Splanchnic Oxygen Consumption Research Articles

Metabolic syndrome and the hepatorenal reflex.

Insufficient hepatic O2 in animal and human studies has been shown to elicit a hepatorenal reflex in response to increased hepatic adenosine, resulting in the stimulation of renal as well as muscle sympathetic nerve activity and activating the renin angiotensin system. Low hepatic ATP, hyperuricemia, and hepatic lipid accumulation reported in metabolic syndrome (MetS) patients may reflect insufficient hepatic O2 delivery, potentially accounting for the sympathetic overdrive associated with MetS. This theoretical concept is supported by experimental results in animals fed a high fructose diet to induce MetS. Hepatic fructose metabolism rapidly consumes ATP resulting in increased adenosine production and hyperuricemia as well as elevated renin release and sympathetic activity. This review makes the case for the hepatorenal reflex causing sympathetic overdrive and metabolic syndrome in response to exaggerated splanchnic oxygen consumption from excessive eating. This is strongly reinforced by the fact that MetS is cured in a matter of days in a significant percentage of patients by diet, bariatric surgery, or endoluminal sleeve, all of which would decrease splanchnic oxygen demand by limiting nutrient contact with the mucosa and reducing the nutrient load due to loss of appetite or dietary restriction.

Metabolic syndrome and the hepatorenal reflex.

Insufficient hepatic O2 in animal and human studies has been shown to elicit a hepatorenal reflex in response to increased hepatic adenosine, resulting in stimulation of renal as well as muscle sympathetic nerve activity and activating the renin angiotensin system. Low hepatic ATP, hyperuricemia, and hepatic lipid accumulation reported in metabolic syndrome (MetS) patients may reflect insufficient hepatic O2 delivery, potentially accounting for the sympathetic overdrive associated with MetS. This theoretical concept is supported by experimental results in animals fed a high fructose diet to induce MetS. Hepatic fructose metabolism rapidly consumes ATP resulting in increased adenosine production and hyperuricemia as well as elevated renin release and sympathetic activity. This review makes the case for the hepatorenal reflex causing sympathetic overdrive and metabolic syndrome in response to exaggerated splanchnic oxygen consumption from excessive eating. This is strongly reinforced by the fact that MetS is cured in a matter of days in a significant percentage of patients by diet, bariatric surgery, or endoluminal sleeve, all of which would decrease splanchnic oxygen demand by limiting nutrient contact with the mucosa and reducing the nutrient load due to the loss of appetite or dietary restriction.

Acquired Liver Injury in the Intensive Care Unit

HE liver plays a key role in the synthesis of proteins, metabolism of toxins and drugs, and in modulation of immunity. In critically ill patients, hypoxic, toxic, and inflammatory insults can affect hepatic excretory, synthetic, and/or purification functions, leading to systemic complications such as coagulopathy, increased risk of infection, hypoglycemia, and acute kidney injury. In severe cases, hepatic encephalopathyorbraindysfunction(acuteliverfailure)may occur. Because of the lack of specificity of standard laboratory investigations, identifying liver injury or dysfunction in critically ill patients remains a significant challenge. In addition, the great heterogeneity of criteria used to define the consequences of liver insults increases the difficulties for the clinician to properly interpret hepatic biochemical abnormalities. In this review, we choose to defineliver injuryas an elevation in serum concentrations of routinely measured hepatic enzymes, including aminotransferases (aspartate aminotransferase [AST]; alanine aminotransferase, [ALT]), alkaline phosphatase (ALP), or!-glutamyl transpeptidase. Hepatic dysfunctionrefers to derangement of pathways related to synthetic or clearance function, including international normalized ratio (INR) and bilirubin.Hepatotoxicity refers to hepatic injury and dysfunction caused by a drug or another noninfectious agent. 1 Acute liver failuredesignates

Effects of Chronic Metabolic Acidosis on Splanchnic Protein Turnover and Oxygen Consumption in Human Beings

