The microcirculation pattern of the small intestine consists of a simple columnar epithelium with goblet cells. Capillary plexuses arise from arterioles in the villus and intestinal crypt, with blood leaving the crypt through venules that enter the portal circulation. Lymphatic vessels, known as lacteals, originate within the villus and eventually form a plexus at the base. The concentration of adenosine in mesenteric venous blood increases fourfold after brief arterial occlusion and during enhanced metabolic activity of the intestinal mucosa. Adenosine acts as a potent vasodilator in the mesenteric vascular bed and is considered a major metabolic mediator of autoregulation. Additionally, potassium ions (K+) and altered plasma osmolality may also contribute to autoregulation.

The small intestine tightly controls oxygen consumption, which remains constant even when arterial perfusion pressure varies between 30 and 125 mm Hg. Intestinal blood flow increases during food ingestion, thanks to the secretion of gastrointestinal hormones such as gastrin and cholecystokinin. These hormones augment intestinal blood flow and are released when food is ingested. The absorption of food also affects intestinal blood flow, with certain products of digestion acting as potent vasodilators. Among these, glucose and fatty acids are the primary mediators of mesenteric hyperemia.

In a normal situation, approximately 25% of cardiac output supplies blood flow to the liver. This blood flow to the liver comes from two sources: the portal vein (about 75%) and the hepatic artery. Since the portal venous blood has already passed through the gastrointestinal capillary bed, a significant portion of its oxygen has been extracted. The hepatic artery delivers the remaining 25% of blood, which is fully saturated with oxygen. As a result, around three-fourths of the oxygen used by the liver is derived from hepatic arterial blood.

The terminal portal venules and hepatic arterioles, which arise from the small branches of the portal vein and hepatic artery, enter the hepatic acinus at its center. From there, blood flows into the sinusoid capillaries, forming the capillary network of the liver. The sinusoid capillaries radiate towards the periphery of the acinus and connect with the terminal hepatic venules. Blood from these venules drains into larger branches of the hepatic veins, which are tributaries of the inferior vena cava.
Simple columnar epithelium with goblet cells •Fig. 17.42 Microcirculation Pattern of the Small Intestine. A, Capillaryplexusesarisefromarteriolesinthevillusandalsointheintestinalcrypt.Bloodleavestheintestinalcryptviavenulesthatentertheportalcirculation.B, Lymphaticvessels(lacteals)originatewithinthevillusandeventuallyformaplexusatthebaseofthevillus.(RedrawnfromKierszenbaumA.Histology and Cell Biology: An Introduction to Pathology. Philadelphia:Mosby;2002.) ). The adenosine concentration in mesenteric venous blood rises fourfold after brief arterial occlusion. It also rises during enhanced metabolic activity of the intestinal mucosa, such as during absorption of food. Adenosine, a potent vasodilator in the mesenteric vascular bed, may be the principal metabolic mediator of autoregulation. However, [K+] and altered plasma osmolality may also contribute to autoregulation.
Oxygen consumption by the small intestine is more rigorously controlled than is blood flow. Experiments have shown that O2 uptake of the small intestine remains constant when arterial perfusion pressure is varied between 30 and 125 mm Hg.
Food ingestion increases intestinal blood flow. Secretion of certain gastrointestinal hormones contributes to this hyperemia. Gastrin and cholecystokinin augment intestinal blood flow, and they are secreted when food is ingested. Absorption of food also affects intestinal blood flow. Undigested food has no vasoactive influence, whereas several products of digestion are potent vasodilators. Among the various constituents of chyme, the principal mediators of mesenteric hyperemia are glucose and fatty acids.
Normally, blood flow to the liver is approximately 25% of cardiac output. Hepatic blood flow is supplied by two sources: the portal vein (≈75%) and the hepatic artery. Because portal venous blood has already passed through the gastrointestinal capillary bed, much of the O2 of the portal vein blood flow has already been extracted. The hepatic artery delivers the remaining 25% of the blood, which is fully saturated with O2. Hence, approximately three fourths of the O2 used by the liver is derived from hepatic arterial blood.
The small branches of the portal vein and hepatic artery give rise to terminal portal venules and hepatic arterioles (
Fig. 17.43 ). These terminal vessels enter the hepatic acinus (the functional unit of the liver) at its center. Blood flows from these terminal vessels into the sinusoid capillaries, which constitute the capillary network of the liver. The sinusoid capillaries radiate toward the periphery of the acinus, where they connect with the terminal hepatic venules. Blood from these terminal venules drains into progressively larger branches of the hepatic veins, which are tributaries of the inferior vena cava.
•Fig. 17.43 Microcirculation of the Hepatic Acinus. Arrows indicatethedirectionofbloodflowfromtheterminalportionsofthehepaticarteryandportalveintothesinusoidcapillaries.Themixtureofarterialandvenousbloodflowsintothecentralveinandthenpassesintothesublobularvein.(RedrawnfromRossMH,PawlingW.Histology:A Text and Atlas: With Correlated Cell and Molecular Biology. Philadelphia:LippincottWilliams&Wilkins;2006.) Periportal space (space of Mall) Capillary Terminal branch of hepatic artery Terminal branch of portal vein Portal canal Arteriosinusoidal branch Lymphatic vessel Bile ductule Inlet venule Hepatic sinusoid Terminal hepatic venule (central vein) Sublobular vein