Splanchnic blood flow

This chapter is relevant to Section G4(ii) and G4(iii)of the 2023 CICM Primary Syllabus, which expects the exam candidate to "describe the distribution of blood volume and flow in the various regional circulations ... including autoregulation... These include, but not limited to, the cerebral and spinal cord, hepatic and splanchnic, coronary, renal and utero-placental circulations". The renal, coronary and hepatic circulatory systems have appeared in the exam so many times that these questions crowd out all the others. In contrast, the splanchnic circulation is forgotten by the examiners, which is puzzling because of its significant importance in our clinical work, where it often kills people by mesenteric ischaemia. The college have made up for this by asking many detailed questions about the mesenteric circulation in the fellowship exam. Moreover, the anatomy of the gastrointestinal blood supply was asked in Question 7 from the first paper of 2018.

In summary:

  • Splanchnic vascular anatomy
    • There are three main vessels: coeliac trunk, superior mesenteric artery and inferior mesenteric artery
    • There is an extensive collateral circulation which protects against ischaemia
    • The venous drainage is into the portal vein, and then into the liver
    • The blood volume in this circulatory region is about 20% of the total
  • Splanchnic blood flow
    • At rest, the total blood flow is 30ml/100g/min (10-20% of total cardiac output)
    • Postprandial blood flow can be up to 35% of total cardiac output
    • Oxygen extraction ratio is low (~ 10%)
    • The splanchnic organs tend to extract more oxygen as flow decreases, and autoregulatory input into blood flow is therefore  minimal under normal circumstances
  • Regulation of splanchnic blood flow:
    • Intrinsic autoregulation:
      • Myogenic autoregulation (stretch-mediated) 
      • Metabolic autoregulation (likely mediated by adenosine)
      • Rapid, but 
    • Autonomic regulation
      • Sympathetic vasoconstriction (noreadrenergic α-1 effect)
      • Parasympathetic vasodilation (acetylcholine-mediated NO release)
    • Humoural and hormonal regulation
      • Vasoactive mediators (of which there are many)
      • Exogenous drugs

As is often the case, in this topic one name keeps appearing in the bylines of the papers, and for splanchnic blood flow that is D. Neil Granger - pretty much anything from the 1980s seems to be perfect for this topic, and much of it seems to be available as free full text. If one had to pick a representative piece, one would have to pick Intestinal Blood Flow (Granger et al, 1980)Fraser et al (1991) is also excellent, even though it is ostensibly supposed to be only about the autonomic nervous system of the gut.

"Splanchnic" circulation

Following from the ancient Greek origin of the word σπλαγχνικός, which basically means "entrails", the casual anatomist will use this term interchangeably with "mesenteric" to describe the blood vessels which supply the digestive tract. However, this is wrong. When you search for "splanchnic circulation" in professional literature, the results generally yield articles like Parks et al (1985), which confidently define it as follows:

"The splanchnic circulation is composed of gastric, small intestinal, colonic, pancreatic, hepatic, and splenic circulations, arranged in parallel with one another".

The attentive reader will note that this definition includes the liver. However, when they were writing the Syllabus Document, the college examiners clearly meant mesenteric instead of splanchnic, because they listed the hepatic circulation separately. Moreover, all the hepatic circulation SAQs do not require any discussion of mesenteric blood supply in their answer. As a result, the circulatory system of the liver gets its own chapter, and this page ends up having to use continue misusing the word "splanchnic", cringing awkwardly at the incorrectness.  