Although metabolic acidosis stimulates protein catabolism, its effects on splanchnic protein turnover and energy expenditure have not been measured in human beings. We investigated the effects of chronic metabolic acidosis (CMA) on splanchnic protein dynamics and oxygen consumption in human beings by using a leucine tracer and mass-balance techniques. Five subjects were studied after 6 days of HCl-, CaCl(2)-, and NH(4)Cl-induced acidosis; 8 subjects served as controls. Blood samples were collected from the radial artery and the hepatic veins. Measurements were performed on plasma and whole-blood samples. Based on plasma measurements, subjects who had undergone CMA had lower rates of splanchnic proteolysis (-35%) and protein synthesis (-50%; P < .05) than controls, as well as a negative leucine kinetic balance (-6.81 +/- 2.48 micromol/kg/min/1.73 m(2) body surface [BS](-1)), compared with the neutral balance in control plasma samples (0.76 +/- 2.11 micromol/kg/min/1.73; P < .05 between groups). Based on measurements from whole blood, splanchnic proteolysis and protein synthesis did not differ significantly between CMA and control samples, and the net leucine kinetic balance was neutral in both groups (CMA, -0.69 +/- 1.57; controls, -0.74 +/- 3.45 micromol/kg/min/1.73). In CMA whole-blood measurements, splanchnic oxygen consumption (44.8 +/- 4.3 mL/min/1.73 m(2) BS) was slightly lower than in controls (57.5 +/- 8.4 mL/min/1.73 m(2) BS; P = NS). Splanchnic protein synthesis correlated with oxygen consumption (r = 0.82; P < .001). CMA reduces splanchnic protein turnover and results in a negative leucine balance--an effect that apparently is offset by the contribution of blood cells to organ leucine (and protein) dynamics. Protein synthesis is a major contributor (about 67%) to energy expenditure in splanchnic organs.

Splanchnic blood flow and oxygen consumption: effects of enteral nutrition and dopexamine in the elderly cardiac surgery patient

Splanchnic blood flow and oxygen consumption: effects of enteral nutrition and dopexamine in the elderly cardiac surgery patient

Splanchnic blood flow and oxygen consumption: effects of enteral nutrition and dopexamine in the elderly cardiac surgery patient

After cardiac surgery, patients are at risk of organ dysfunction because of decreased perfusion. Different measures have been used to increase the splanchnic blood flow. We compared the effects of enteral nutrition and dopexamine on the cardiac output, splanchnic blood flow and oxygen consumption. Sixteen patients undergoing cardiac surgery were included. Indocyanine green extraction and thermodilution were used for repeated measurements of the splanchnic blood flow and cardiac output. On the first post-operative day, indocyanine green infusion was started. Patients were randomized to start with dopexamine (Dpx group) or enteral nutrition (EN group). After 180 min, both groups received a combination of dopexamine and enteral nutrition. Blood gases from the hepatic vein and pulmonary and radial arteries were analysed repeatedly. In the Dpx group, the cardiac index increased with dopexamine infusion, but not when enteral nutrition was added. In the EN group, enteral nutrition alone did not increase the cardiac index, but dopexamine addition increased the cardiac index in this group. The splanchnic blood flow increased initially in the Dpx group, but then returned to baseline and remained constant on addition of enteral nutrition. In the EN group, the splanchnic blood flow initially remained at baseline, but increased after dopexamine addition. There was no difference between the groups with regard to systemic or splanchnic oxygen consumption or the oxygen extraction ratio. In the Dpx group, lactate increased from baseline with no further increase on addition of enteral nutrition. Lactate was unchanged in the EN group. Dopexamine and enteral nutrition caused no adverse effects on oxygen consumption or the oxygen extraction ratio. Enteral nutrition did not increase the splanchnic blood flow or cardiac index. Dopexamine increased the systemic blood flow with only a transient effect on the splanchnic blood flow. Dopexamine increased the lactate concentration, possibly indicating a more ischaemic condition.

Splanchnic Oxygen Consumption Is Impaired during Severe Acute Normovolemic Anemia in Anesthetized Humans

Splanchnic Oxygen Consumption Is Impaired during Severe Acute Normovolemic Anemia in Anesthetized Humans

Splanchnic Oxygen Consumption Is Impaired during Severe Acute Normovolemic Anemia in Anesthetized Humans

