The hepatic circulation is a low-pressure vascular bed that accommodates large volumes of blood (1).Total hepatic blood flow in humans is approximately 1,500 mL/min and accounts for 15% to 20% of cardiac output. The liver, like the lung, receives a dual blood supply; 70% of total hepatic blood flow is from the portal vein, and 30% from the hepatic artery. Blood from the hepatic artery and portal vein supplies the liver sinusoids and ultimately drains into the hepatic vein. Any one of these segments of the hepatic circulation – the hepatic artery, portal vein, sinusoids, hepatic vein – may be inflicted by disease, with sometimes devastating consequences. This chapter examines the structure and function of the hepatic macrocirculation, with an emphasis on cirrhotic portal hypertension as a paradigm of hepatic vascular disease and endothelial cell (EC) heterogeneity.

HISTORY

The hepatic vasculature has been the subject of interest for millennia. Indeed, seminal observations of patients with portal hypertension, and its major complications of ascites and esophageal variceal hemorrhage, provided a strong foundation for our present-day knowledge of the hepatic circulation (Table 134–1). Several important themes emerge from a consideration of the history of the field. First, there is noticeable change in methodology over time from physical examination to gross anatomy, followed by studies in physiology and pathology, and culminating in methods at the interface of organ and cell physiology and molecular biology. Second, studies of the diseased liver have provided profound insights into the physiology of the normal hepatic vasculature.