Anatomy of the splanchnic circulation

The major vessels and their branches are:

  • Coeliac trunk
    • Left gastric artery
    • Common hepatic artery
    • Splenic artery
  • Superior mesenteric artery
    • Inferior pancreaticoduodenal artery
    • Intestinal (jejunal and ileal) arteries
    • Ileocolic artery
    • Right colic artery
    • Middle colic artery
  • Inferior mesenteric artery
    • Left colic artery
    • Sigmoid arteries
    • Superior rectal artery

The structures supplied by each branch are:

  • Coeliac trunk:
    • Abdominal part of the oesophagus
    • Stomach
    • Superior half of the duodenum
    • Liver
    • Superior half of the pancreas
    • Spleen
  • Superior mesenteric artery:
    • Intestine, from the lower half of the duodenum down to the splenic flexure of the large intestine
  • Inferior mesenteric artery:
    • Colon, from the splenic flexure down to the sigmoid and superior portion of the rectum

Venous structures:

  • Oesophagus is drained by branches of the azygous veins and the inferior thyroid vein
  • Mesenteric circulation drains via the superior and inferior mesenteric vein
    • These two vessels are then joined by the splenic vein
    • These form the portal vein
    • This then splits to form the right and left branches in the liver
    • From the portal vein, blood drains via the hepatic vein into the inferior vena cava
  • Lower third of the rectum and anus drain into the middle rectal vein, which drins directly into the IVC

It is of course completely pointless to accurately describe the layout of the mesenteric anatomy to the CICM exam candidate, as they should never have to encounter it in the wild. Occasionally, the interpretation of imaging might be called for, or the discussion of embolised branches, but realistically the ICU trainee would almost never be called upon to make diagnostic or management decisions on the basis of raw untreated anatomy. From this, it follows that even a discussion of the splanchnic circulation which represents the vessels schematically, or which just lists the names of the arterial and venous branches, would be educationally meaningless. It does not help that these vessels are normally subject to endless individual variation. In case a detailed anatomical review of these variations is required, one can find authoritative answers in excellent reference resources such as Kornblith et al (1992) or Rosenblum et al (1997). Instead, the following broad generalisations or unique features can be mentioned here, as they may actually have relevance to the intensive care practitioner:

  • Significant collateral circulation exists. There is a significant amount of collateral flow between major mesenteric vessels, and between the splanchnic circulation and the rest of the systemic arterial system. This has implications: for ischaemia to occur, at least two of the three major vessels need to be occluded or experiencing critical stenosis. Important sites of collateral flow include the pancreas (made by the gastroduodenal branch of the coeliac artery and the pancreaticoduodenal branch of the SMA) and the splenic flexure (where branches of the SMA and IMA create the Arc of Riolan and the Marginal Artery of Drummond)
  • Extensive anastomosis between arterial branches is seen in the mesenteric circulation particularly, where many arteries from different vascular territories mesh freely before "arborising" into a shared capillary network. This is protective against embolic phenomena, as none of these vessels are "end vessels".
  • The microcirculation of the villus features a counter-current mechanism, which allows arterial oxygen to "escape" into the countercurrent venous blood, thereby predisposing the intestinal mucosa to ischaemia (Shepherd & Kiel, 1992).
  • The venous drainage is into the liver, rather than back into the heart. Mesenteric venous blood drains from the gut into the portal venous circulation, a valveless system of high-flow low-resistance vessels which supply the liver with 75% of its blood and 50% of its oxygen.
  • The total capacity of the system is vast. Particularly the veins. The mesenteric circulation can contain up to 20% of the total circulating blood volume (Brooksby & Donald, 1971), some of which can be liberated as a sort of emergency autotransfusion in animals (and potentially also in man).

Splanchnic blood flow

The discussion of splanchnic blood flow must necessarily be split into the discussion of blood flow through the three major arteries, as they are rather different. Of these, the coeliac trunk is the largest, most proximal, and has the highest blood flow, followed by the SMA. The IMA is the smallest and has the lowest blood flow. Two important points need to be made, which have some sort of vague critical care relevance:

  • The flow is distributed unequally. The main recipients of the blood flow, among the organs, are the pancreas and small intestine. The stomach and large bowel are comparatively under perfused.
  • Absorptive surfaces get more blood flow. In each hollow viscus, the mucosa and submucosa enjoy greater perfusion than the muscularis layer.

