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61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010
Joint Meeting mit der Brasilianischen Gesellschaft für Neurochirurgie am 20. September 2010

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

21. - 25.09.2010, Mannheim

Influence of moderate hypothermia on myogenic tone and cerebrovascular reactivity of rat isolated cerebral arteries

Meeting Abstract

Suche in Medline nach

  • Zeliha Guel - Neurochirurgische Forschung, Medizinische Fakultät Mannheim der Universität Heidelberg, Germany
  • Rudolf Schubert - Kardiovaskuläre Physiologie, Medizinische Fakultät Mannheim der Universität Heidelberg, Germany
  • Lothar Schilling - Neurochirurgische Forschung, Medizinische Fakultät Mannheim der Universität Heidelberg, Germany

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocP1868

doi: 10.3205/10dgnc339, urn:nbn:de:0183-10dgnc3391

Veröffentlicht: 16. September 2010

© 2010 Guel 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: Moderate hypothermia is considered a worthwhile approach to achieve neuroprotection in patients suffering from severe ischemic or traumatic brain damage. The present study was performed to characterize the effects of moderate hypothermia (HT) on cerebroarterial function including spontaneous myogenic tone, myogenic response, and reactivity upon receptor-mediated and -independent stimuli.

Methods: Superior cerebellar arteries were obtained from Wistar rats and small segments mounted on micropipettes in a temperature-controlled organ bath at 37°C. Diameter was continuously measured under isobaric conditions. After development of spontaneous tone at 37°C vessels were exposed to stepwise changes of transmural pressure to elicit myogenic responses or exposed to increased concentrations of the extracellular K+ concentration [K+]e, to sarafotoxin 6c (S6c) or bradykinin (Bk) as well as sodium nitroprusside (SNP) (to elicit NO-mediated, endothelium-dependent and -independent dilation), or to U46619 (a thromboxane A2 analogue) and endothelin-1 (ET-1) to induce receptor-mediated constriction. All stimuli were applied under normothermia (NT, 37°C) or after decreasing bath temperature to moderate HT (32°C).

Results: Prior to induction of HT myogenic tone at 70 mmHg was 27.9+1.7% (mean+SEM; n=22). Tone decreased somewhat over time indicating some run-down. This decrease was slightly more pronounced under HT than under NT (p<0.10 ). Diameter responses upon pressure changes (70 to 40mmHg and 70 to 100 mmHg) did not reveal significant differences between NT and HT suggesting that the myogenic autoregulation was unaffected by the temperature decrease. Increasing [K+]e to 7.5mM resulted in a ditation of 26.3+3.5% (NT, n=10) and 15.6+2.1% (HT, n=10; p<0,05 vs NT). Further, increasing [K+]e to 60mM induced a constriction which was comparable in NT (14.3+3.3% , n=10) and HT (11.6+2.9% , n=10, p>0.05). Dilations upon S6c, Bk and SNP did not differ under NT and HT conditions. Similarly, constriction induced by U46619 and ET-1 were fully comparable in NT and HT.

Conclusions: In conclusion, in isolated cerebral arteries moderate HT slightly decreased myogenic tone and dilatation to moderate increases in [K+]e the latter being considered an important factor of metabolic coupling. In contrast, NO mediated dilations were not affected by HT. Furthermore, constrictory responses were unaltered under HT. Taken together these effects might suggest a dysregulation of cerebral perfusion during moderate hypothermia.