Continuous veno-venous hemodiafiltration alleviates multiple organ dysfunction syndrome in dogs

Abstract

Context: Multiple organ dysfunction syndrome (MODS) is a major cause of death in critically patients. It has been hypothesized that inactivation or removal of pro-inflammatory molecules may prevent or reverse MODS.

Objective: The purpose of this paper was to investigate the efficacy of continuous veno-venous hemodiafiltration (CVVHDF) as treatment for MODS in an established animal model.

Materials and methods: Male Beagle dogs (n = 18) were used to establish the model and were randomly assigned to a CVVHDF, sham, or control group. The serum levels of ALT, AST, Cr, BUN, PaO₂, and PaCO₂ were measured as functional makers of major organs. Apoptosis, DLA-DR expression, and cytokine levels of peripheral monocytes were determined.

Results: The MODS model was successfully established. After CVVHDF treatment, the WBC and neutrophil counts were lower and the monocyte count and percentage were greater, but these were unchanged in the sham and control groups. Apoptosis of CD14+ monocytes was significantly lower in the CVVHDF group than in the sham and control groups. The fraction of DLA-DR⁺ monocytes and IL-1β secretion was significantly greater in the sham and control groups than in the CVVHDF group. Moreover, IL-4 secretion increased significantly in the CVVHDF group but not in the control group.

Discussion and Conclusion: Our study of an experimental model of MODS indicated that MODS leads to significant disruption of physiological and immune functions. CVVHDF treatment alleviated some of these symptoms due to the improvement of monocyte function, reduction of monocyte apoptosis, and increase of anti-inflammatory cytokines.

Keywords::

• Multiple organ dysfunction syndrome
• Hemodiafiltration
• Septic shock
• Hemorrhagic shock
• Monocytes; CD14

Declarations of interest

This study was supported by the National Natural Science Foundation of China (Grant No.: 30960146) and the Xinjiang Uygur Autonomous Region Natural Science Fund (Grant No.: 200821114).