Splanchnic and Hepatic Circulation

Splanchnic and Hepatic Circulation

Splanchnic Circulation Overview

The splanchnic circulation supplies the GI tract, spleen, pancreas, and liver. At rest, it receives ~25% of cardiac output. Oxygen consumption is also high (~25% of total O₂ use). The gut can draw on this large vascular reserve: in haemorrhage, splanchnic vasoconstriction diverts 200–300 mL of blood to the systemic circulation.

Autoregulation

Myogenic autoregulation occurs in the stomach, small intestine, and colon, and is most prominent in the mucosa (which has the highest O₂ demand). Metabolic autoregulation: after meals, local metabolite accumulation (adenosine, CO₂, H⁺) causes vasodilation → mucosal blood flow increases up to 6-fold (fed state hyperaemia). This is essential to match O₂ delivery to the increased metabolic demands of digestion and absorption.

Neurogenic Control

The sympathetic nervous system (splanchnic nerves, α-adrenoceptors) causes vasoconstriction. In haemorrhage, sympathetic activation can reduce splanchnic blood flow to 25% of normal, diverting blood to vital organs. Parasympathetic stimulation causes mild vasodilation and increases secretion.

Villus Microcirculation and Countercurrent Exchange

Within each villus, arterioles run up the centre and venules return along the periphery. This arrangement creates a countercurrent exchange system: O₂ short-circuits from arteriole to venule at the villus base — approximately 80% of O₂ is shunted. The villus tip therefore receives only ~20% of the O₂ delivered. This makes the villus tip highly susceptible to hypoperfusion: in shock, mesenteric ischaemia, or severe haemorrhage, villus tips necrose → mucosal barrier breaks down → translocation of bacteria/endotoxin → systemic sepsis (gut as motor of multi-organ failure).

Hepatic Circulation

The liver receives ~25% of cardiac output (~1.5 L/min at rest). Its dual blood supply: portal vein (~75% of hepatic blood flow, nutrient-rich but low O₂) and hepatic artery (~25% of flow, high O₂). Both merge in hepatic sinusoids, where hepatocytes extract nutrients, process toxins, and synthesise plasma proteins. The hepatic venous outflow drains via hepatic veins into the inferior vena cava. Normal portal pressure is 5–10 mmHg; portal hypertension (>12 mmHg) drives the clinical complications of cirrhosis.