Changes in the microcirculation during human endotoxemia measured with near-infrared spectroscopy

Objective

Aiming at a better understanding of the microcirculatory deficits that characterize the septic condition, we measured local hemoglobin oxygen saturation (= tissue oxygen saturation [StO₂]) using near-infrared spectroscopy (NIRS) (Hutchinson Technology, USA) before and during experimental human endotoxemia. The baseline StO₂ may represent the vasodilatory state, the decline in StO₂ during ischemia the tissue oxygen consumption, the slope of increase in StO₂ after the ischemic period vascular reactivity, and the area under the curve after reperfusion the flow debt repayment.

Methods

Five healthy subjects received an i.v. dose of 2 ng/kg E. coli O:113 lipopolysaccharide (LPS) and five subjects served as controls. Before, 2 and 4 hours after the administration of LPS/placebo the StO₂ was measured in the thenar skeletal muscle before, during and after a 1.5-min period of arterial occlusion (inflating an upper-arm cuff 50 mmHg above the systolic blood pressure). Data are expressed as the mean ± SEM. Differences were tested by paired Student t tests. P < 0.05 was considered to indicate significance.

Results

The control subjects showed that time itself did not change the response to ischaemia as measurements at t = 0, 2 and 4 hours demonstrated similar changes in StO₂. LPS administration induced the expected flu-like symptoms, fever, and the decrease in mean arterial pressure and the increase in heart rate. Experimental endotoxemia resulted in an increase in the baseline StO₂ from 79 ± 4% at t = 0 to 87 ± 4% at t = 2 hours (P = 0.07) and 94 ± 1% at t = 4 hours (P = 0.049) after LPS administration. The decline in StO₂ during ischemia and the slope of increase during reperfusion was not influenced by endotoxemia. However, the area under the curve after reperfusion decreased from 18 ± 4 AU at t = 0, to 10 ± 4 at t = 2 hours (P = 0.04) and 6 ± 1 AU at t = 4 hours (P = 0.03) after the administration of LPS.

Conclusion

During human endotoxemia the vasodilatory state is represented by an increase in baseline StO₂. Oxygen consumption during ischemia and vascular reactivity after reperfusion is not influenced by endotoxemia. After the ischemic period, during reperfusion, flow debt repayment significantly decreases during endotoxemia. NIRS is a valuable tool that will facilitate future experiments that study inflammatory-associated changes in the microcirculation.