E further periods. These processes were very similar in both the liver and kidney and occurred throughout the organ, showing that the surface findings can be extensive to deeper areas (Figure 1). In contrast, the small bowel SDF images showed that gut surface microcirculation was composed primarily of high-flow capillaries and only the vascular density was focally reduced in sepsis; besides, the perivascular PX-478 web tissues could not be identified, showing that the vascular and tissue architectural pattern in the gut differs substantially from solid organs, suggesting a different pathophysiology response of the intestinal microcirculation in sepsis. The gut histology showed generalized cell edema and varying necrosis phases in muscle layers of the intestine in sepsis, and such events could not be suspected by SDF. Conclusion: Organ dysfunction in sepsis is better detectable in solid organs by SDF imaging as compared with gut muscular compartment.P95 Preliminary results for the use of proteinase K to achieve release of LPS from the Alteco LPS Adsorber?after perfusion with LPS containing blood E Hansen1*, L Pierre2, S Blomqvist1,2 1 Alteco Medical AB, Lund, Sweden; 2Faculty of Medicine, Lund University, Sweden Critical Care 2012, 16(Suppl 3):P95 Background: The effect of Alteco LPS Adsorber?to remove LPS from the circulation is based on the incorporation of a synthetic peptide that binds to the lipid A moiety of LPS, the binding capacity in one adsorber exceeding 7.5 g LPS. Positive clinical effects of the adsorber when used in patients with Gram-negative sepsis have been reported [1]. Measurement of LPS in human blood, however, is hampered by difficulties such as contamination and interference. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28388412 The aim of this pilot study was to evaluate a method to release LPS from the LPS adsorber after perfusion with LPS containing blood. Methods: Two adsorbers (A1, A2) containing the active peptide and one dummy adsorber (D) with no peptide were used. Whole blood (500 ml) from healthy pigs was collected in a bag containing heparin, 37 g LPS was added. A roller pump was used to recirculate the blood through the adsorber. The pump flow was set at 150 ml/minute and the duration of the perfusion was 2 hours. After the end of perfusion the adsorbers were rinsed with 500 ml Krebs solution. A solution of 20 mg proteinase K in 50 ml Tris buffer with pH 7.4 was prepared and 2.5 ml CaCl2 was added. The adsorbers were kept at 37 and the proteinase K solution [2] was perfused throughCritical Care 2012, Volume 16 Suppl 3 http://ccforum.com/supplements/16/SPage 47 ofFigure 1(abstract P93) Organ SDF and histological findings in sham and sepsis groups at the 6-hour period. Arrows indicate vascular and perivascular tissue derangements.the adsorbers at 5 ml/minute for 6 hours. Samples for LPS analysis (chromogenic LAL) [3] were drawn before the perfusion and then after 30, 240 and 360 minutes. The enzyme activity was checked using a synthetic substrate [4]. Results: The concentrations of LPS before and during perfusion with proteinase K are shown in Table 1.Conclusion: The LPS values found before the start of the perfusion indicate contamination of the solution. The increase in LPS seen in all adsorbers after 30 minutes is probably due to traces of blood components. The later increase in LPS after treatment with proteinase K in the active adsorbers indicates that the adsorber is effective in capturing LPS from whole blood and that proteinase K is able to dislodge LPS bound t.