Page 46 - Effects of radiotherapy and hyperbaric oxygen therapy on oral microcirculation Renee Helmers

Chapter 2
the complex interactions associated with several factor (including anesthesia protocol) may have superseded the magnitude of the vasoconstrictive response opposing the expected observable effect during HB hyperoxia. Furthermore, it is difficult to explain why the measured calcium levels were low in comparison to the reference values; two possible explanations are that the diet from domesticated animals may have been more varied and different compared to the standardized diet associated with controlled experiments and there may be calibration discrepancies between different blood gas instruments used by other studies. Fourth, hyperglycemia is commonly observed when anesthetic and sedative agents such as dexmedetomidine and/or midazolam11,52 are used; this is true for both human and animal models and was also measured across all time points. Vasoconstriction may not have been directly attributed to hyperglycemia during NB hyperoxia as no vasoconstriction response was observed despite decreased TCD/PVD during HB hyperoxia. Interestingly in vitro research on glucose incubated rabbit aortic rings showed that raised glucose levels contributed directly to endothelium-derived increased synthesis of vasoconstrictor prostanoids;45 however this finding may not directly apply to microcirculatory vascular responses. Although difficult to explain based on our observations and the available literature, one may speculate that the effects of HBO on activation of leukocytes, microthrombi, hematology, and altered hemorheological properties may have contributed to the decreases in TVD/ PVD during the HB segment of our experiments. Rabbits have an unpredictable tendency of displaying oscillations in hematological values, which is why it may be possible that some hematological components may have contributed towards denser blood volume and failed vasoconstriction registrations in the microcirculation during hyperbaria. Increases in RBC deformability and mean cell volume under HBO conditions have been reported.1 From the present animal model it is difficult to pin an exact explanation on a vasoregulatory mechanism that would equally satisfy both NB and HB hyperoxic scenarios. Given the complex interplay of multiple factors, it appears that final blood vessel caliber settings may be the result of many influences. Furthermore, the hemodynamic effects associated with NB/HB hyperoxia observed in the present model are in line with reviewed reports on HR and blood pressure.40 Interestingly the levels of paO2 during HB hyperoxia did not reach >600 mmHg, it is possible that the effects of hyperoxia may have induced pulmonary vascular paralysis17 and as a consequence resulted in lowered tensions in blood gas values.
44