Systemic and splanchnic hemodynamics, metabolism and PCO₂-gap during septic shock induced by live E. coli infusion in dogs

Full text

Background

The effects of intravenous live bacteria infusion on the time course of splanchnic oxygenation variables have not been adequately defined, as well as the effects of large volume crystalloid infusion on these variables.

Methods

Twenty-seven anesthetized mongrel dogs (17.1± 1.77 kg) were challenged by a 15 min intravenous infusion of live E. coli (6 × 10⁹ CFU/kg) and followed for 90 min. The animals were then randomized in two groups over 60 min: CT (controls, n=13), no fluid infusion or LR (lactated Ringer's 32 ml/kg/h, n=14). Cardiac index (CI in l/min/m²), mean arterial pressure (MAP in mmHg), mesenteric blood flow (MBF in ml/min, ultrasonic flowprobe), oxygen-derived variables, lactate levels (in mmol/l) and gastric PCO₂ (gastric tonometry in mmHg) were assessed throughout the 165 min experimental protocol. PCO₂-gap was defined as the difference between gastric and arterial PCO₂ and lactate flux was defined by the standard formula: ([portal lactate levels-arterial lactate levels]×MBF).

Results

Data are presented as mean ± SE. E.coli infusion significantly reduced MAP, CI, MBF, and increased PCO₂-gap in both groups. Fluid infusion increased CI, systemic DO₂ and stabilized PCO₂-gap. Although MBF was similar in both groups, only controls presented gut lactate production. Table 1 shows the time course of MAP, CI, MBF, lactate flux and PCO₂-gap of the two groups.

Conclusion

Although large-volume crystalloid infusion fails to restore mesenteric and gastric mucosal perfusion, it seems to prevent gut lactate production in a canine model of experimental septic shock.

Table 1 Time course of MAP, CI, MBF, Lactate Flux and PCO₂-gap at baseline, 15, 105 and 165 min.