Page 45 - Effects of radiotherapy and hyperbaric oxygen therapy on oral microcirculation Renee Helmers

Hyperoxia-driven microvascular changes
demonstrating translational similarities.3,51 In our model no microvascular vasoconstriction was observed during HB hyperoxia, this finding was surprising
and controversial; we can only hypothesize that the absence of vasoconstriction
may have been due to discordance in vascular regulatory signals and/or hemodynamic shear stresses in relation to the observed denser blood volume. 2 Furthermore regarding microthrombi, recent investigations indicate engaging
of platelet activation via thrombin and arachidonic acid pathways in patients30 subjected to similar hyperbaric conditions as presented in this report. It is important to consider that the unseen microthrombi and activated leukocytes in the microcirculation may have been due to the overshadowing effects of vasodilation and dense blood volume described in the microcirculation during HB hyperoxia. For example, recall that the SDFI relies on hemoglobin in RBCs absorbing green light, this poses a technical challenge and makes discerning microthrombi from free RBCs in dense blood volume difficult and does not exclude their presence in the microcirculation under HB conditions. Under influence of HBO conditions the absence of vasoconstriction may be an advantageous mechanism enabling maximum tissue blood perfusion despite the contemplated presence of activated immune cells and/or circulating microthrombi; this is supported by the Øbv that remained near baseline values during the first three HB time points (T4, T5, and T6) and the small increase in vasodilation (though not significant) that was observed during HB normoxia (T7) and NB normoxia at the end of the experiments (T8).
Several considerations need to be addressed based on the present model. First, in pilot experiments we found that 10 min was sufficient time to enable transition towards oxygen acclimatization from normoxia to hyperoxia and back to normoxia (data not published). Second, the sequence of the experiments presented in the protocol was not randomized and the duration of anesthesia may have influenced the HB hyperoxia segment of the investigation. Third, the measured calcium levels were below the normal reference range. Vascular smooth muscle cell contractility is regulated by intracellular calcium concentrations that in turn set vascular tone and blood pressure. Interestingly though despite being low already at baseline, circulating calcium levels decreased (though not significant) during hyperoxia under both NB and HB conditions; these minute oscillations seem to indicate that calcium consumption may have been present during hyperoxia. We cannot explain why no direct vasoconstriction was measured during HB hyperoxia. We can only speculate that
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