Search

The mechanism by which hyperoxia decreases blood flow is still not understood. Hyperoxemia-induced vasoconstriction is known to occur in many organs, including brain and retina, skeletal muscle, and myocardium. Whether this also occurs in skin is unknown. This study was conducted in healthy volunteers exposed intermittently to 100% oxygen (FIO2 1.0). Perfusion of forearm skin was measured by laser Doppler imaging (LDI). In series 1, it was measured in 7 subjects before, during, and after 15 min of oxygen breathing. In series 2, flow was measured, also during air and O2 breathing, after perfusion was raised by (a) sympathetic blockade (induced by a topically applied local anesthetic) (n = 9) and by (b) current-induced vasodilation (n = 8). In normal unperturbed skin, there was no significant change with hyperoxia. When basal perfusion was raised by topical anesthesia or by current, there was also no change in mean perfusion overall with hyperoxia. However, areas with the highest perfusion (upper decile) showed a significant perfusion decrement with hyperoxia (− 30% and − 20%, respectively; p < 0.001). Vasoconstriction with hyperoxia has been demonstrated in human skin. The fact that it is observed only when flow is increased above basal levels and then only in high-flow vessels suggests that cutaneous blood flow control is primarily regulated by variables other than oxygen.

O2 transport and O2 diffusion interact in providing O2 to tissue, but the extent to which diffusion may be critical in the heart is unclear. If O2 diffusion limits mitochondrial oxygenation, a change in blood O2 affinity at constant total O2 transport should alter cardiac O2 consumption (VO2) and function. To test this hypothesis, we perfused isolated isovolumically working rabbit hearts with erythrocytes at physiological blood-gas values and P50 (PO2 required to half-saturate hemoglobin) values at Ph of 7.4 of 17 ▒ 1 Torr (2,3-bisphosphoglycerate depletion) and 33 ▒ 5 Torr (inositol hexaphosphate incorporation). When perfused at 40 and 20% of normal coronary flow, mean VO2 decreased from the control value by 37 and 46% (P < 0.001), and function, expressed as cardiac work, decreased by 38 and 52%, respectively (P < 0.001). Perfusion at higher P50 during low-flow ischemia improved VO2 by 20% (P < 0.001) and function by 36% (P < 0.02). There was also modest improvement at basal flow (P < 0.02 and P < 0.002, respectively). The improvement in VO2 and function due to the P50 increase demonstrates the importance of O2 diffusion in this cardiac ischemia model.