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62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

07. - 11. Mai 2011, Hamburg

Accelerated clot formation to update the experimental subarachnoid-hemorrhage model in the rat

Meeting Abstract

Suche in Medline nach

  • A. Ehlert - Klinik für Neurochirurgie, A.K. St. Georg, Hamburg
  • B. Tiemann - Versuchstierhaltung, Universitätsklinikum Hamburg-Eppendorf, Hamburg
  • G. Manthei - Klinik für Neurochirurgie, A.K. St. Georg, Hamburg
  • K.H. Frosch - Klinik für Neurochirurgie, A.K. St. Georg, Hamburg

Deutsche Gesellschaft für Neurochirurgie. Polnische Gesellschaft für Neurochirurgen. 62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH). Hamburg, 07.-11.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. DocP 051

doi: 10.3205/11dgnc272, urn:nbn:de:0183-11dgnc2729

Veröffentlicht: 28. April 2011

© 2011 Ehlert et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Objective: The experimental subarachnoid hemorrhage (SAH) in the rat is considered to be a bad model for human SAH, since the induction of blood clots, vasospasm or neurological deficits can only be achieved at short-term if at all. Continuous clot formation from induced bleeding, which is considered to be a conditio sine qua non, cannot be achieved in the area of the basal cisterns. Following SAH, humans show persistent clot formation, partly due to endogenous membrane-bound tissue factor (mTF). However, this has not described for rats and a very fast blood wash out has reported due to anatomical variances. We have therefore accelerated the clotting time to improve clot formation.

Methods: TF was added step-by-step to citrated rat blood and an acceleration of the clotting time in routine hematology labs from about 19.55 to 12.4 sec (quick) was achieved. After the induction of SAH in 14 Wistar rats by injection of 0.3 ml native fresh blood via a catheter, we injected 0.08 ml TF to accelerate the clotting process and to achieve a sufficient blood clot in the target area near the circulus arteriosus. For proper positioning, we catheterized the middle cranial fossa accordingly.

Results: All animals treated survived and showed clinical signs of meningeal irriation such as sensitivity to light and noise; some animals developed movement deviations and apparent hemiparesis. On autopsy on the first until the seventh post-operative day (POD), compact clots were found in the target area, until the 14th POD clear clots continued to exist and new formations developed (n=11/14) that looked like connective tissue. CSF testing in two animals revealed clear evidence of old blood on the ninth and eleventh POD and regarding the remaining 3/14 animals, there were no pathological brain findings between the eleventh and 21st POD. On the third and fourth POD, an MRI of two of the animals was carried out (brains without pathological findings on the 21th POD). In the T2-weighted images, we found signs of ischemia for both animals.

Conclusions: We present an experimental SAH model in the rat with reproducible, long-lasting clot formation at the brain-supplying arteries and with potentially corresponding ischemia in the target vessels. The clots that were persistent for more than a week were followed by new formations that resembled connective tissue at the brain surface and their vessels developed. This model may limit the number of model SAHs in large animals and primates.