HYPERTENSION-INDUCED ENHANCED MYOGENIC CONSTRICTION OF CEREBRAL ARTERIES IS PRESERVED AFTER TRAUMATIC BRAIN INJURY.

Szarka, N [Szarka, Nikolett (Idegtudomány, agy...), szerző] Transzlációs Medicina Intézet (PTE / ÁOK); Amrein, K [Amrein, Krisztina (PhD Orvostudomány), szerző] Idegsebészeti Klinika (PTE / ÁOK); Horvath, P [Horváth, Péter (Idegsebészet, Neu...), szerző] Idegsebészeti Klinika (PTE / ÁOK); Klinikai Idegtudományi Doktori Iskola (PTE / DI); Ivic, I [Ivic, Ivan (Gerontology, Phys...), szerző] Transzlációs Medicina Intézet (PTE / ÁOK); Czeiter, E [Czeiter, Endre (Idegsebészet), szerző] Idegsebészeti Klinika (PTE / ÁOK); Buki, A [Büki, András (Idegsebészet, ide...), szerző] MTA-PTE Klinikai Idegtudományi Képalkotó Kutató... (PTE / KCS); Koller, A [Koller, Ákos (Szív és vérkeringés), szerző] Idegsebészeti Klinika (PTE / ÁOK); Toth, P [Tóth, Péter József (Idegsebészet, cer...), szerző] Idegsebészeti Klinika (PTE / ÁOK)

Angol nyelvű Tudományos Szakcikk (Folyóiratcikk)
Megjelent: JOURNAL OF NEUROTRAUMA 0897-7151 34 (14) pp. 2315-2319 2017
  • SJR Scopus - Neurology (clinical): D1
Azonosítók
Szakterületek:
    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 form pressure/volume overload, but 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. Thus, 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 thus should be targeted differently in normotensive and hypertensive patients following TBI.
    Hivatkozás stílusok: IEEEACMAPAChicagoHarvardCSLMásolásNyomtatás
    2021-04-21 03:10