Femoral AVGs are a suitable alternative to upper limb vascular access, with acceptable primary and secondary patency rates. Infection occurred in approximately one-quarter of cases, whereas steal was uncommon.

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Primary endothelial cells (ECs) are the preferred cellular source for luminal seeding of tissue-engineered (TE) vascular grafts. Research into the potential of ECs for vascular TE has focused particularly on venous rather than arterial ECs. In this study we evaluated the functional characteristics of arterial and venous ECs, relevant for vascular TE. Porcine ECs were isolated from femoral artery (PFAECs) and vein (PFVECs). The proliferation rate was comparable for both EC sources, whereas migration, determined through a wound-healing assay, was less profound for PFVECs. EC adhesion was lower for PFVECs on collagen I, measured after 10 min of arterial shear stress. Gene expression was analysed by qRT-PCR for ECs cultured under static conditions and after exposure to arterial shear stress and revealed differences in gene expression, with lower expression of EphrinB2 and VCAM-1 and higher levels of vWF and COUP-TFII in PFVECs than in PFAECs. PFVECs exhibited diminished platelet adhesion under flow and cell-based thrombin generation was delayed for PFVECs, indicating diminished tissue factor (TF) activity. After stimulation, prostacyclin secretion, but not nitric oxide (NO), was lower in PFVECs. Our data support the use of venous ECs for TE because of their beneficial antithrombogenic profile.

The use of extended criteria donors is an effective way of reducing the shortage of deceased donor organs. Evidence of significant liver trauma in a deceased donor usually rules out transplantation of the liver. The aim of this study was to evaluate the use and outcomes of donor livers with preprocurement trauma. Records of all 312 deceased donors with a history of trauma between January 1986 and September 2007 were reviewed. Donors with macroscopic liver injuries were identified, and data from recipient medical records were obtained. Data on declined donor offers were also evaluated. The median donor age was 20 (range, 10-57) years, and 9 of 15 (60%) were male. The liver injuries were predominantly lacerations (grades 1-5) and vascular injury. The right lobe was resected because of extensive damage in 3 cases. This resulted in 2 left lobes (back-table cut-down) and 1 left lateral segment allograft (in situ split). For the 15 recipients, the median age was 43 (3-69) years. Primary nonfunction was not seen. There was no difference in survival between whole and partial allografts. Three deaths occurred within 3 months post-transplantation. During the same period, 42 of 1405 donor offers (3%) were declined because of extensive liver trauma or major ongoing intra-abdominal hemorrhage. In conclusion, the use of donor livers with preexisting trauma leads to acceptable outcomes. Strategies to deal with trauma include resection of the right lobe if required. Use of deceased donor livers with injury is a safe way to expand the donor pool. Liver Transpl 15: 321-325, 2009.

BackgroundAutologous arteriovenous (AV) fistulas are the first choice for vascular access but have a high risk of non-maturation due to insufficient vessel adaptation, a process dependent on nitric oxide (NO)-signaling. Chronic kidney disease (CKD) is associated with oxidative stress that can disturb NO-signaling. Here, we evaluated the influence of CKD on AV fistula maturation and NO-signaling.MethodsCKD was established in rats by a 5/6th nephrectomy and after 6 weeks, an AV fistula was created between the carotid artery and jugular vein, which was followed up at 3 weeks with ultrasound and flow assessments. Vessel wall histology was assessed afterwards and vasoreactivity of carotid arteries was studied in a wire myograph. The soluble guanylate cyclase (sGC) activator BAY 60–2770 was administered daily to CKD animals for 3 weeks to enhance fistula maturation.ResultsCKD animals showed lower flow rates, smaller fistula diameters and increased oxidative stress levels in the vessel wall. Endothelium-dependent relaxation was comparable but vasorelaxation after sodium nitroprusside was diminished in CKD vessels, indicating NO resistance of the NO-receptor sGC. This was confirmed by stimulation with BAY 60–2770 resulting in increased vasorelaxation in CKD vessels. Oral administration of BAY 60–2770 to CKD animals induced larger fistula diameters, however; flow was not significantly different from vehicle-treated CKD animals.ConclusionsCKD induces oxidative stress resulting in NO resistance that can hamper AV fistula maturation. sGC activators like BAY 60–2770 could offer therapeutic potential to increase AV fistula maturation.

