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Pregled bibliografske jedinice broj: 893881

Hyperbaric oxygenation affects mechanisms of vascular reactivity


Drenjančević, Ines; Mihaljević, Zrinka; Matić, Anita; Unfirer, Sanela; Mišir, Mihael; Mihalj, Martina; Bilić-Dujmušić, Nikolina; Jukić, Ivana; Stupin, Ana; Gros, Mario; Kibel, Aleksandar
Hyperbaric oxygenation affects mechanisms of vascular reactivity // 4th Congress of Croatian Physiological Society and 2nd Regional Congress of the Physiological Societies - Abstract Book
Dubrovnik, Hrvatska, 2017. str. /-/ (pozvano predavanje, međunarodna recenzija, sažetak, znanstveni)


Naslov
Hyperbaric oxygenation affects mechanisms of vascular reactivity

Autori
Drenjančević, Ines ; Mihaljević, Zrinka ; Matić, Anita ; Unfirer, Sanela ; Mišir, Mihael ; Mihalj, Martina ; Bilić-Dujmušić, Nikolina ; Jukić, Ivana ; Stupin, Ana ; Gros, Mario ; Kibel, Aleksandar

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
4th Congress of Croatian Physiological Society and 2nd Regional Congress of the Physiological Societies - Abstract Book / - , 2017, /-/

Skup
4th Congress of Croatian Physiological Society and 2nd Regional Congress of the Physiological Societies

Mjesto i datum
Dubrovnik, Hrvatska, 21-24.09.2017

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Hyperbaric oxigenation, vascular function

Sažetak
Hyperbaric oxygenation (HBO2) has become widely accepted adjuvant therapy for various conditions with deprived tissue oxygenation, such as diabetic foot and ulcers, ischemic injuries, sepsis, skin flap transplantations. Besides its beneficiary effects on the tissue perfusion, HBO2 exhibits high toxicity at higher pressures, due to increased oxidative stress and barotrauma. Mechanisms of beneficiary as well as pathophysiological effects of HBO2 on vascular function are intensively investigated and include studies in macrovessels, as well as in microvessels, in different animal models and in humans. For example, our studies in diabetic rats demonstrated significantly reduced dilation of cerebral resistance vessels in response to acetylcholine, which is restored with HBO2, possibly mediated by effect of CYP450- epoxygenases’ vasodilating metabolites EETs on KATP channels. Similarly, in aortic ring studies, it appears that HBO2 enhances NO production and EETs production while oxidative stress was not increased. Intermittent HBO2 shifts the arachidonic acid metabolites production / sensitivity demonstrated in genetically modified rats, diabetic rats and in human. Several enzymatic pathways, most prominently CYP450 hydroxylases and epoxygenases are affected by HBO2 ; this occurs in healthy as well as in diseased vasculature. HBO2 changes vascular function by changing mRNA and protein expression, and subsequently production of mediators, such as EETs and NO. In the model of experimental stroke in diabetic female rats, HBO2 exhibited beneficial effects by reducing brain infarct size. Contrary to intermittent HBO2, acute hyperbaric oxygenation immediately after exposure impairs endothelial dependent vasorelaxation (ACh), NO- dependent which is temporary, reversible and caused by increased superoxide levels. This has been proved on functional level (restored relaxation after TEMPOL in vitro) and by direct measurements of released superoxide in aortic tissue. There is a delay in antioxidative enzyme expression in acute HBO2 treatment which may contribute to impaired vasorelaxation.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

Napomena
Funded by: VIF2017-MEFOS-4 ; PI: Ines Drenjančević



POVEZANOST RADA


Projekt / tema
219-2160133-2034 - Djelovanje kisika na vaskularnu funkciju u zdravlju i bolesti (Ines Drenjančević, )

Ustanove
Medicinski fakultet, Osijek