gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Rat subarachnoid hemorrhage model: pathophysiological mechanism of cerebral salt wasting

Meeting Abstract

  • S. Schlaffer - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • H. Tam - Department of Medicine, Georgetown University, Washington, DC, USA
  • J. Verbalis - Department of Medicine, Georgetown University, Washington, DC, USA
  • M. Buchfelder - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • A. Kleindienst - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocP05-09

DOI: 10.3205/09dgnc301, URN: urn:nbn:de:0183-09dgnc3015

Veröffentlicht: 20. Mai 2009

© 2009 Schlaffer et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Electrolyte disorders that result from acute brain damage as traumatic brain injury or subarachnoid hemorrhage (SAH) are yet not completely understood. One potential sequela, cerebral salt wasting (CSW), results often in severe hyponatremia, which to date has not been explained by alterations of peripheral hormone levels. Experimental and anatomical evidence suggests that hypothalamic dysfunction not only influences pituitary endocrine function, but also the peripheral sympathetic system via direct descending neuronal connections. Controlled clinical trials are difficult and potentially dangerous in this very ill population. Therefore, studies using an animal model that mimics the clinical features of CSW offer the best opportunity to understand the underlying pathophysiology.

Methods: In male Wistar rats (325–350 g), SAH was induced by injecting 200µl of autologous blood into the great cistern (n=10). A second group underwent additional bilateral renal denervation (n=10). The rats were housed in metabolic cages, and the daily sodium excretion as well as serum sodium, osmolality and vasopressin (AVP) were measured for 10 days.

Results: Serum sodium (141.5 mmol/l day 0, 142.0 mmol/l day 5), osmolality (303.5 mosmol/kg day 0, 307.2 mosmol/kg day 5) remained stable, while the initial increase of AVP normalized over the investigation period (46.99 pg/ml day 0, 8.14 pg/ml day 5). As compared to control rats, sodium excretion was increased on day 1 (p=0.002) and on day 4 (p=0.026). Sufficient renal denervation was confirmed by significantly reduced kidney catecholamine levels (p<0.001). While early natriuresis was unaffected, denervation prevented late natriuresis (p=0.002).

Conclusions: The rat model of SAH is suitable for studying CSW. We conclude that the renal sympathetic system contributes substantially to natriuresis following SAH, and may be the underlying pathophysiological factor for CSW.