/ml), plasma atrial natriuretic peptide concentration (82 + 8 pg/ml), plasma renin activity (0.8 + 0.15 pmol of angiotensin I h−1 ml−1), heart rate (92 + 6 beats/min) and mean arterial pressure (111 + 4 mmHg). 5. In the control experiments, urine volume, sodium excretion and fractional sodium excretion remained in a low range during positive end-expiratory pressure, whereas potassium excretion increased. In the expansion experiments, urine volume, sodium excretion and fractional sodium excretion increased continuously. Glomerular filtration rate was decreased during positive end-expiratory pressure in the control experiments when compared with the expansion experiments (3.4 + 0.3 versus 3.9 + 0.2 ml min−1 kg−1 body weight). 6. Arterial blood gases and plasma osmolality did not change in either protocol. 7. It is suggested that the striking increase in antidiuretic hormone may play a part in the circulatory control mechanisms that maintain mean arterial pressure during positive end-expiratory pressure when the extracellular volume is not expanded.