The process of thrombin generation involves numerous plasma proteases and cofactors. Interaction with the vessel wall, in particular endothelial cells (ECs), influences this process but data on this interaction is limited. We evaluated thrombin generation on EA.hy926, human coronary arterial ECs (HCAECs) and patient-derived human venous ECs (HVECs) by means of a modified calibrated automated thrombogram (CAT) method and especially looked into contribution of the intrinsic and extrinsic pathways. Thrombin generation was measured in presence of confluent ECs with normal pooled and factor XII-deficient (FXII-deficient) platelet-poor plasma, with/without active site inhibited factor VIIa (ASIS) to block the extrinsic pathway and corn trypsin inhibitor for blocking contact activation (intrinsic pathway). Fetal bovine serum (FBS) was removed from culture conditions as FXIIa from the serum retained on ECs apparently, thereby inducing strong contact activation. In serum-free conditions, EA.hy926 and patient-derived HVECs induced thrombin generation mainly via the contact activation pathway with minor influence of ASIS on peak height and very low thrombin generation curves in FXII-deficient plasma. HVECs derived from coronary arterial bypass graft (CABG) patients showed increased thrombin generation compared to control patients, which could be ascribed to increased contact activation. Contribution of the extrinsic pathway on patient-derived ECs was limited. We conclude that the CAT method in combination with serum-free cultured ECs offers a valuable high-throughput method to evaluate endothelial influences on thrombin generation, which appears to involve predominantly contact activation on ECs. Contact activation-mediated thrombin generation was increased on ECs from CABG patients compared to controls.

reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. carbon dioxide 30 [27][28][29][30][31][32][33][34][35] mmHg and median temperature 37.1 [36.8-37.3]°C. After removal of artefacts, the mean monitoring time was 22 h08 (8 h54). All patients had impaired cerebral autoregulation during their monitoring time. The mean IAR index was 17 (9.5) %. During H 0 H 6 and H 18 H 24 , the majority of our patients; respectively 53 and 71 % had an IAR index > 10 %. Conclusion According to our data, patients with septic shock had impaired cerebral autoregulation within the first 24 hours of their admission in the ICU. In our patients, we described a variability of distribution of impaired autoregulation according to time. ReferencesSchramm P, Klein KU, Falkenberg L, et al. Impaired cerebrovascular autoregulation in patients with severe sepsis and sepsis-associated delirium. Crit Care 2012; 16: R181. Aries MJH, Czosnyka M, Budohoski KP, et al. Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury. Crit. Care Med. 2012.

Vascular tissue engineering relies on the combination of patient-derived cells and biomaterials to create new vessels. For clinical application, data regarding the function and behavior of patient-derived cells are needed. We investigated cell growth and functional characteristics of human venous endothelial cells (HVECs) from coronary arterial bypass graft (CABG), chronic kidney disease (CKD), and control patients. HVECs were isolated from venous specimens that were obtained during elective surgical procedures by means of collagenase digestion. Gene expression, proliferation, migration, secretory functions, and thrombogenic characteristics were evaluated using high-throughput assays. A total of 48 cell batches (14 control, 19 CABG, and 15 CKD subjects) were assessed. Proliferation, population doubling times, and migration of HVECs derived from CABG and CKD patients did not differ from controls. Thrombomodulin expression was higher in CABG-HVECs compared with controls. HVEC-induced thrombin formation in plasma did not differ between groups, and the contact activation pathway was the major contributor to coagulation. Patient-derived HVECs were able to attach and survive on polycaprolactone scaffolds that were coated with fibrin. HVECs from cardiovascular-diseased and CKD patients showed comparable functional characteristics with HVECs derived from uncompromised patients. We, therefore, conclude that endothelial cells from aged patients with comorbidities can be safely used for isolation and in vitro expansion for vascular tissue engineering.