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Changes in the microcirculation during human endotoxemia measured with near-infrared spectroscopy
© BioMed Central Ltd 2006
Published: 21 March 2006
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.
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.
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.
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.