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Yokoyama Y, Baveja R, Sonin N, et al. Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow. Am J Physiol Gastrointest Liver Physiol. 2001;280(1):G21-31doi: 10.1152/ajpgi.2001.280.1.G21.
Yokoyama, Y., Baveja, R., Sonin, N., Clemens, M. G., & Zhang, J. X. (2001). Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow. American journal of physiology. Gastrointestinal and liver physiology, 280(1), G21-31. https://doi.org/10.1152/ajpgi.2001.280.1.G21
Yokoyama, Y, et al. "Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow." American journal of physiology. Gastrointestinal and liver physiology vol. 280,1 (2001): G21-31. doi: https://doi.org/10.1152/ajpgi.2001.280.1.G21
Yokoyama Y, Baveja R, Sonin N, Clemens MG, Zhang JX. Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow. Am J Physiol Gastrointest Liver Physiol. 2001 Jan;280(1):G21-31. doi: 10.1152/ajpgi.2001.280.1.G21. PMID: 11123194.
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Am J Physiol Gastrointest Liver Physiol. 2001 Jan;280(1):G21-31. doi: 10.1152/ajpgi.2001.280.1.G21.

Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow.

American journal of physiology. Gastrointestinal and liver physiology

Y Yokoyama, R Baveja, N Sonin, M G Clemens, J X Zhang

Affiliations

  1. Department of Biology, University of North Carolina at Charlotte, Charlotte, North Carolina 28223, USA.

PMID: 11123194 DOI: 10.1152/ajpgi.2001.280.1.G21

Abstract

The present study was undertaken to investigate hepatic microcirculatory response following partial portal vein ligation (PPVL) in rats. Portal pressure was markedly increased 2-6 wk after PPVL, but no significant reduction in sinusoidal perfusion and hepatocellular injury were detected. However, marked neovascularization was observed in PPVL rats using intravital microscopy and scanning electron microscopy (SEM). Extremely high red blood cell velocity (2,000-4,900 microm/s) was seen in these vessels. Injection of fluorescein sodium via the carotid artery revealed that the neovessels originated from the hepatic arterial vasculature. This was further confirmed by clamping the common hepatic artery and phenylephrine injection from the carotid artery. These vessels maintained sufficient flow after massive sinusoidal shutdown elicited by the portal infusion of endothelin receptor B agonist IRL-1620. SEM also showed extensive neovascularization at the hilum. Additionally, clamping the portal vein decreased sinusoidal perfusion only by 9.5% in PPVL, whereas a 71.2% decrease was observed in sham. These results strongly suggest that the liver maintains its microcirculatory flow by vascular remodeling from the hepatic arterial vasculature following PPVL.

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