Reversible Decrease of Oxygen Consumption by Hyperoxia*

Heterogeneous sensitivity of cerebral and muscle tissues to acute normobaric hyperoxia at rest

“…This seemingly paradoxical response has been confirmed by others (McLeod et al, 2003;Tisdall et al, 2009), and has been attributed to a maldistribution of blood flow and a functional O 2 shunting in the cerebral microcirculation (Bergofsky and Bertun, 1966;Bredle et al, 1988;Reinhart et al, 1991). It has also been shown that the decrease in O 2 extraction concurs with an increase in mixed venous O 2 tension (Lodato, 1989;Reinhart et al, 1991); a finding that agrees with the notion of a metabolic autoregulatory response that by way of blood perfusion strives to maintain the O 2 supply to the tissue in balance with O 2 demand in cases of a surfeit of O 2 (Tsai et al, 2003). Cerebral Δ[tHb] was significantly reduced during the first 20 min of the HYPER trial, but thereafter did not differ significantly between the trials.…”

Hemodynamic, biochemical and morphological changes induced by aminoguanidine in normal and septic sheep

“…Hyperoxia was not intended in our experiments, and changes in FiO2 were meant only to prevent hypoxia by the sepsis-induced pulmonary dysfunction. Hyperoxia could interfere with the effects of aminoguanidine, probably by causing a decrease in oxygen consumption possibly by the generation of oxygen free radicals [39,40]. In particular, generation of oxygen free radicals could lead to a decrease in the bioactivity of NO, especially under septic conditions (in which oxygen free radical generation is more marked).…”

Hyperoxia Exacerbates Myocardial Ischemia in the Presence of Acute Coronary Artery Stenosis in Swine

“…However, hypocapnic hyperoxia resulted in a drop on global circumferential strain in the healthy animals. [33][34][35] High oxygen tensions seem to decrease capillary density with a consecutive reduction of oxygen diffusion and thus extraction. Increasing CO 2 levels seem to attenuate this effect.…”