Most textbooks seem to quote a total blood flow of  30ml/100g/min, but of course the total flow of blood to the splanchnic circulation can vary considerably, depending on what and when you ate, and can vary from 10% to 35% of the total cardiac output. To illustrate the point, Rosenblum et al (1997) report coeliac axis flows varying from 300ml/min to 1200 ml/min. Perko et al (1998) reported total splanchnic blood flow of around 1600ml/min on average for resting adults, and around 3000ml/min for the same adults after they horfed down a bucket of Swedish glog. In short, splanchnic blood flow is highly variable. Which brings us to...

Autoregulation of splanchnic blood flow

Clearly, one of the characteristics of the splanchnic circulation is the ability to change its vascular resistance and invite influence the rate of splanchnic blood flow according to some change in conditions. This can, for lack of a better word, be called "autoregulation", in the sense that it appears as if the blood vessels of the gut are being influenced by something the gut is doing, but in fact most of the mechanisms of control are external, and most of them are designed to optimise the benefit to the rest of the organism rather than catering for the metabolic demands of abdominal organs. This topic is covered in just the right amount of detail by Parks & Jacobson (1985). 

In brief, there are three main levels of control over the splanchnic circulation:

  • Intrinsic autoregulation:
    • Myogenic autoregulation (stretch-mediated) 
    • Metabolic autoregulation (likely mediated by adenosine)
  • Autonomic regulation
    • Sympathetic vasoconstriction (noradrenergic α-1 effect)
    • Parasympathetic vasodilation (acetylcholine-mediated NO release)
  • Humoural and hormonal regulation
    • Vasoactive mediators (of which there are many)
    • Exogenous drugs

Intrinsic autoregulation of splanchnic blood flow

Yes, the gut has some mechanisms to ensure that it maintains some sort of stable flow, in the event that systemic blood pressure is fluctuating wildly, or if its metabolic needs are not being met. These mechanisms are not especially unique. There are two main ones: myogenic regulation and metabolic regulation. They are common to all (well, most) arterial circulatory regions, and are described well enough in the chapter which deals with the mechanisms of peripheral vascular resistance. In summary:

  • Myogenic regulation is triggered by vessel stretch and is an intrinsic property of the vascular smooth muscle
  • Metabolic regulation can be loosely described as "regulation of blood flow which is determined by metabolic demand" and seems to be a response to the release of metabolic endproducts by the tissue, particularly the products of anaerobic metabolism.  Carbon dioxide, lactate, potassium ions, adenosine, nitric oxide and hydrogen ions have all been implicated.

Now, those might sound familiar, but Granger and Kvietys (1981) caution that it is not what you might expect after reading about the autoregulatory capacity of other regional circulations:

"... it is not the intense phenomenon seen in other organs (e.g. kidney, brain) since a reduction in perfusion pressure is usually accompanied by a reduction in blood flow, while resistance falls by a modest amount"

So, don't expect the intestine to attentively self-manage like the brain. Fortunately, it does not need to, because of its ascetic disinterest in metabolic substrate. Under normal circumstances, according to Granger & Norris (1980) at rest the oxygen extraction ratio of the gut is about 5-10%. This means, it really does not need to do very much to autoregulate its blood flow, and if perfusion pressure drops it can just extract more oxygen. Thus, when the investigators dropped the MAP to 30 mmHg, the oxygen extraction ratio increased to 80% (i.e. tenfold) with only 30% change in vascular resistance. 

To summarise, there is some intrinsic (myogenic, metabolic) autoregulation of blood flow in the mesenteric circulation, but under most conditions it is a rather relaxed affair, as the gut is not viewed as a mission-critical organ. However, everything changes as soon as you have a meal.

