SECRETION OF BRAIN NATRIURETIC PEPTIDE IN PATIENTS WITH ANEURYSMAL SUBARACHNOID HEMORRHAGE

Background Subarachnoid haemorrhage is commonly associated with natriu resis and hyponatraemia. One possible explanation for these features i s a defect in the central regulation of renal sodium reabsorption with increased secretion of a natriuretic factor. We investigated whether excess sodium secretion in patients with subarachnoid haemorrhage is r elated to increased secretion of natriuretic peptides or to the presen ce of digoxin-like immunoreactive substances. Methods We measured the plasma concentrations of digoxin-like immunoreactive substances (by a fluorescence polarisation immunoassay) and natriuretic peptides, aldos terone, renin, and antidiuretic hormone (by radioimmunoassay) in ten p atients with aneurysmal subarachnoid haemorrhage, ten patients undergo ing elective craniotomy for cerebral tumours, and 40 healthy controls of similar age and sex distribution. Samples were collected before sur gery, 1 h, 4 h, and 12 h after surgery, then daily until 7 days postop eratively in the two groups of patients. Findings All patients with su barachnoid haemorrhage, but none of the tumour patients, showed increa sed urine output and urinary excretion of sodium (p=0.018 for comparis on of means of curves to 7 days). The patients with subarachnoid haemo rrhage had much higher plasma concentrations of brain natriuretic pept ide (BNP) than controls, on admission (mean 15.1 [SE 3.8] vs 1.6 [1.0] pmol/L, p<0.001) and throughout the study period, accompanied by lowe r than normal aldosterone concentrations and normal plasma concentrati ons of atrial and C-type natriuretic peptides (ANP, CNP). The patients with tumours had similar plasma concentrations of ANP, BNP, and CNP t o the controls. We did not detect digoxin-like immunoreactive substanc es in either group of patients. Interpretation Salt-wasting of central origin may induce hyponatraemia in patients with aneurysmal subarachn oid haemorrhage, possibly as a result of increased secretion of BNP wi th subsequent suppression of aldosterone synthesis.