Bacterial translocation aggravates mesenteric microcirculation changes induced by sepsis

Introduction

Considering that systemically exacerbated or impaired inflammatory response with alteration of the micro-circulation flow is a universal feature related to septic shock, regarding the current theory of sepsis that considers bacterial translocation (BT) as the main etiological factor for the induction of systemic infection, we sought to examine the additional effect of BT in pre-established sepsis, evaluating intestinal microcirculation injury by intravital microscopy.

Methods

Adult female Wistar rats (200–250 g) were submitted to the combination induction of sepsis plus BT, and mesenteric microcirculation of the small bowel was monitored for up to 2 hours by intravital microscope under general anesthesia (n = 5/each group). Non-lethal, semi-lethal and lethal sepsis were induced by jugular vein inoculation of 10⁷, 10⁹ or 10¹⁰ CFU/ml/100 g body weight of Escherichia coli R-6, respectively. The BT process was induced soon after sepsis induction by oroduodenal inoculation of 5 ml E. coli R-6 10¹⁰ CFU/ml/100 g body weight confined to the small intestine. In control groups, animals were submitted to BT or sepsis alone.

Results

BT alone was able to provoke capillary hemorrhages and obstruction of capillaries and venulas of low flow, from 30 min after inoculation, which worsened up to 2 hours. In the sepsis group, although hemorrhagic lesions were not seen, obstruction of venules extended to even high-flow venules, and the severity of microcirculation obstructions were directly proportional to the intensity of sepsis. Only lethal sepsis showed arteriolar obstruction. Most sepsis-related alterations initiated 25 min after inoculation and worsened up to 2 hours of the observation period. When the BT process was added to the sepsis, non-lethal sepsis microcirculation injuries were as intense as semi-lethal sepsis lesions, and the semi-lethal sepsis microcirculation injuries became as the lethal sepsis microcirculation injuries.

Conclusion

The BT process, when associated with the pre-existing sepsis, augments significantly the mesenteric micro-circulation injuries, showing that BT can be the additional triggering factor for the installment of multiple organ failure in sepsis shock.