In conscious humans, reduction in hemoglobin concentration to 5 g/dl did not produce inadequate systemic oxygenation. However, systemic measures of inadequate oxygenation may not be sufficiently sensitive to detect inadequate oxygenation in individual organs such as splanchnic organs. The authors tested the hypothesis that acute normovolemic anemia to hemoglobin less than 6.0 g/dl in anesthetized humans reduces splanchnic oxygen consumption because of diminished whole body oxygen delivery. Elective spine (n = 12) and abdominal (n = 7) surgery patients underwent acute normovolemic anemia to decrease the hemoglobin concentration close to 6.0 g/dl. The authors assessed the development of supply-dependent conditions in systemic and regional vascular beds by two primary measures before and after acute normovolemic anemia: oxygen consumption and surrogate biochemical markers of anaerobic metabolism, including plasma lactate, regional lactate kinetics, and ketone body ratio. When hemoglobin was reduced from 13.6 +/- 1.2 to 5.9 +/- 0.3 g/dl, oxygen supply dependency occurred in the splanchnic and preportal tissues but not at the systemic level. Regional supply dependency was accompanied by biochemical markers of anaerobic metabolism. In anesthetized humans, a reduction in hemoglobin to 5.9 g/dl by acute normovolemic anemia diminished splanchnic and preportal whole body oxygen delivery and impaired splanchnic and preportal oxygen consumption. This was accompanied by increased plasma levels of regional lactate and an increased beta-hydroxybutyrate-to-acetoacetate ratio. These findings suggest that the risk to the gastrointestinal tract during acute normovolemic anemia may be underestimated.

Efeitos iniciais da reposição volêmica com solução salina hipertônica a 7,5% na perfusão e oxigenação esplâncnica após choque hemorrágico

To evaluate the effects of SSH resuscitation on systemic and splanchnic hemodynamic variables in an experimental model of controlled hemorrhagic shock. Ten mongrel dogs were bled (20 ml/min) to a target mean arterial pressure (MAP) of 40+/-5 mmHg. After 30 minutes of shock, animals received SSH infused in 5-minute and they were observed for 60 minutes thereafter. Systemic hemodynamics were evaluated through a Swan-Ganz and arterial catheters while gastrointestinal tract perfusion by a catheter inside the portal vein, an ultrasonic flowprobe around portal vein blood flow (PVBF) and a gastric tonometer. Splanchnic oxygen delivery and consumption, intramucosal pH and veno-arterial, portal-arterial and mucosal-arterial pCO2-gradients (D(ap-a)pCO2, D(vp-a)pCO2 e D(t-a)pCO2, respectively) were assessed. Hemorrhage (29.8+/-2.4 ml/Kg) induced significant decreases in MAP (125+/-6 to 42+/-1 mmHg), in CO (1.9+/-0.2 to 0.6+/-0.1 L/min), and PVBF (504+/-73 to 126+/-12 ml/min) while significant increases were detected in D(ap-a)pCO2 (5.3+/-0.8 to 19.9+/-1.6 mmHg) D(vp-a)pCO2 (5.4+/-1.4 to 22.6+/-2.1 mmHg) and D(t-a)pCO2 (6.1+/-1.1 to 43.8+/-7.5 mmHg). SSH infusion promoted only partial benefits in systemic and splanchnic blood flows. Reduced pCO2 gradients but fewer effects in D(t-a)pCO2 were observed. The SSH infusion promoted partial systemic and splanchnic hemodynamic benefits. Those benefits were especially poor at the splanchnic microcirculation, as evaluated by D(t-a)pCO2. In addition, systemic and regional oxygen-derived variables do not reflect the regional microcirculation disturbances. Gastrointestinal tonometry clearly represents a useful tool for monitoring splanchnic perfusion in patients in hemodynamic shock.

Effect of meal and propranolol on whole body and splanchnic oxygen consumption in patients with cirrhosis

Our aim was to measure whole body energy expenditure after a mixed liquid meal, with and without simultaneous propranolol infusion, in patients with cirrhosis. We also wanted to investigate the effect of propranolol on substrate fluxes and oxygen uptake in the tissues drained by the hepatic vein and azygos vein in the postprandial period in these patients. Whole-body oxygen uptake, hepatic blood flow, hepatic venous pressure gradient and net-hepatic fluxes of oxygen, lactate, glucose, glycerol, and free fatty acids (FFA) were measured in 12 patients with alcoholic cirrhosis before and for 2 h after ingestion of a mixed liquid meal (700 kcal). Half of the patients (n = 6) were randomized to a treatment group receiving intravenous infusion of propranolol in combination with the meal. The meal-induced energy expenditure was significantly lower in patients given propranolol [15.0 +/- 18.9 vs. 67.0 +/- 26.1 kJ/120 min (means +/- SD), P < 0.01]. Meal-induced whole body oxygen uptake was lower in patients receiving propranolol (19.2 +/- 38 vs. 135.7 +/- 61 mmol/120 min, P < 0.01), and the meal-induced increase in splanchnic oxygen uptake was nonexistent when propranolol was administered in combination (-13.2 +/- 34.8 vs. 110.4 +/- 34.8 mmol/120 min, P = 0.04). Postprandially, the propranolol group had a tendency toward a reduced splanchnic glucose output, and the FFA uptake was significantly reduced. Propranolol reduces meal-induced whole body oxygen uptake and energy expenditure as well as splanchnic oxygen uptake. The splanchnic reduction in oxygen consumption can explain almost the entire reduction in whole body oxygen consumption.

