Effect of lung protective ventilation strategy on extrapulmonary organs inflammatory response in an acute respiratory distress syndrome rabbit model

Objective

To evaluate the influence of a lung protective ventilation strategy on extrapulmonary organ inflammatory response in an acute respiratory distress syndrome (ARDS) rabbit model.

Methods

The ARDS rabbit models were duplicated by alveoli-lavaged saline. The rabbits were divided into six groups: (1) normal, (2) ARDS group, (3) low volume (VT) with best end-expiratory pressure (PEEP) (LVBP), (4) normal volume with best PEEP (NVBP), (5) low-volume with high PEEP (LVHP), and (6) high-volume zero PEEP (HVZP). Tumor necrosis factor alpha (TNF-α) and IL-10 levels in liver and intestine homogenates were measured by ELISA and their mRNA expression was measured by RT-PCR.

Results

In the LVBP group, the mRNA expression of TNF-α and IL-10 in liver was lower than the NVBP, LVHP, and HVZP groups. But there was no difference between LVBP and ARDS groups. TNF-α mRNA expression in the LVHP group was higher than the LVBP group in liver tissue, but significantly lower than the HVZP group. Compared with the LVBP group, the TNF-α and IL-10 concentrations in liver were increased markedly in NVBP, LVHP, and HVZP. But there was no difference between the LVBP and ARDS groups. Live TNF-α and IL-10 concentrations were highest in the HVZP group, which was higher than the LVBP and LVHP groups. In the LVBP group, the mRNA expression of TNF-α and IL-10 in intestine was lower than the NVBP, LVHP, and HVZP groups. But there was no difference between the LVBP and ARDS groups. As compared with the LVBP group, the TNF-α and IL-10 concentrations of intestine in NVBP, LVHP, and HVZP were increased markedly, but there was no difference between the LVBP and ARDS groups.

Conclusions

A lung protective ventilation strategy can downregulate inflammatory mediator expression in the liver and intestine of ARDS rabbits and may prevent the occurrence of multiple organ dysfunction syndrome.