Mesenteric Microcirculatory Dysfunctions and Translocation of Indigenous Bacteria in a Rat Model of Strangulated Small Bowel Obstruction

Abstract

PRUPOSE Bacterial translocation has been shown to occur in critically ill patients after extensive trauma, shock, sepsis, or thermal injury. The present study investigates mesenteric microcirculatory dysfunctions, the bacterial translocation phenomenon, and hemodynamic/metabolic disturbances in a rat model of intestinal obstruction and ischemia.METHODSAnesthetized (pentobarbital 50 mg/kg, i.p.) male Wistar rats (250–350 g) were submitted to intestinal obstruction or laparotomy without intestinal obstruction (Sham) and were evaluated 24 hours later. Bacterial translocation was assessed by bacterial culture of the mesenteric lymph nodes (MLN), liver, spleen, and blood. Leukocyte-endothelial interactions in the mesenteric microcirculation were assessed by intravital microscopy, and P-selectin and intercellular adhesion molecule (ICAM)-1 expressions were quantified by immunohistochemistry. Hematocrit, blood gases, lactate, glucose, white blood cells, serum urea, creatinine, bilirubin, and hepatic enzymes were measured.RESULTSAbout 86% of intestinal obstruction rats presented positive cultures for E. coli in samples of the mesenteric lymph nodes, liver, and spleen, and 57% had positive hemocultures. In comparison to the Sham rats, intestinal obstruction induced neutrophilia and increased the number of rolling (~2-fold), adherent (~5-fold), and migrated leukocytes (~11-fold); this increase was accompanied by an increased expression of P-selectin (~2-fold) and intercellular adhesion molecule-1 (~2-fold) in the mesenteric microcirculation. Intestinal obstruction rats exhibited decreased PaCO2, alkalosis, hyperlactatemia, and hyperglycemia, and increased blood potassium, hepatic enzyme activity, serum urea, creatinine, and bilirubin. A high mortality rate was observed after intestinal obstruction (83% at 72 h vs. 0% in Sham rats).CONCLUSIONIntestinal obstruction and ischemia in rats is a relevant model for the in vivo study of mesenteric microcirculatory dysfunction and the occurrence of bacterial translocation. This model parallels the events implicated in multiple organ dysfunction (MOD) and death.

The Effects of Low and High Tidal Volume and Pentoxifylline on Intestinal Blood Flow and Leukocyte-Endothelial Interactions in Mechanically Ventilated Rats

“…However, we previously found positive correlations between the expression of P-selectin and intercellular molecules with leukocyte-endothelial interactions at the mesentery and lungs after hemorrhagic shock/reperfusion and sepsis. 7,19,24 And in the present study we found significant differences in leukocyte-endothelial interactions between the groups, which were not associated with hemodynamics. The increased leukocyte adhesion and migration to the perivascular tissue at the mesentery (distant locale) may have been induced by systemic inflammation biotrauma, which was prevented by low V T and attenuated by pentoxifylline.…”

“…However, leukocyte over-activation and increased leukocyte accumulation in the perivascular tissue can be associated with an exaggerated pro-inflammatory immune response that can contribute to widespread microvascular injury and consequent endothelial damage. 7,[24][25][26] Hypoperfusion of the gastrointestinal vascular bed has been suggested as a potential mechanism for the development of several complications from mechanical ventilation in critically ill patients. [8][9][10] We recently found that high intrathoracic pressure generated by high V T (10 mL/kg) and high PEEP (10 cm H 2 O) increased leukocyte-endothelial interactions in rat mesentery, as compared to PEEP values of 0 and 5 cm H 2 O, with no significant differences in mean arterial blood pressure between the groups.…”

“…[1][2][3] However, PEEP increases intrathoracic pressure, which can reduce venous return and cardiac output, and redistribute blood flow away from the splanchnic vasculature. [4][5][6] Hypoperfusion and ischemia in the gastrointestinal tract are associated with loss of tract barrier and systemic inflammation, 7 which may play a pivotal role in the pathogenesis of several complications associated with mechanical ventilation, [8][9][10] including multiple-organ failure in patients with severe sepsis and cardiac failure, a situation that usually has a very poor outcome. [11][12][13] Therapies directed at improving microcirculation and local/systemic cellular perfusion may improve outcomes.…”

Bacterial translocation and mortality on rat model of intestinal ischemia and obstruction

“…As consequence, bacterial translocation and systemic inflammatory occur [7][8][9] . Zanoni et al 10 proposed a model modification, adding ischemia to intestinal obstruction, by ligature of terminal ileum blood vessels (7 to 10 cm of extension), promoting bacterial translocation and inflammatory response.…”

Estudo dos efeitos do etil-piruvato, salina hipertônica e do Ringer lactato sobre a resposta da microcirculação mesentérica em modelo de sepse induzida por Escherichia coli em ratos

“…O desencadeamento da sepse foi induzido por inoculação de bactérias vivas de E. coli obtidas de nódulos linfáticos mesentéricos em modelo de obstrução intestinal (Zanoni et al, 2009) (Trzeciak et al, 2007).…”