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Enhanced myogenic response of cerebral arteries induced by pre‐existing hypertension is intact after traumatic brain injury
Author(s) -
Szarka Nikolett,
Amrein Krisztina,
Czeiter Endre,
Buki Andras,
Koller Akos,
Toth Peter J
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.684.3
Subject(s) - medicine , traumatic brain injury , cerebral autoregulation , cerebral blood flow , cerebral perfusion pressure , blood pressure , ischemia , autoregulation , cardiology , cerebral arteries , cerebral circulation , anesthesia , myogenic contraction , psychiatry , smooth muscle
Traumatic brain injury (TBI) impairs pressure‐induced myogenic autoregulation of cerebral blood flow (CBF), which is associated with increased mortality and bad functional outcome of TBI patients. When blood pressure drops lack of myogenic autoregulatory function of cerebral vessels exposes brain tissue to hypoperfusion and ischemia; in case of high blood pressure it allows high blood volume to penetrate the brain exacerbating disruption of the blood brain barrier, development of hemorrhages and elevation of intracranial pressure. Hypertension, the most important cardiovascular risk factor in TBI patients, enhances myogenic tone of cerebral arteries via increased vascular production of 20‐hydroxyeicosatrienoic acid (HETE), which protects brain tissue form pressure/volume overload but leads to increased susceptibility to cerebral ischemia. Although both effects may potentiate the vascular consequences of TBI, it is not known how hypertension modulates the effect of TBI on myogenic responses of cerebral vessels. To establish the effect of TBI on cerebral myogenic responses in hypertension we studied isolated middle cerebral arteries (MCA) of normotensive and spontaneously hypertensive rats (SHR) after severe impact acceleration diffuse brain injury. We found that TBI diminished myogenic constriction of MCAs in normotensive animals, but the 20‐HETE mediated enhanced myogenic tone in SHRs was not affected by traumatic brain injury. These results suggest that following brain trauma hypertensive patients may be protected from high blood pressure, but are likely to be more prone to cerebral ischemia when blood pressure drops, and therefore require different therapeutic strategies than normotensive patients. Support or Funding Information This work was supported by grants from the Marie Curie Actions SMARTER 7 th Framework Program of the European Union 606998 (to NSz and AK), the Hungarian Academy of Sciences (the Bolyai Research Scholarship BO/00634/15 to PT), the Hungarian Brain Research Program (Grant No. KTIA_13_NAP‐A‐II/8 to PT, ECz and AB) and the Hungarian Scientific Research Fund (K108444 to AK).