Hyperbaric oxygenation affects mechanisms of vascular reactivity (CROSBI ID 652087)
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Podaci o odgovornosti
Drenjančević, Ines ; Mihaljević, Zrinka ; Matić, Anita ; Unfirer, Sanela ; Mišir, Mihael ; Mihalj, Martina ; Bilić-Dujmušić, Nikolina ; Jukić, Ivana ; Stupin, Ana ; Gros, Mario ; Kibel, Aleksandar
engleski
Hyperbaric oxygenation affects mechanisms of vascular reactivity
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.
hyperbaric oxigenation, vascular function
Funded by: VIF2017-MEFOS-4 ; PI: Ines Drenjančević
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Podaci o prilogu
/-/.
2017.
objavljeno
Podaci o matičnoj publikaciji
4th Congress of Croatian Physiological Society and 2nd Regional Congress of the Physiological Societies - Abstract Book
Podaci o skupu
4th Congress of Croatian Physiological Society and 2nd Regional Congress of the Physiological Societies
pozvano predavanje
21.09.2017-24.09.2017
Dubrovnik, Hrvatska