This tissue was used as internal control tissue: it was from the same patient and experienced similar surgical handling as the isolated jejunum, while it was not subjected to IR. Arterial blood was sampled preoperatively, before the isolated jejunum was subjected to ischemia, immediately upon reperfusion and every half hour during reperfusion until the last part of the isolated jejunum was collected at the end of the study protocol. Simultaneous with the second and every next arterial blood sample, blood was drawn from the venule draining the isolated jejunal segment by Kartogenin direct puncture to assess concentration VR23 gradients across the isolated jejunal segment. All blood samples were directly transferred to pre-chilled EDTA vacuum tubes and kept on ice. At the end of the study all blood samples were centrifuged at 4000 rpm, 4uC for 15 minutes to obtain plasma. Plasma was kept on ice and immediately stored in aliquots at 280uC until analysis. The total reperfusion time was determined by the duration of the surgical procedure, with a maximum of 240 minutes. Reperfused ischemic intestine samples were obtained from every patient. Healthy jejunum samples, serving as internal controls, were obtained from 12 patients. Development of IR induced organ damage is generally described to be characterized by an excessive and vigorous inflammatory response. This inflammatory response is mainly triggered by apoptosis of cells that cannot be resolved in time by phagocytic cells and will become necrotic in time. Such necrotic cells are a source of damage associated molecular patterns or alarmins which recruit and activate innate immune cells, aimed at restoration of homeostasis and tissue repair. However, in the context of ischemia and reperfusion such an inflammatory reaction often results in additional tissue damage. It has been demonstrated in the kidney as well as other organs that IR induced inflammation and subsequent organ damage are dependent on the development of widespread apoptosis.Rapid clearance of apoptotic cells as well as therapeutic strategies to reduce apoptosis have been shown to be critical in preventing the mostly harmful IR induced inflammatory response.