Liver Transplant After Normothermic Regional Perfusion From Controlled Donors After Circulatory Death: The Norwegian Experience.

BACKGROUND: In order to meet the increasing demand for donor organs, the concept of donation after circulatory death (DCD) was reintroduced in Norway, first as a pilot study, followed by the use of DCD as institutional practice. We report the current Norwegian experience with liver transplant after DCD. METHODS: After acceptance from next of kin, life support was withdrawn from patients with devastating brain injury and cardiac arrest observed. After a 5-minute "no-touch" period, extracorporeal membrane oxygenation for post mortem normothermic regional perfusion (NRP) by extracorporeal membrane oxygenator circuit was established. Data from all liver transplant recipients receiving controlled DCD (cDCD) livers in Oslo were analyzed. RESULTS: From 2015 to 2017, a total of 8 patients underwent liver transplant with cDCD and NRP liver grafts in Norway. Median Model for End-Stage Liver Disease score was 26 (range, 6-40). There were no cases of delayed graft function or graft loss. Seven patients have reached 1 year of follow-up, and 1 patient has reached 6 months. Two patients have recurrence of primary disease (primary sclerosing cholangitis and steatohepatitis). All patients had normalized liver function at last follow-up. Two patients underwent procedures for biliary complications. In 1 patient, leakage from the cystic duct was successfully handled endoscopically by stenting. In the other patient, a suspected stricture on magnetic resonance imaging led to an endoscopic retrograde cholangiopancreatography, which did not confirm signs of biliary stenosis. There was 1 instance of hepatic artery stenosis, which was managed with endovascular technique. CONCLUSION: The results after liver transplant using cDCD with NRP are good. The rate of complications seems to be within the same range as when using conventional donation after brain death grafts.

Caveolin expression changes in the neurovascular unit after juvenile traumatic brain injury: signs of blood-brain barrier healing?

Traumatic brain injury (TBI) is one of the major causes of death and disability in pediatrics, and results in a complex cascade of events including the disruption of the blood-brain barrier (BBB). A controlled-cortical impact on post-natal 17-day-old rats induced BBB disruption by IgG extravasation from 1 to 3 days after injury and returned to normal at day 7. In parallel, we characterized the expression of three caveolin isoforms, caveolin 1 (cav-1), caveolin 2 (cav-2) and caveolin 3 (cav-3). While cav-1 and cav-2 are expressed on endothelial cells, both cav-1 and cav-3 were found to be present on reactive astrocytes, in vivo and in vitro. Following TBI, cav-1 expression was increased in blood vessels at 1 and 7 days in the perilesional cortex. An increase of vascular cav-2 expression was observed 7 days after TBI. In contrast, astrocytic cav-3 expression decreased 3 and 7 days after TBI. Activation of endothelial nitric oxide synthase (eNOS) (via its phosphorylation) was detected 1 day after TBI and phospho-eNOS was detected both in association with blood vessels and with astrocytes. The molecular changes involving caveolins occurring in endothelial cells following juvenile-TBI might participate, independently of eNOS activation, to a mechanism of BBB repair while, they might subserve other undefined roles in astrocytes.