This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Diringer, M. Articles by Hanley, D. F. Search for Related Content PubMed PubMed Citation Articles by Diringer, M. Articles by Hanley, D. F.

Stroke, Vol 19, 1119-1124, Copyright © 1988 by American Heart Association

ARTICLES

Plasma atrial natriuretic factor and subarachnoid hemorrhage

M Diringer, PW Ladenson, BJ Stern, J Schleimer and DF Hanley
Department of Neurology, Johns Hopkins Hospital, Baltimore, MD 21205.

Hyponatremia is common following aneurysmal subarachnoid hemorrhage and has been linked to the syndrome of inappropriate secretion of antidiuretic hormone. However, the demonstration of volume depletion and natriuresis in some patients has suggested that salt wasting is a more likely etiology. Atrial natriuretic factor appears to play a role in both central and peripheral regulation of sodium homeostasis. To investigate the behavior of circulating atrial natriuretic factor following subarachnoid hemorrhage, we studied 25 patients with intracranial aneurysms: 21 after acute subarachnoid hemorrhage and four without evidence of recent rupture. Atrial natriuretic factor was measured by radioimmunoassay of extracted plasma (normal value, 20.8 +/- 24.6, mean +/- 3 SD). Mean +/- SEM plasma atrial natriuretic factor concentration was elevated to 84 +/- 25 pg/ml on Day 1, rose to 134 +/- 29 pg/ml on Day 3, and fell to 86 +/- 17 pg/ml by Day 7 after subarachnoid hemorrhage (p less than 0.01). In two patients (9.5%) who developed hyponatremia after aneurysm rupture, plasma concentrations were no different from that in the group as a whole; concentrations in patients with no evidence of recent subarachnoid hemorrhage were not elevated. Neither fluid administration nor timing of surgery could account for the elevated concentrations. We conclude that concentrations of circulating atrial natriuretic factor are elevated after subarachnoid hemorrhage but do not solely account for the accompanying hyponatremia.

This article has been cited by other articles:

				E. Berendes, H. Van Aken, C. Raufhake, C. Schmidt, G. Assmann, and M. Walter Differential Secretion of Atrial and Brain Natriuretic Peptide in Critically Ill Patients Anesth. Analg., September 1, 2001; 93(3): 676 - 682. [Abstract] [Full Text] [PDF]

				A Albanese, P Hindmarsh, and R Stanhope Personal practice: Management of hyponatraemia in patients with acute cerebral insults Arch. Dis. Child., September 1, 2001; 85(3): 246 - 251. [Abstract] [Full Text] [PDF]

				G. E. Sviri, M. Feinsod, and J. F. Soustiel Brain Natriuretic Peptide and Cerebral Vasospasm in Subarachnoid Hemorrhage : Clinical and TCD Correlations Stroke, January 1, 2000; 31(1): 118 - 122. [Abstract] [Full Text] [PDF]

				M. Walter, E. Berendes, A. Claviez, and M. Suttorp Inappropriate Secretion of Natriuretic Peptides in a Patient With a Cerebral Tumor JAMA, July 7, 1999; 282(1): 27 - 28. [Full Text] [PDF]

				M. Tomida, M. Muraki, K. Uemura, and K. Yamasaki Plasma Concentrations of Brain Natriuretic Peptide in Patients With Subarachnoid Hemorrhage Stroke, August 1, 1998; 29(8): 1584 - 1587. [Abstract] [Full Text] [PDF]