Acute portal hypertension without liver dysfunction enhances bacterial translocation to the lung

Introduction

Based on current knowledge, patients with cirrhosis have a higher risk of infection and are more likely to die as a result of those infections. Also, increasing evidence has attributed the bacterial translocation (BT) phenomenon as the most possible etiology of sepsis and MODS. Thus, in this study we examined the isolated portal hypertension (PH) role, without liver dysfunction, in an experimental BT model at a very acute phase of PH, in order to evaluate whether the infection in cirrhotic patients might be related only to the increased portal blood pressure factor with its consequential intestinal venous congestion.

Methods

Adult female Wistar rats (200–250 g) were submitted to PH induction by partial portal ligature (decrease of 50% of portal flow) or PH-sham surgery, and 2 days later were subject to a BT experiment (5 ml Escherichia coli R-6 10¹⁰ CFU/ml/100 g body weight confined to the small intestine) or a BT-sham experiment (saline only) under general anesthesia. Following 2 hours of the BT process, samples of the mesenteric lymph node, liver, spleen and lung were collected for culture and the animals were sacrificed. Groups: G1 (PH-Sham + BT-Sham), G2 (PH + BT-sham), G3 (PH-Sham + BT with inoculum) and G4 (PH + BT with inoculum) (n = 8/group).

Results

All cultures of G1 were negative; however, when PH factor was added (G2), the native Gram-negative intestinal bacteria translocated significantly to extraintestinal sites with exception of the lung: MLN (5/8, 62.5% positive); liver (2/8, 25% positive); spleen (1/8,12.5% positive) and lung (0/8, 0%). In the conventional BT experiment, all samples were 100% positive with exception of the lung (3/8, 37% positive). Again, when PH factor was added (G4), even the lung was 100% positive, showing that PH factor is a significant factor related to BT even for native microflora. Also, the increased BT index to the lung might be related to the portal blood shunt to the systemic circulation by bypassing the bacterial clearance role of the liver and reaching directly the lung microcirculation, even at the early phase of PH. This fact can be related to the high incidence of pulmonary insufficiency in cirrhotic patients.

Conclusion

PH factor increases native flora BT and promotes a higher index of BT to the lung when intestinal bacterial overgrowth factor is present in the rat model of BT.