Hepatic platelet and leukocyte adherence during endotoxemia

INTRODUCTION: Liver microcirculation disturbances are a cause of hepatic failure in sepsis. Increased leukocyte-endothelial interaction, platelet adherence and impaired microperfusion cause hepatocellular damage. The time course and reciprocal influences of ongoing microcirculatory events during endotoxemia have not been clarified. METHODS: Male Wistar rats (232 ± 17 g) underwent cecal ligation and puncture (CLP). Intravital microscopy (IVM) was performed 0, 1, 3, 5, 10 and 20 hours after CLP. Mean erythrocyte velocity, leukocyte and platelet rolling in postsinusoidal venules and sticking of leukocytes and platelets in postsinusoidal venules and hepatic sinusoids were determined. Heart rate (HR), mean arterial pressure (MAP) and portal venous blood flow (PBF) were measured. Blood count and investigation of hepatic enzyme release was performed after each IVM time point. RESULTS: Hepatic platelet-endothelial adherence in liver sinusoids and postsinusoidal venules occurred one hour after the induction of endotoxemia. Leukocyte-endothelial interaction started three to five hours after CLP. A decrease of hepatic microperfusion could be observed at three hours in sinusoids and ten hours in postsinusoidal venules after CLP, although PBF was reduced one hour after CLP. HR remained stable and MAP decreased ten hours after CLP. Hepatic enzymes in blood were significantly elevated ten hours after CLP. CONCLUSION: Hepatic platelet-endothelial interaction is an early event during endotoxemia. Leukocyte adherence occurs later, which underlines the probable involvement of platelets in leukocyte recruitment. Although PBF is reduced immediately after CLP, the later onset of hepatic microperfusion decrease makes the existence of autoregulatory liver mechanisms likely

Data for: Genetic pathogenesis of hereditary trichilemmal cyst formation

These data belong to the submitted manuscript JID-2018-1015 Merged exome data of 5 individuals with hereditary trichilemmal cysts Sanger sequencing data of an analyzed family cohort with hereditary form of trichilemmal cysts Sanger sequencing data of 14 patients with hereditary trichilemmal cysts Sanger sequencing data of allele-specific PCRs TRPC4 overexpression experimental data Kir3.1 overexpression experimental data Overexpression DAG concentration measurements experimental dat

Data for: Genetic pathogenesis of hereditary trichilemmal cyst formation

These data belong to the submitted manuscript JID-2018-1015Merged exome data of 5 individuals with hereditary trichilemmal cysts Sanger sequencing data of an analyzed family cohort with hereditary form of trichilemmal cystsSanger sequencing data of 14 patients with hereditary trichilemmal cysts Sanger sequencing data of allele-specific PCRsTRPC4 overexpression experimental dataKir3.1 overexpression experimental dataOverexpression DAG concentration measurements experimental dat

Data for: Genetic pathogenesis of hereditary trichilemmal cyst formation

These data belong to the submitted manuscript JID-2018-1015 Merged exome data of 5 individuals with hereditary trichilemmal cysts Sanger sequencing data of an analyzed family cohort with hereditary form of trichilemmal cysts Sanger sequencing data of 14 patients with hereditary trichilemmal cysts Sanger sequencing data of allele-specific PCRs TRPC4 overexpression experimental data Kir3.1 overexpression experimental data Overexpression DAG concentration measurements experimental dat