Starts: 
Thursday, April 11, 2019 -
12:00 to 13:00
Specific location: 
Room 201

BMC Seminar Thursday 11th of April at 12:00 in room 201 Læknagarður

Speaker: Dr. Aleksandar Kibel, assistant professor at the Department of Physiology and Immunology at the Faculty of Medicine, University of Osijek, as well as an internal medicine specialist and cardiology subspecialist at the Department for Heart and Vascular Diseases, Osijek University Hospital, Croatia.

Title: The effect of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) - the role of CYP enzymes

Abstract: Hyperbaric oxygenation is the therapeutic or experimental application of 100% oxygen at a pressure level higher than atmospheric pressure. Treatment with hyperbaric oxygen can be a beneficial adjuvant therapy in various disorders characterized by compromised tissue oxygenation and perfusion. However, the effects of hyperbaric oxygenation cannot be simply explained as a compensation of the oxygen deficit. Hyperbaric oxygenation has a much broader influence and has the ability to alter protein expression, modulate signaling pathways and affect vascular structure and function. The objective of our work was to assess the effects of hyperbaric oxygenation on vascular reactivity to angiotensin II and angiotensin-(1-7) and to investigate the role of epoxyeicosatrienoic acids (EETs) and specific cytochrome P450 (CYP) enzymes in the modulation of vascular reactivity by hyperbaric oxygenation. Data from functional studies on isolated aortic ring preparations, as well as mRNA and protein expression studies will be presented, showing that hyperbaric oxygenation significantly increases vascular responses to ANG-(1-7), what could explain some of the observed positive effects of hyperbaric oxygenation in pathologic conditions. EETs seem to play an important role in the mechanism of this modulation. Hyperbaric oxygenation increases the expression of specific CYP isoforms, but it is also possible that it increases the vascular sensitivity to EETs. The changes in vascular reactivity were not a consequence of a possible change in arterial pressure, oxidative stress or ANG-(1-7) blood levels. Hyperbaric oxygenation does not significantly alter reactivity to ANG II in either healthy or diabetic rats. The findings contribute in broadening our understanding of the mechanisms underlying the influence of hyperbaric oxygenation.

 

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