Small-Dose Epoprostenol Decreases Systemic Oxygen Consumption and Splanchnic Oxygen Extraction During Normothermic Cardiopulmonary Bypass

Normothermic, nonpulsatile cardiopulmonary bypass (CPB) impairs systemic and splanchnic oxygen transport and increases gastrointestinal permeability. It is an important therapeutic goal to avoid splanchnic dysoxia during CPB. Small-dose prostacyclin therapy improves splanchnic oxygen transport and microcirculation in septic patients. In this study, we sought to determine if during cardiac surgery, the prostacyclin analog epoprostenol improves the balance of systemic and splanchnic oxygen transport. Eighteen patients undergoing cardiac valve replacement were randomized to receive either epoprostenol (3 ng x kg(-1) x min(-1)) or placebo during, and for 1 hour after, surgery. Systemic and splanchnic oxygen delivery, consumption, and extraction and arterial, mixed venous, and hepato-venous lactate concentrations were measured before, during, and after CPB. Gastrointestinal permeability was measured 1 day before and 1 day after surgery using the triple sugar permeability test. During CPB, the epoprostenol group had decreased systemic oxygen consumption and splanchnic oxygen extraction (P = 0.024). These effects were not present 1 hour after the end of epoprostenol infusion. The study was not adequately powered to determine whether epoprostenol altered the trend towards increased lactate metabolism and increased postoperative gastrointestinal permeability, nor could we demonstrate any differences between groups in clinically relevant end-points. In conclusion, these findings suggest that during normothermic CPB, small-dose epoprostenol therapy may reduce systemic oxygen consumption and splanchnic oxygen extraction.

Influence of Enteral and Parenteral Nutrition on Splanchnic Hemodynamics in Septic Patients

Enteral nutrition is believed to augment splanchnic perfusion, thereby preserving splanchnic integrity, whereas parenteral nutrition does not offer this benefit. In an effort to study this, we compared splanchnic oxygen exchange and blood flow in critically ill, septic patients to normal controls during enteral or total parenteral nutrition. Splanchnic oxygen exchange and hepatic blood flow characteristics in 14 critically ill, septic patients were compared to 19 normal controls while fasting and during nutrient administration. Nutrients were delivered as intraduodenal feedings or parenteral nutrition. Splanchnic hemodynamics were measured at baseline, 90 min, and 210 min during nutrient administration. Hepatic blood flow index (HBFI) by indocyanine green dye (ICG) clearance, splanchnic oxygen consumption index (SplVO(2)I), and hepatic venous oxygen saturation (ShvO(2)) were measured using hepatic venous catheterization. Plasma volume (PV) was measured from the volume of ICG distribution. Results were analyzed using population means (+/-SD) and one-way analysis of variance. There was no statistical change in HBFI, SplVO(2)I, PV or ShvO(2) over the study time interval within any group (p < 0.05), irrespective of whether enteral or parenteral nutrition was the nutrient source. Septic patients, whether fasting or receiving nutrition, demonstrated higher HBFI and SplVO(2)I levels, whereas ShvO(2) levels were uniformly lower throughout the study compared to normal controls. Critically ill patients exhibited a hyperdynamic splanchnic state as indicated by the marked increase in HBFI and SplVO(2)I. However, neither nutrient regimen at clinically relevant rates altered splanchnic hemodynamics over the course of study. Thus, enteral nutrients do not appear to offer hemodynamic protection to the splanchnic system in critically ill patients.

Splanchnic oxygen transport, hepatic function and gastrointestinal barrier after normothermic cardiopulmonary bypass.

