Effects of High-Volume Continuous Hemofiltration on Experimental Pancreatitis Associated Lung Injury in Pigs

Abstract

To investigate the effect of high-volume continuous hemofiltration on experimental pancreatitis associated lung injury (PALI) in pigs. Animals had severe acute pancreatitis (SAP) induced by intraductal injection of sodium taurocholate and trypsin and were randomly assigned to three groups: 1) Controls, 2) Low-volume (LV) (20 ml/kg/h) continuous venovenous hemofiltration (CVVH) and 3) High-volume (HV) (100 ml/kg/h) CVVH at the onset of the induction of SAP. Systemic and pulmonary hemodynamic index were monitored intermittently. At the same time, arterial oxygen tension (PaO 2 ), cytokines and activated NF- ê B levels of peripheral blood mononuclear cell were measured. After the animals died, the degree of microscopic lung injury was judged and scored. The median survival times of control, low-volume and high-volume groups were respectively 41 h, 50 h and 65 h. Temperatures in high-volume CVVH group were more steady than in control and LV CVVH groups (p<0.01). MPAP was significantly decreased by 4-5 mmHg in the HV CVVH group after 12 h of treatment. PaO(2) was significantly higher in HV group than in LV group at 6 h , 12 h, 24 h and 48 h (p<0.01). HV CVVH resulted in significant reductions not only in interstitial edema and atelectasis but also hemorrhages, hyaline membranes, microthrombi and total lung injury histology score. Plasma cytokines in the high-volume group were significantly lower than in the LV and control groups. In the HV group, the expression of NF- ê B activation at 6 h, 12 h and 24 h was lower than in the control and LV groups respectively. CVVH can reduce pulmonary edema and the severity of PALI in pigs with high-volume CVVH being significantly better than low-volume CVVH. The beneficial effects of CVVH on arterial oxygenation and pulmonary function may be connected with improvements in systemic hemodynamics, reduction in plasma cytokine concentration and decreased activity of NF- ê B in peripheral blood mononuclear cells.