Inflammation and Hemoglobin Oxygen Affinity

In septic patients, oxygen delivery is often impaired, yet the specific impact of inflammation on erythrocyte oxygen transport characteristics remains largely unexplored. This study examined the direct effects of endotoxin-induced inflammation on the oxygen dissociation curve (ODC) and evaluated dexamethasone and noradrenaline as potential pharmacological interventions to modulate hemoglobin oxygen-binding properties during inflammation. Blood samples from ten healthy male volunteers were allocated to four groups: control, lipopolysaccharide (LPS), LPS with dexamethasone, and LPS with noradrenaline. Samples were incubated at 37 °C for two hours. ODCs were determined, providing p50 values and Hill coefficients. Blood gas analysis, 2,3-bisphosphoglycerate levels, and interleukin-6 (IL-6) levels were measured to assess metabolic parameters and inflammatory response. p50 values and Hill coefficients showed no significant differences between LPS-stimulated samples and controls. LPS effectively induced inflammatory activation with significantly elevated IL-6 levels (1416 (1226–1778) vs. 3 [2–4] ng/l, p = 0.002). Dexamethasone co-treatment significantly increased p50 values compared to LPS alone (29.2 (28.1–29.7) vs. 26.9 (25.7–27.9) mmHg, p = 0.030) and altered Hill coefficients (2.47 (2.32–2.56) vs. 2.65 (2.57–2.86), p = 0.002), indicating a rightward shift of the ODC. Noradrenaline demonstrated anti-inflammatory effects with reduced IL-6 levels (1212 (1068–1427) vs. 1416 (1226–1778) ng/l, p = 0.013) but did not significantly alter oxygen-binding properties. Acute inflammation does not directly alter hemoglobin oxygen-binding properties. The novel dexamethasone-induced rightward shift of the ODC may facilitate oxygen release to tissues and could have important clinical implications for steroid therapy in septic patients.