Increased angiogenesis and permeability in the mesenteric microvasculature of rats with cirrhosis and portal hypertension: an in vivo study
Article first published online: 3 AUG 2006
Volume 26, Issue 7, pages 889–898, September 2006
How to Cite
Geerts, A. M., De Vriese, A. S., Vanheule, E., Van Vlierberghe, H., Mortier, S., Cheung, K.-J., Demetter, P., Lameire, N., De Vos, M. and Colle, I. (2006), Increased angiogenesis and permeability in the mesenteric microvasculature of rats with cirrhosis and portal hypertension: an in vivo study. Liver International, 26: 889–898. doi: 10.1111/j.1478-3231.2006.01308.x
- Issue published online: 3 AUG 2006
- Article first published online: 3 AUG 2006
- Received 20 January 2006,accepted 4 May 2006
- endothelial nitric oxide synthase;
- intravital microscopy;
- portal hypertension;
- vascular endothelial growth factor
Abstract: Background: In vivo evidence for angiogenesis in the splanchnic vasodilation in portal hypertension (PHT) and cirrhosis is lacking. Vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) are mediators of angiogenesis. The present study visualises in vivo structural changes (angiogenesis and vascular hyperpermeability) and examines the presence of VEGF and eNOS in the mesenteric microvasculature of animal models of PHT with and without cirrhosis.
Methods: Portal hypertension was induced by partial portal vein ligation (PPVL) and cirrhosis was induced by common bile duct ligation (CBDL) in rats. The mesenteric microcirculation was examined by intravital microscopy. Expression of VEGF, eNOS and CD31 in mesenteric tissue were studied by immunohistochemistry.
Results: An increased mesenteric angiogenesis was observed in PPVL and CBDL rats compared with Sham-operated and control rats, as shown by intravital microscopy and CD 31 staining. VEGF and eNOS expression was higher in CBDL and PPVL rats compared with control groups and correlated positively with vascular density. Macromolecular leakage was increased in cirrhotic rats compared with control and PPVL rats.
Conclusion: Our study provides in vivo evidence of an increased angiogenesis in the mesenteric microvasculature of animal models of PHT and cirrhosis. Increased VEGF and eNOS expression in the mesentery of PPVL and CBDL rats may suggest their contribution. Microvascular permeability in the mesenteric vessels was only increased in cirrhotic rats.