Mechanisms of organ failure and abnormal oxygen metabolism during sepsis

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This study was based on our previous findings that abnormal dependency of systemic oxygen consumption (VO_2) on systemic oxygen delivery (DO_2) occurred during the supply-independent range of DO_2 in a rabbit IL-1β-induced septic shock model (SHOCK 14:193-9,2000). In the present series of study, we identified the organ responsible for the development of the abnormal oxygen metabolism during sepsis. Hemodynamics during hyperdynamic sepsis was reproduced by 1 mg/kg i.v. administration of lipopolysaccharide (LPS) to rabbits. Each animal was monitored invasively with an arterial catheter, a Swan-Ganz catheter, and an ultrasonic probe placed on the superior mesenteric vein (SMV). In addition, mucosal blood flow of the ileum was monitored by the surface Doppler scan method. The animals developed hypotension with metabolic acidosis by 90 min after the administration of LPS in the presence of the consistent or somewhat increased cardiac output. This vasomotor shock persisted by 240 min after the administration of LPS. The SMV blood flow was increased approximately by 50% from the baseline value. In contrast, mucosal blood flow of the ileum was decreased initially by 67% from the baseline value approximately by 120 min after LPS, and returned gradually to the baseline value by 240 min. The heterogeneity of the blood flow assessed by a relative dispersion of the blood flow to an area of ileal mucosa was significantly increased after LPS regardless of a period of time. These results suggest a significant role of the gut tissue in the development of systemic abnormalities in hemodyamics and oxygen metabolism.