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J Neurotrauma. 2017 Jul 15;34(14):2315-2319. doi: 10.1089/neu.2016.4962. Epub 2017 Apr 26.

Hypertension-Induced Enhanced Myogenic Constriction of Cerebral Arteries Is Preserved after Traumatic Brain Injury.

Szarka N1,2, Amrein K1,3, Horvath P1, Ivic I2, Czeiter E1,3, Buki A1,3, Koller A1,4,5, Toth P1,2,3,6.

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1 Department of Neurosurgery and Szentagothai Research Center, University of Pecs , Pecs, Hungary .
2 Department of Translational Medicine, University of Pecs , Pecs, Hungary .
3 MTA-PTE Clinical Neuroscience MR Research Group , Pecs, Hungary .
4 Institute of Natural Sciences, University of Physical Education , Budapest, Hungary .
5 Department of Physiology, New York Medical College , Valhalla, New York.
6 Reynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, Oklahoma.


Traumatic brain injury (TBI) was shown to impair pressure-induced myogenic response of cerebral arteries, which is associated with vascular and neural dysfunction and increased mortality of TBI patients. Hypertension was shown to enhance myogenic tone of cerebral arteries via increased vascular production of 20-hydroxyeicosatrienoic acid (HETE). This adaptive mechanism protects brain tissue from pressure/volume overload; however, it can also lead to increased susceptibility to cerebral ischemia. Although both effects may potentiate the detrimental vascular consequences of TBI, it is not known how hypertension modulates the effect of TBI on myogenic responses of cerebral vessels. We hypothesized that in hypertensive rats, the enhanced myogenic cerebrovascular response is preserved after TBI. Therefore, we investigated the myogenic responses of isolated middle cerebral arteries (MCA) of normotensive and spontaneously hypertensive rats (SHR) after severe impact acceleration diffuse brain injury. TBI diminished myogenic constriction of MCAs isolated from normotensive rats, whereas the 20-HETE-mediated enhanced myogenic response of MCAs isolated from SHRs was not affected by TBI. These results suggest that the optimal cerebral perfusion pressure values and vascular signaling pathways can be different and, therefore, should be targeted differently in normotensive and hypertensive patients following TBI.


20-HETE; autoregulation; cerebral blood flow; high pressure

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