Der Anaesthesist
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Plasma renin-activity and plasma aldosterone were measured by radioimmunoassay in 15 female patients before and 16 hours after intraabdominal surgery. Plasma renin was increased in all patients and plasma aldosterone in 12 patients after operation. Plasma renin and plasma aldosterone were correlated significantly (r=0.66, p less than 0.01) in the whole group. ⋯ It is proposed that postoperative hyperaldosteronism is at least partly mediated through the renin-angiotensin-system. An absolute or relative sodium deficit appears to be an unlikely explanation for the stimulation of the renin-angiotensin-system in the postoperative period. The postoperative increase of plasma renin and consequently plasma aldosterone is possibly a consequence of anaesthetic induced impaired kidney perfusion and/or catecholamine mediated stimulation of renin release.
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In 8 volume expanded dogs with an equilibrium between input and renal output of sodium and water neuroleptanalgesia of 6 hours duration with a total of 9 mg/kg of droperidol and 0.35 mg/kg of fentanyl was performed. Under anaesthesia GFR was increased by about 10% (p less than 0,02) compared with the conscious state, whilst renal sodium and water excretion was reduced by about 50%. From this we conclude that active tubular transport of sodium is augmented under neuroleptanalgesia. ⋯ Plasma volume and intravascular protein did not change under neuroleptanalgesia compared with the conscious state. Urine osmolality and negative free water clearance (TcH2O) increased by about 60% under droperidol and fentanyl. In volume expanded dogs under neuroleptanalgesia intravenous application of 0.5-1.0 mg of atropine resulted in a temporary water diuresis.