Abstract
Microvascular exchange in the liver is quite peculiar owing to the porosity of the sinusoidal endothelial cells; the pores in the sinusoidal endothelium allow free passage of macromolecules, which allows the hepatocyte to take up tightly protein bound drugs (1). One of the major changes occurring in cirrhosis is sinusoidal capillarization (2), which leads to a profound impediment of passage of substances into the space of Disse. Sinusoidal capillarization was first described by Hans Popper on a morphological level (2); he—rightfully—predicted that this phenomenon would have important bearings on hepatic function. It lasted almost 20 yr until sinusoidal capillarization was demonstrated functionally using the multiple indicator dilution technique (3)—this study was quite a feat because it applied this demanding technique to humans before studying the phenomenon in animal models. Another important aspect of altered microvascular exchange is loss of the sinusoidal fenestrations that, at least in alcoholic liver disease, occurs before significant fibrosis is seen (4).
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Reichen, J. (2005). Evaluation of Portal Hemodynamics Using Indicator Dilution and Noninvasive Techniques. In: Sanyal, A.J., Shah, V.H. (eds) Portal Hypertension. Clinical Gastroenterology. Humana Press. https://doi.org/10.1007/978-1-59259-885-4_10
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DOI: https://doi.org/10.1007/978-1-59259-885-4_10
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