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. Author manuscript; available in PMC: 2019 Jun 24.
Published in final edited form as: Clin Pharmacol Ther. 2018 Jan 17;104(3):553–563. doi: 10.1002/cpt.979

Figure 5.

Figure 5

Effect of ethyl nitrite (ENO) on tissue oxygenation (StO2) and oxygen utilization in humans. (a) Calf muscle oxygenation measured with near infrared spectroscopy during hypoxia and dosing with 1–100 ppm ENO; each dose was administered for 20 min (no washout). Initiation of hypoxia (time 0; normoxic baseline) produced a significant decline in StO2 (*P < 0.05). For doses >10 ppm ENO, calf oxygenation increased, reaching normoxic levels at 40 ppm. At study completion, muscle StO2 was at normoxic (prehypoxic) levels (P=1.00). (b) Consistent with an ENO-induced increase in peripheral oxygen utilization there was a direct linear relationship between muscle StO2 and arterial-venous oxygen content difference (A-V Δ O2, mL/dL; r=0.44). (c) Brain StO2 declined with hypoxia, then remained significantly lower than the prehypoxic starting point throughout ENO dosing (*P < 10−7). (d) Consistent with the persistent decrease in cerebral oxygenation, there was no relationship between brain StO2 and A-V Δ O2 difference (r=0.09).