Splanchnic Organs Research Articles

Mast cell-mediated splanchnic cholestatic inflammation

Splanchnic mast cells increase in chronic liver and in acute-on-chronic liver diseases. We administered Ketotifen, a mast cell stabilizer, and measured the mast cells in the splanchnic organs of cholestatic rats. These groups were studied: sham-operated rats (S; n = 15), untreated microsurgical cholestasic rats (C; n = 20) and rats treated with Ketotifen: early (SK-e; n = 20 and CKe; n = 18), and late (SK-l; n = 15 and CK-l; n = 14). The cholestatic rats showed systemic and splanchnic impairments, such as ascites, portal hypertension, and biliary proliferation and fibrosis. The rats also showed a splanchnic increase of TNF-α, IL-1β and MCP-1, and a reduction of IL-4, IL-10 and antioxidants. An increase of VEGF in the ileum and mesenteric lymphatic complex was associated with a liver reduction of TGF-β1. Ketotifen reduces the degree of hepatic insufficiency and the splanchnic inflammatory mediators, as well as VEGF and TGF-ß1 levels. Ketotifen also reduces the connective tissue mast cells in the mesenteric lymphatic complex of cholestatic rats, while increases the hepatic mucosal mast cells. In cholestatic rats, Ketotifen improves liver function and ascites, and also reduces pro-inflammatory mediators in the splanchnic area. The decrease in connective tissue mast cells in the mesenteric lymphatic complex due to the administration of Ketotifen would lead to the improvement of the inflammatory splanchnic response, and consequently the abovementioned complications.

Heterogeneity and Variability in Pressure Autoregulation of Organ Blood Flow: Lessons Learned Over 100+ Years.

Pressure autoregulation is an organ's intrinsic ability to maintain blood flow despite changes in perfusion pressure. The purpose of this review is to discuss autoregulation's heterogeneity among different organs and variability under different conditions, a very clinically relevant topic. Systematic search of Ovid MEDLINE; nonsystematic search of PubMed, Google Scholar, and reference lists. Animal or human studies investigating the potency or variation of pressure autoregulation of any organs or the association between autoregulation and outcomes. Two authors screened the identified studies independently then collectively agreed upon articles to be used as the basis for this review. Study details, including subjects, organ investigated, methods of blood pressure intervention and blood flow measurement, and values of the lower limit, upper limit, and plateau were examined. Comparative canine studies were used to demonstrate the heterogeneity of pressure autoregulation among different organs and validate the proposed scale for organ categorization by autoregulatory capacity. Autoregulatory variability is discussed per organ. The association between cerebral autoregulation and outcome is summarized. The organs with robust autoregulation are the brain, spinal cord, heart, and kidney. Skeletal muscle has moderate autoregulation. Nearly all splanchnic organs including the stomach, small intestine, colon, liver, and pancreas possess weak autoregulation. Autoregulation can be readily affected by a variety of clinically relevant factors. Organs with weak or weakened autoregulation are at a greater risk of suboptimal perfusion when blood pressure fluctuates. Cerebral autoregulation and outcomes are closely related. These lessons learned over 100+ years are instructive in clinical care.

The Organ Handling of Soluble Klotho in Humans

Background: Chronic kidney disease (CKD) reduces both Klotho expression and its shedding into circulation, an effect that accelerates progression and cardiovascular complications. However, the mechanisms that regulate Klotho release by the human kidney are still unknown. Methods: We measured plasma Klotho across the kidney, splanchnic organs and lung in 22 patients (71 ± 2 years, estimated glomerular filtration rate [eGFR] 60 ± 5.4 mL/min 1.73 m²) during elective diagnostic cardiac catheterizations. Results: Although the Klotho average renal vein concentrations were remarkably higher (by ∼9%) than arterial values, the kidney removed Klotho (or was at zero balance) in 7 subjects, indicating that the kidney contribution to systemic Klotho is not constant. Klotho fractional enrichment across the kidney was inversely related to plasma sodium (r = 0.43, p = 0.045) and acid uric acid levels (r = 0.38, p = 0.084) and directly, to renal oxygen extraction (r = 0.56, p = 0.006). In multivariate analysis, renal oxygen extraction was the only predictor of the enrichment of Klotho across the kidney, suggesting the dependence of renal Klotho release on tubular hypoxia or oxidative metabolism. Klotho balance was neutral across the lung. In patients with eGFR <60 mL/min, Klotho was also removed by splanchnic organs (single pass fractional extraction ∼11%). Conclusions: The present study identifies kidney oxygen uptake as a predictor of Klotho release, and splanchnic organs as a site for Klotho removal. This study provides new understanding of kidney Klotho release and suggests that modulating kidney oxygen metabolism could increase Klotho delivery, as an option to slow disease progression and blunt organ damage.

A metabolic approach during normothermic regional perfusion in uncontrolled donors after circulatory death-A pilot study.

The use of donation after circulatory death (DCD) has increased significantly to face the persistent mismatch between supply and demand of organs for transplantation. While controlled (c) DCDs have warm ischemic time (WIT) that can be estimated, the WIT is often inexact and extended in uncontrolled DCD (uDCD), making assessment of injury difficult. We aimed at investigating the effects of cold ischemia on potential donor organ damage in the course of nRP by assessing the dynamic variations of transaminases and creatinine values in 17 uDCD donors. In our series, lactate values did not show significant changes during the study period (P=0.147). Creatinine values did not significantly changed while transaminases progressive increased throughout the study period, even if it was significant only for AST (P=0.035). According to our data, nRP duration affects splanchnic organs, being the liver sensitive to hypoperfusion, and serial biochemical measurements could help in detecting organ functional status.

Ammonia-Nitrogen Added to Low-Crude-Protein Diets Deficient in Dispensable Amino Acid–Nitrogen Increases the Net Release of Alanine, Citrulline, and Glutamate Post–Splanchnic Organ Metabolism in Growing Pigs

Dietary ammonia is rapidly absorbed but poorly used for urea synthesis in pigs fed low-crude-protein (low-CP) diets deficient in dispensable amino acid (DAA)-nitrogen. We explored the effect of dietary ammonia on net amino acid (AA) balances in portal-drained viscera (PDV) and livers of pigs fed a diet deficient in DAA-nitrogen. Eight barrows with an initial body weight (BW) of 26.5±1.4 kg (mean + SD) were surgically fitted with 4 catheters each (portal, hepatic, and mesenteric veins and carotid artery). The pigs were restricted-fed (2.8×191 kcal/kg BW0.60) for 7 d, and every 8 h a diet deficient in DAA-nitrogen supplemented with increasing amounts of ammonia-nitrogen (CP=7.76%, 9.27%, and 10.77% for the control and low- and high-ammonia diets, respectively). The treatment sequence was based on a 3×3 Latin-square design with 3 consecutive periods. On the last day of each period, blood flows in portal and hepatic veins were determined with a continuous infusion of ρ-amino hippuric acid into the mesenteric vein. Consecutive blood samples were taken for AA concentration in blood plasma, and AA balances were calculated for PDV and the liver. Cumulative release of citrulline (Cit) and proline (Pro) increased with ammonia supplementation in PDV but decreased for glutamine (Gln) and glycine (Gly) (Gln: -19.32±3.56, -32.50±3.73, and -42.11±3.55 mmol/meal for the control and low- and high-ammonia groups, respectively; P≤0.05). Cumulative release of alanine (Ala), glutamic acid (Glu), and Gln increased with ammonia supplementation across the liver (P≤0.05). When combined, PDV+liver, the cumulative release of Ala, Cit, and Glu increased with ammonia-nitrogen supplementation (P≤0.05). Dietary ammonia could be used as a nitrogen supplement to increase the synthesis of Ala, Cit, and Glu across splanchnic organs in pigs fed a diet deficient in DAA-nitrogen.

Fructose metabolism and noncommunicable diseases: recent findings and new research perspectives.

There is increasing concern that dietary fructose may contribute to the development of noncommunicable diseases. This review identifies major new findings related to fructose's physiological or adverse effects. Fructose is mainly processed in splanchnic organs (gut, liver, kidneys) to glucose, lactate, and fatty acids, which can then be oxidized in extrasplanchnic organs and tissues. There is growing evidence that splanchnic lactate production, linked to extrasplanchnic lactate metabolism, represents a major fructose disposal pathway during and after exercise. Chronic excess fructose intake can be directly responsible for an increase in intrahepatic fat concentration and for the development of hepatic, but not muscle insulin resistance. Although it has long been thought that fructose was exclusively metabolized in splanchnic organs, several recent reports provide indirect that some fructose may also be metabolized in extrasplanchnic cells, such as adipocytes, muscle, or brain cells; the quantity of fructose directly metabolized in extrasplanchnic cells, and its physiological consequences, remain however unknown. There is also growing evidence that endogenous fructose production from glucose occurs in humans and may have important physiological functions, but may also be associated with adverse health effects. Fructose is a physiological nutrient which, when consumed in excess, may have adverse metabolic effects, mainly in the liver (hepatic insulin resistance and fat storage). There is also concern that exogenous or endogenously produced fructose may be directly metabolized in extrasplanchnic cells in which it may exert adverse metabolic effects.

Effects of GIP on regional blood flow during normoglycemia and hyperglycemia in anesthetized rats.

The incretin hormone glucose‐dependent insulinotropic polypeptide (GIP) potentiates glucose‐stimulated insulin secretion, and affects β‐cell turnover. This study aimed at evaluating if some of the beneficial effects of GIP on glucose homeostasis can be explained by modulation of islet blood flow. Anesthetized Sprague–Dawley rats were infused intravenously with different doses of GIP (10, 20, or 60 ng/kg*min) for 30 min. Subsequent organ blood flow measurements were performed with microspheres. In separate animals, islets were perfused ex vivo with GIP (10−6–10−12 mol/L) during normo‐ and hyperglycemia and arteriolar responsiveness was recorded. The highest dose of GIP potentiated insulin secretion during hyperglycemia, but had no effect in normoglycemic rats. The highest GIP concentration decreased blood perfusion of whole pancreas, pancreatic islets, duodenum, colon, liver and kidneys. The decrease in blood flow was unaffected by ganglion blockade or adenosine receptor inhibition. In contrast to this, in single perfused islets GIP induced a dose‐dependent arteriolar dilation. Thus, high doses of GIP exert a direct dilatory effect on islet arterioles in isolated islets, but induce a generalized vasoconstriction in splanchnic organs, including the whole pancreas and islets, in vivo. The latter effect is unlikely to be mediated by adenosine, the autonomic nervous system, or endothelial mediators.

Fructose-containing caloric sweeteners as a cause of obesity and metabolic disorders.

Compared with other carbohydrates, fructose-containing caloric sweeteners (sucrose, high-fructose corn syrup, pure fructose and fructose-glucose mixtures) are characterized by: a sweet taste generally associated with a positive hedonic tone; specific intestinal fructose transporters, i.e. GLUT5; a two-step fructose metabolism, consisting of the conversion of fructose carbones into ubiquitous energy substrates in splanchnic organs where fructolytic enzymes are expressed, and secondary delivery of these substrates to extrasplanchnic tissues. Fructose is a dispensable nutrient, yet its energy can be stored very efficiently owing to a rapid induction of intestinal fructose transporters and of splanchnic fructolytic and lipogenic enzymes by dietary fructose-containing caloric sweeteners. In addition, compared with fat or other dietary carbohydrates, fructose may be favored as an energy store because it uses different intestinal absorption mechanisms and different inter-organ trafficking pathways. These specific features make fructose an advantageous energy substrate in wild animals, mainly when consumed before periods of scarcity or high energy turnover such as migrations. These properties of fructose storage are also advantageous to humans who are involved in strenuous sport activities. In subjects with low physical activity, however, these same features of fructose metabolism may have the harmful effect of favoring energy overconsumption. Furthermore, a continuous exposure to high fructose intake associated with a low energy turnover leads to a chronic overproduction of intrahepatic trioses-phosphate production, which is secondarily responsible for the development of hepatic insulin resistance, intrahepatic fat accumulation, and increased blood triglyceride concentrations. In the long term, these effects may contribute to the development of metabolic and cardiovascular diseases.

Arterioportal shunting, splanchnic capillary perfusion, and the effects of colloids during capnoperitoneum in neonatal and adolescent pigs

Clinical and experimental data indicate that neonates are sensitive to the CO2 pneumoperitoneum. An impaired splanchnic perfusion during laparoscopy in adults has been reported. We recently confirmed that intravenous colloids improve macrocirculatory function in neonates. We aimed to determine the impact of CO2 pneumoperitoneum on the perfusion of splanchnic organs in the young including effects of colloid application. Male piglets (n = 25) were divided into four groups: (1) neonatal controls, (2) neonates with crystalloid restitution, (3) neonates with colloidal restitution, and (4) adolescents with crystalloid restitution. Animals were ventilated and subjected to a 3-h, 10mmHg CO2 pneumoperitoneum followed by 2h resuscitation. Hepatic, splanchnic, and arteriovenous shunt perfusion was assessed via central and portal venous catheters. Capillary organ flow was detected by fluorescent microspheres. The rate of bile flow was measured. The neonatal crystalloid group showed a significant decrease in the intestinal capillary perfusion at the end of the recovery period. This was not detectable in the adolescent and colloid group. There was a significant increase in microcirculatory arterioportal shunt flow during the CO2 pneumoperitoneum in both neonatal groups but not in the sham and adolescent groups (p < 0.05). Hepatic arterial perfusion increased after insufflation in all groups and dropped during capnoperitoneum to levels of about 70% baseline. There was no significant impairment of splanchnic perfusion or bile flow as a result of the pneumoperitoneum in all groups. Capillary perfusion of the abdominal organs was stable during capnoperitoneum and recovery in adolescents and neonates with colloid restitution, but not with crystalloid restitution. Significant arterioportal shunting during capnoperitoneum could affect hepatic microcirculation in neonates. Our data confirm that moderate pressure capnoperitoneum has no major effect on the perfusion of abdominal organs in neonates with adequate substitution.

Ammonia Nitrogen Added to Diets Deficient in Dispensable Amino Acid Nitrogen Is Poorly Utilized for Urea Production in Growing Pigs

Background: Including ammonia in low-crude protein (CP) diets deficient in dispensable amino acid (DAAs) increases nitrogen retention in growing pigs.Objective: We investigated the absorption and metabolism of dietary ammonia nitrogen in the portal-drained viscera (PDV) and liver of pigs fed a diet deficient in DAA nitrogen.Methods: Eight pigs with an initial mean ± SD body weight (BW) of 26.5 ± 1.4 kg were surgically fitted with 4 catheters each (portal, hepatic and mesenteric veins, and carotid artery). The pigs were fed (2.8 × 191 kcal/kg BW0.60), for 7 d and every 8 h, a diet deficient in DAA nitrogen supplemented with increasing amounts of ammonia nitrogen (CP: 7.76%, 9.27%, and 10.77%; indispensable amino acid nitrogen:total nitrogen ratio: 0.71, 0.59, and 0.50 for control and low- and high-ammonia diets, respectively). The treatment sequence was based on a Latin square design with 3 consecutive periods. On the last day of each period, blood flows in the portal and hepatic veins were determined with a continuous infusion of ρ-amino hippuric acid into the mesenteric vein. Serial blood samples were taken to determine ammonia and urea nitrogen concentration. Net balances of ammonia and urea nitrogen were calculated for the PDV and liver.Results: Cumulative (8 h) ammonia nitrogen appearance in the portal vein increased (P ≤ 0.05) with ammonia intake (433, 958, and 1629 ± 60 mg ammonia nitrogen/meal for control and low- and high-ammonia diets, respectively). The cumulative hepatic uptake of ammonia nitrogen increased (P ≤ 0.05) with ammonia nitrogen supply. The cumulative urea nitrogen appearance in the hepatic vein tended to increase (P ≤ 0.10) only in high-ammonia treatment (-92.5, -59.4, and 209.7 ± 92 mg urea nitrogen/meal for control and low- and high-ammonia diets, respectively) and, relative to the control diet, represented -6.0% and 11% of ammonia nitrogen intake.Conclusion: Dietary ammonia nitrogen is poorly utilized for urea production across splanchnic organs when pigs are fed diets deficient in DAA nitrogen.

Correction to 'Starvation effects on nitrogen and carbon stable isotopes of animals: an insight from meta-analysis of fasting experiments'.

[This corrects the article DOI: 10.1098/rsos.170633.].

Factors associated with increased pancreatic enzymes in septic patients: a prospective study

BackgroundThe perfusion of splanchnic organs is deeply altered in patients with septic shock. The aim of the study is to identify the predictive factors of septic shock-induced increase of serum lipase and amylase and to assess and evaluate its prognostic impact.MethodsWe conducted a prospective observational study. All adult patients admitted with septic shock were eligible for our study. Serum lipase and amylase were measured on admission. Patients with and those without increased pancreatic enzymes were compared. Predictive factors of pancreatic insult identified by the univariate analysis were integrated in a stepwise multivariate analysis. Odds ratios (OR) with the 95% confidence interval (CI) were calculated accordingly. Second, the sensitivity and the specificity of amylase and lipase to predict intensive care unit (ICU) mortality were identified through the Receiver Operator Curve.ResultsFifty patients were included. Median [quartiles] age was 68.5 [58–81] years. The APACHE II score was 26 [20–31]. Twenty-three patients (46%) had increased serum amylase and/or serum lipase. Diabetes mellitus (OR = 16; 95% CI [1.7–153.5]; p = 0.016), increased blood urea nitrogen (OR = 1.12; 95% CI [1.02–1.20], p = 0.016), and decreased C-reactive protein (OR = 0.97; 95% CI [0.96–0.99]; p = 0.027) were identified as independent factors predicting increased pancreatic enzymes. Twenty patients (40%) died in the ICU. Neither serum amylase level nor serum lipase level was significantly different between survivors and non-survivors (respectively 49 [27.7–106] versus 85.1 [20.1–165] UI/L; p = 0.7 and 165 [88–316] versus 120 [65.5–592] UI/L; p = 0.952).ConclusionIncrease of pancreatic enzymes is common in patients with septic shock. Diabetes and impaired renal function are predictive of increased pancreatic enzymes. Such finding does not carry any negative prognostic value.

Fructose Metabolism from a Functional Perspective: Implications for Athletes.

Substantial amounts of fructose are present in our diet. Unlike glucose, this hexose cannot be metabolized by most cells and has first to be converted into glucose, lactate or fatty acids by enterocytes, hepatocytes and kidney proximal tubule cells, which all express specific fructose-metabolizing enzymes. This particular metabolism may then be detrimental in resting, sedentary subjects; however, this may also present some advantages for athletes. First, since fructose and glucose are absorbed through distinct, saturable gut transporters, co-ingestion of glucose and fructose may increase total carbohydrate absorption and oxidation. Second, fructose is largely metabolized into glucose and lactate, resulting in a net local lactate release from splanchnic organs (mostly the liver). This 'reverse Cori cycle' may be advantageous by providing lactate as an additional energy substrate to the working muscle. Following exercise, co-ingestion of glucose and fructose mutually enhance their own absorption and storage.

Colestasis microquirúrgica: un modelo de inflamación esplácnica

Introduction: The ligation of the common bile duct in rats is a reliable experimental model of the cirrhosis associated with portal hypertension. This condition induces a splanchnic inflammation, in which mast cells might be involved. Methods: In order to verify this hypothesis, were measured the density of connective tissue mast cells (RMCP-I) (RMCP: rat mast cell protease) and mucosal mast cells (RMCP-II) in the splanchnic organs of pseudo-operated rats and in rats with microsurgical extrahepatic cholestasis. Results: A statistically significant increase (p<0.05) in the density of both types cells in the liver and ileum of cholestatic rats with reference to the pseudo-operated rats was observed. Conclusions: These results suggest the possible key role that mast cells could play in the visceral organs. Being splanchnic modulators of the inflammatory response, angiogenesis and fibrotic remodelling, which occur in cirrhosis.

Mature peritoneal macrophages take an avascular route into the injured liver and promote tissue repair.

Mature peritoneal macrophages take an avascular route into the injured liver and promote tissue repair.

The Role of the Vagal Nucleus Tractus Solitarius in the Therapeutic Effects of Obesity Surgery and Other Interventional Therapies on Type 2 Diabetes

The current treatment for obesity-related type 2 diabetes is not able to achieve sufficient metabolic control. New remission prospects have been offered through bariatric surgery and other interventional therapies. The aim of the study is to illustrate the mechanism by which such therapies affect the autonomic system, in particular the afferent vagal activity. The first and most important terminal of this activity is the brainstem vagal nucleus tractus solitarius. Its function, on which the vagal efferent inputs that control the splanchnic organs depend, is conditioned by the level of synaptic transmission within it. In conclusion, on the basis of such a view, a selective pharmacological modulation of such transmission as the target for future medical treatment of obesity and related type 2 diabetes is proposed.

Functional vascular anatomy of the peritoneum in health and disease.

The peritoneum consists of a layer of mesothelial cells on a connective tissue base which is perfused with circulatory and lymphatic vessels. Total effective blood flow to the human peritoneum is estimated between 60 and 100 mL/min, representing 1-2 % of the cardiac outflow. The parietal peritoneum accounts for about 30 % of the peritoneal surface (anterior abdominal wall 4 %) and is vascularized from the circumflex, iliac, lumbar, intercostal, and epigastric arteries, giving rise to a quadrangular network of large, parallel blood vessels and their perpendicular offshoots. Parietal vessels drain into the inferior vena cava. The visceral peritoneum accounts for 70 % of the peritoneal surface and derives its blood supply from the three major arteries that supply the splanchnic organs, celiac and superior and inferior mesenteric. These vessels give rise to smaller arteries that anastomose extensively. The visceral peritoneum drains into the portal vein. Drugs absorbed are subject to first-pass hepatic metabolism. Peritoneal inflammation and cancer invasion induce neoangiogenesis, leading to the development of an important microvascular network. Anatomy of neovessels is abnormal and characterized by large size, varying diameter, convolution and blood extravasation. Neovessels have a defective ultrastructure: formation of large "mother vessels" requires degradation of venular and capillary basement membranes. Mother vessels give birth to numerous "daughter vessels". Diffuse neoangiogenesis can be observed before appearance of macroscopic peritoneal metastasis. Multiplication of the peritoneal capillary surface by neoangiogenesis surface increases the part of cardiac outflow directed to the peritoneum.

Interorgan handling of fibroblast growth factor-23 in humans.

Fibroblast growth factor-23 (FGF-23) accumulates in blood of patients with chronic kidney disease (CKD) and is associated both with cardiovascular complications and disease progression. However, our knowledge of the sites and mechanisms that regulate plasma FGF-23 is still incomplete. We measured plasma intact FGF-23 across the kidney, splanchnic organs, and lung in 11 patients [estimated glomerular filtration rate (eGFR) 60 ± 6 ml/min] during elective diagnostic cardiac catheterizations. In these patients FGF-23 was removed by the kidney, with a fractional extraction (FE) of ∼22%. The FE of FGF-23 across the kidney was similar to that of creatinine (∼17%, P = NS). In addition, the FGF-23 FE by the kidney was significantly directly related to eGFR (r = 0.709 P = 0.018) and to kidney creatinine FE (r = 0.736 P = 0.013) but only as a trend to plasma phosphate levels (r = 0.55, P = 0.18). There was no difference in FGF-23 levels in blood perfusing splanchnic organs and cardiopulmonary bed. However, the arterial-venous difference of FGF-23 across the lung was directly related to FGF-23 pulmonary artery levels, suggesting that the lung, and possibly the heart, participate in the homeostasis of plasma FGF-23 when its systemic levels are increased. Our data show that the human kidney is the only site for FGF-23 removal from blood and suggest that FGF-23 is predominantly removed by glomerular filtration. The kidney ability to remove FGF-23 from the circulation likely accounts for the early increase in blood of FGF-23 in patients with CKD.

Pathogenesis of Portal Hypertension: Extrahepatic Mechanisms

Chronic liver diseases, including hepatic cirrhosis, chronic hepatitis, alcoholic liver disease, and hepatocellular carcinoma, are one of the commonest causes of death and liver transplantation in adults worldwide. They are accompanied by profound disturbances that are not limited to the intrahepatic circulation, but involve also the splanchnic and systemic vascular beds. These hemodynamic disturbances are responsible for the development of portal hypertension, the most frequent and severe of cirrhosis. This syndrome is characterized by a pathological increase of blood pressure in the portal vein and concomitant increases in splanchnic blood flow and portosystemic collateral vessel formation. Increased blood flow in splanchnic organs draining into the portal vein augments in turn the portal venous inflow. Such increased portal venous inflow perpetuates and exacerbates portal pressure elevation and determines the formation of ascites during chronic liver disease. In addition, portosystemic collateral vessels include the gastroesophageal varices, which are particularly prone to rupture causing massive gastroesophageal bleeding. Collateral vessels are also responsible for other major consequences of chronic liver disease, including portosystemic encephalopathy and sepsis. Extrahepatic mechanisms are clearly of major importance for disease progression and aggravation of the portal hypertensive syndrome. Accordingly, most of the therapies currently used in portal hypertension do not act inside the liver but they actually target the increased splanchnic blood flow. This paper reviews the consequences of the splanchnic circulatory abnormalities in portal hypertension and the complex signals capable of increasing vasodilatation, hyporesponsiveness to vasoconstrictors and angiogenesis in the splanchnic vascular bed and the portosystemic collateral circulation in this pathological setting.

Review of splanchnic oximetry in clinical medicine.

Global tissue perfusion and oxygenation are important indicators of physiologic function in humans. The monitoring of splanchnic oximetry through the use of near-infrared spectroscopy (NIRS) is an emerging method used to assess tissue oxygenation status. Splanchnic tissue oxygenation (SrSO2) is thought to be potentially of high value in critically ill patients because gastrointestinal organs can often be the first to suffer ischemic injury. During conditions of hypovolemia, cardiac dysfunction, or decreased oxygen-carrying capacity, blood flow is diverted toward vital organs, such as the brain and the heart at the expense of the splanchnic circulation. While monitoring SrSO2 has great potential benefit, there are limitations to the technology and techniques. SrSO2 has been found to have a relatively high degree of variability that can potentially make it difficult to interpret. In addition, because splanchnic organs only lie near the skin surface in children and infants, and energy from currently available sensors only penetrates a few centimeters deep, it can be difficult to use clinically in a noninvasive manner in adults. Research thus far is showing that splanchnic oximetry holds great promise in the ability to monitor patient oxygenation status and detect disease states in humans, especially in pediatric populations.