Plasma Concentrations of Brain Natriuretic Peptide in Patients With Subarachnoid Hemorrhage

Abstract

Background and Purpose-Hyponatremia after subarachnoid hemorrhage (SAH) is commonly associated with diuresis and natriuresis, but the causes are still controversial. We investigated whether brain natriuretic peptide (BNP) was related to such hyponatremia. Methods-Plasma BNP concentrations were measured by immunoradiometric assay in 18 patients at 0 to 2 days (period 1), 7 to 9 days (period 2), and Ͼ14 days (period 3) after SAH. Plasma concentrations of antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and noradrenaline were also measured during period 2. Results-The 11 patients with hyponatremia (serum sodium concentration of Ͻ135 mEq/L) had much higher plasma BNP concentrations during each period than did healthy controls (PϽ0.05), whereas the 7 patients with normonatremia did not show statistically higher values. In the patients with hyponatremia, the plasma BNP concentration during period 2 was statistically higher than that during periods 1 and 3 (PϽ0.05). The plasma noradrenaline concentration during period 2 was higher in patients with hyponatremia than in those with normonatremia (PϽ0.05), whereas the plasma concentrations of ADH and ANP during period 2 were not statistically different between the hyponatremic and normonatremic patients. Key Words: hyponatremia Ⅲ natriuretic peptide, brain Ⅲ subarachnoid hemorrhage H yponatremia after SAH has been reported to have an incidence of 30% to 40%. Recent studies have demonstrated that this phenomenon is frequently associated with hypovolemia, which is caused not by the syndrome of inappropriate secretion of ADH but by CSW. Conclusions-We1,2,3 However, the cause of CSW is still controversial. Some authors have reported that ANP 4,5 and digoxinlike peptides 6 may cause the hyponatremia, while others have suggested that these agents are not involved. 7,8 BNP, which was isolated from porcine brain in 1988, 9 causes natriuresis and diuresis. It has recently become possible to measure BNP accurately by immunoradiometric assay. We investigated whether BNP was related to hyponatremia after SAH by measuring plasma BNP concentrations with use of an immunoradiometric assay in patients with acute SAH. Subjects and Methods Patients and ManagementEighteen patients (4 men and 14 women without cardiac, renal, or endocrine diseases; meanϮSD age, 62.3Ϯ10.8 years) with SAH verified by CT scan were investigated from January 1995 through December 1996. All patients underwent cerebral angiography and aneurysm clipping within 48 hours of the onset, except for 1 patient in whom angiography failed to identify the source of hemorrhage. Each patient received intravenous fluid at approximately 2500 to 3000 mL/d to maintain a central venous pressure of 4 to 12 cm H 2 O. Sodium administration ranged from 280 to 320 mEq/d in patients without hyponatremia, while sodium loss was replaced according to urinary excretion when hyponatremia occurred. When symptomatic vasospasm occurred, ozagrel sodium (Xanbon, Kissei Pharmaceutical Co Ltd) was intravenously administered at 80 mg/d in pa...

Hyponatraemia

“…Increased plasma concentrations of a natriuretic polypeptide released from the brain have been reported (Yamanoto et al, 1987;Berendes et al, 1997) in patients with CSWS. A recent study showed increased circulating plasma brain natriuretic peptide concentrations in patients with CSWS following subarachnoid haemorrhage (Tomida et al, 1998). The pathophysiology of CSWS is not yet fully established, however, and although increased plasma concentrations of natriuretic peptides may be responsible for the natriuresis and hyponatraemia, the mechanism behind the increased secretion has not been identi®ed.…”

Predictors of increased cumulative serum levels of the N-terminal prohormone of brain natriuretic peptide 4 days after acute spontaneous subarachnoid hemorrhage

“…Initially, the effects of BNP on fluid and salt balance were explored. 4,24,27 Later, BNP and vasospasm were studied. Results from these studies indicated that it was the clinically apparent brain ischemia, rather than the angiographic or transcranial Doppler defined vasospasm, that was associated with the BNP increase.…”

Analysis of the serum components in acute period after subarachnoid hemorrhage

“…Troponin I (Tn-I) is elevated in approximately 20-30% of patients with the peak level within 1-2 days from the onset of SAH (21,24). Serum level of the brain natriuretic peptide (BNP) was also found to be increased soon after SAH and returning to baseline in 1 to 2 weeks (34). Increased BNP level is a predictor of worse neurologic outcomes and early in-hospital mortality (36).…”