title: The neuro-cardio-endocrine response to acute subarachnoid haemorrhage.
abstract: OBJECTIVE
  Whereas cardiac hormones increase after subarachnoid haemorrhage (SAH), and may contribute to sodium wastage and hyponatraemia, there is controversy concerning the relative roles of atrial natriuretic peptide (ANP) vs. brain natriuretic peptide (BNP) and the factors initiating their secretion. Noting previous work linking stress hormone responses with cardiac injury after SAH, we have studied responses in stress hormones, markers of cardiac injury and the temporal changes in ANP and BNP and related them to changes in sodium status post ictus and during recovery from acute SAH.
  
  
  METHODS
  Eighteen patients with verified SAH of variable severity were studied in a single unit for a 14-day period post ictus under controlled conditions of sodium and fluid intake. All received a standardized protocol of daily dexamethasone and nimodipine throughout the study. Severity was graded using criteria of Hess and Hunt at admission. Stress hormones (AVP, catecholamines and admission plasma cortisol), markers of cardiac injury (ECG and daily plasma troponin T) and cardiac hormones (ANP and BNP) were measured daily and related to severity, plasma sodium and renin-aldosterone activity. Hormone levels (ANP, BNP and endothelin) in cerebrospinal fluid (CSF) were also measured in nine patients.
  
  
  RESULTS
  Intense neurohormonal activation (AVP, cortisol and catecholamines) at admission was associated with increased levels of both plasma ANP and BNP whereas levels in CSF were unaffected. In individual patients plasma levels of ANP and BNP were strongly correlated (P < 0.001). Cardiac events (abnormal ECG and/or elevated troponin) occurred in six of seven patients graded severe but neither stress hormones nor cardiac peptides differed significantly in patients with mild (n = 11) vs. severe (n = 7) SAH. During the course of a progressive fall in plasma sodium concentration (P = 0.001), there was a delayed activation of renin-aldosterone which was inversely correlated with declining levels of plasma ANP/BNP (P < 0.002).
  
  
  CONCLUSIONS
  Excessive secretion of both ANP and BNP occurs in all patients after acute subarachnoid haemorrhage and is unrelated to severity, stress hormone activation or markers of cardiac injury. Inhibition of renin-aldosterone by cardiac hormones may impair renal sodium conservation and contribute to developing hyponatraemia. In the absence of evidence for activation of natriuretic peptides within the brain, the prompt and consistent increase in both ANP and BNP strongly supports the view that the heart is the source of increased natriuretic peptide secretion after acute subarachnoid haemorrhage.
authors.affiliation: Department of Neurosurgery, Christchurch Hospital, PB 4710, Christchurch, New Zealand. eric.espiner@chmeds.ac.nz
authors.forename: Eric A
authors.initials: EA
authors.lastname: Espiner
authors.forename: Robert
authors.initials: R
authors.lastname: Leikis
authors.forename: Richard D
authors.initials: RD
authors.lastname: Ferch
authors.forename: Martin R
authors.initials: MR
authors.lastname: MacFarlane
authors.forename: Janusz A
authors.initials: JA
authors.lastname: Bonkowski
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Frampton
authors.forename: A Mark
authors.initials: AM
authors.lastname: Richards
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D001127:Arginine Vasopressin / Q000652:urine; D009320:Atrial Natriuretic Factor / Q000097:blood* / Q000134:cerebrospinal fluid; D003401:Creatine / Q000652:urine; D004562:Electrocardiography; D016232:Endothelins / Q000134:cerebrospinal fluid; D004837:Epinephrine / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood* / Q000134:cerebrospinal fluid; D009638:Norepinephrine / Q000097:blood; D012964:Sodium / Q000097:blood / Q000652:urine; D013345:Subarachnoid Hemorrhage / Q000097:blood* / Q000134:cerebrospinal fluid / Q000503:physiopathology; D013997:Time Factors; D020107:Troponin T / Q000097:blood
chemical_list: D016232:Endothelins; D020107:Troponin T; D001127:Arginine Vasopressin; D020097:Natriuretic Peptide, Brain; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D003401:Creatine; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine