Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Increased sinusoidal flow is not the primary stimulus to liver regeneration. | Mortensen et al. Comparative Hepatology 2010 9 2 http content 9 1 2 COMPARATIVE HEPATOLOGY RESEARCH Open Access Increased sinusoidal flow is not the primary stimulus to liver regeneration Kim E Mortensen 1 Lene N Conley2 Ingvild Nygaard1 Peter Sorenesen2 Elin Mortensen3 Christian Bendixen2 Arthur Revhaug4 Abstract Background Hemodynamic changes in the liver remnant following partial hepatectomy PHx have been suggested to be a primary stimulus in triggering liver regeneration. We hypothesized that it is the increased sinusoidal flow per se and hence the shear-stress stimulus on the endothelial surface within the liver remnant which is the main stimulus to regeneration. In order to test this hypothesis we wanted to increase the sinusoidal flow without performing a concomitant liver resection. Accordingly we constructed an aorto-portal shunt to the left portal vein branch creating a standardized four-fold increase in flow to segments II III and IV. The impact of this manipulation was studied in both an acute model 6 animals 9 hours using a global porcine cDNA microarray chip and in a chronic model observing weight and histological changes 7 animals 3 weeks . Results Gene expression profiling from the shunted segments does not suggest that increased sinusoidal flow per se results in activation of genes promoting mitosis. Hyperperfusion over three weeks results in the whole liver gaining a supranormal weight of of the total body weight versus the normal . Contrary to our hypothesis the weight gain was observed on the non-shunted side without an increase in sinusoidal flow. Conclusions An isolated increase in sinusoidal flow does not have the same genetic microscopic or macroscopic impact on the liver as that seen in the liver remnant after partial hepatectomy indicating that increased sinusoidal flow may not be a sufficient stimulus in itself for the initiation of liver regeneration. Background Since Higgins and Anderson formalized