Autonomic control of splanchnic blood flow

The greatest changes which occur in splanchnic blood flow during routine use are due to eating. This is handled largely by the sympathetic and parasympathetic fibres which innervate the blood vessels of the gut. Fraser et al (1991) offer the best overview for this topic.  The main role of the autonomic nervous system is to increase blood flow to the gut for digestion, and to redirect it away from the gut during times of increased haemodynamic demand. Thus:

  • Sympathetic stimulation:
    • Decreases gastric (and especially mucosal) blood flow
    • Markedly decreases intestinal blood flow (an α-1 mediated effect); though after a time some sort "autoregulatory escape" occurs, which is probably mediated by the release of vasodilator peptides in a negative feedback response
    • Decreases blood flow to the colon
  • Parasympathetic stimulation:
    • Increases gastric blood flow (though this effect does not appear to be acetylcholine-mediated)
    • Increases intestinal blood flow, and this is clearly a parasympathetic phenomenon, but it is not by means of vagal stimulation. The vagus apparently does not play any role in this, as direct vagal stimulation has no vasodilatory effect, but there definitely is postprandial vasodilation happening, and it is definitely blocked by atropine.
    • Increases colonic and rectal blood flow

Neurohormonal and humoral control of splanchnic blood flow

There turns out to be a vast array of circulating vasoactive substances, and all of them have some effect on the splanchnic circulation. It would literally be easier to list hormones which don't influence the splanchnic circulation. An excellent table is offered by Harper (2016), and it is reproduced here with zero modification. Theoretically, it would possible to track down references for each of these influences, but it did not seem essential, considering especially the fact that CICM have never asked about this in any of the past papers.

Vasoactive Mediators of the Splanchnic Circulation
Vasodilators Vasoconstrictors
  • Parasympathetic activation
  • Hypercapnia
  • Hypoxia
  • Alkalosis
  • Acetylcholine
  • Bradykinin
  • Adenosine
  • Gastrin
  • Secretin
  • Cholecystokinin
  • Vasoactive intestinal polypeptide
  • Substance P
  • Prostaglandins
  • Gastric inhibitory polypeptide
  • Leukotrienes
  • Nitric oxide
  • Dopamine
  • Sympathetic activation
  • Hypocapnia
  • Hyperoxia
  • Acidosis
  • Vasopressin and analogs
  • Angiotensin II
  • Prostaglandins
  • Peptide YY
  • Neuropeptide Y


Parks, Dale A., and Eugene D. Jacobson. "Physiology of the splanchnic circulation." Archives of internal medicine 145.7 (1985): 1278-1281.

Kornblith, Paul L., Scott J. Boley, and Brian S. Whitehouse. "Anatomy of the splanchnic circulation." Surgical Clinics of North America 72.1 (1992): 1-30.

Rosenblum, Jordan D., Catherine M. Boyle, and Lewis B. Schwartz. "The mesenteric circulation: anatomy and physiology." Surgical Clinics 77.2 (1997): 289-306.

Brooksby, Gerald A., and David E. Donald. "Dynamic changes in splanchnic blood flow and blood volume in dogs during activation of sympathetic nerves." Circulation research 29.3 (1971): 227-238.

Perko, M. J., et al. "Mesenteric, coeliac and splanchnic blood flow in humans during exercise." The Journal of Physiology 513.3 (1998): 907-913.

Granger, D. Neil, and Peter R. Kvietys. "The splanchnic circulation: intrinsic regulation." Annual review of physiology 43.1 (1981): 409-418.

Granger, HARRIS J., and CARRIE P. Norris. "Intrinsic regulation of intestinal oxygenation in the anesthetized dog." American Journal of Physiology-Heart and Circulatory Physiology 238.6 (1980): H836-H843.

Granger, D. N., et al. "Intestinal blood flow." Gastroenterology 78.4 (1980): 837-863.

Fink, Gregory D., and John W. Osborn. "The splanchnic circulation." Primer on the Autonomic Nervous System. Academic Press, 2012. 211-213.

Fraser, Kathleen A., and Samuel S. Lee. "Autonomic regulation of splanchnic circulation." Canadian Journal of Gastroenterology 5 (1991).

Shepherd, A. P., and J. W. Kiel. "A model of countercurrent shunting of oxygen in the intestinal villus." American Journal of Physiology-Heart and Circulatory Physiology 262.4 (1992): H1136-H1142.

Geboes, Karel, Karen P. Geboes, and Geert Maleux. "Vascular anatomy of the gastrointestinal tract." Best Practice & Research Clinical Gastroenterology 15.1 (2001): 1-14.