The effect of non-pulsatile, normothermic cardiopulmonary-bypass (CPB) on the splanchnic blood-flow and oxygen-transport, the hepatic function and the gastrointestinal barrier were observed in a prospective observational study in 31 adults undergoing cardiac valve replacement surgery. The splanchnic (i.e. hepatic) blood-flow (HBF) was measured by the constant infusion of indocyanine-green (ICG) using a hepatic-venous catheter. Liver function was examined by calculation of lactate uptake, ICG extraction and the monoethylglycinexylidide (MEGX) test. A day before and after surgery the gastrioduodenal and intestinal permeability was measured by determination of sucrose and lactulose/mannitol excretion. Splanchnic blood flow and oxygen delivery did not decrease during and after surgery while splanchnic oxygen consumption (P < 0.0125) and arterial lactate concentrations increased. The splanchnic lactate uptake paralleled the lactate concentration. After but not during CPB an increase of systemic oxygen consumption was observed. The MEGX test values decreased on the first day after surgery. The ICG extraction was attenuated during the operation. The gastroduodenal and the intestinal permeability increased significantly postoperatively (P < 0.002, respectively, P < 0.001). There was no correlation between these findings and the duration of CPB. There was a significant correlation of the intestinal permeability but not of the gastroduodenal permeability between the prior and after surgery values (P < 0.001). Increased oxygen consumption during CPB may indicate an inflammatory reaction due to the pump beginning in the splanchnic area or a redistribution of the splanchinc blood flow during the CPB. Normothermic CPB does not lead to a significant or prolonged reduction of liver function. Normothermic CPB causes an increase of gastrointestinal permeability. The intestinal barrier function prior to surgery was accountable for the degree of loss of intestinal barrier function following surgery.

Pneumoperitoneum for laparoscopic cholecystectomy is not associated with compromised splanchnic circulation.

To investigate the influence of increased intra-abdominal pressure during pneumoperitoneum on splanchnic circulation. Open study. University hospital, Sweden. Five otherwise healthy patients (mean age of 34 years), undergoing laparoscopic cholecystectomy. Arterial and hepatic vein catheterization and simultaneous arterial and hepatic vein blood gas sampling in the awake state, during anaesthesia, after the establishment of pneumoperitoneum (intra-abdominal pressure level 11-13 mmHg) and after 30 and 60 minutes of pneumoperitoneum. Hepatic blood flow was estimated by the continuous infusion method and used as a measure of splanchnic blood flow. Splanchnic oxygen consumption was calculated according to the Fick principle. Splanchnic blood flow and splanchnic oxygen consumption were not affected by pneumoperitoneum at this level of intra-abdominal pressure.

The effect of insulin and glucagon on splanchnic oxygen consumption.

The purpose of these experiments was to measure the influence of insulin and glucagon on the splanchnic oxygen consumption. Two experiments were performed. In one experiment, the influence of hyperinsulinaemia was investigated in six healthy subjects, who were studied during a euglycaemic hyperinsulinaemic clamp. In another experiment, the influence of glucagon was investigated in seven healthy subjects, who were studied twice during a pancreatic islet clamp with either supplementation of insulin and glucagon, or of insulin alone. In both situations the measurements were performed during euglycaemia. Splanchnic oxygen consumption and net substrate balances were studied by the arterio-hepatic venous catheterisation technique and measurement of splanchnic blood flow in all experiments. During the euglycaemic hyperinsulinaemic clamp, the splanchnic blood flow increased significantly and the splanchnic oxygen consumption decreased by about 20%, while the net splanchnic glucose output reversed to a net uptake. In the pancreatic islet clamp experiments there was a significant difference between the net splanchnic glucose outputs whether glucagon and insulin or only insulin was supplemented. In spite of this, the splanchnic oxygen consumption decreased by about 20% in both situations, i.e. independent of glucagon supplementation. In both experiments there was a pronounced inhibition of lipolysis, which led to decreased fatty acids availability to the liver. This resulted in a concomitant decrease in hepatic ketone body formation. This decrease could account for about 30% of the decrease in splanchnic oxygen consumption. The reduction in splanchnic oxygen consumption can be explained by decreased ketogenesis, decreased protein synthesis and changes in splanchnic fuel selection, while changes in the rate of gluconeogenesis does not seem to play a significant role.

Effect of prone position on hepato-splanchnic hemodynamics in acute lung injury.

To evaluate the effects of prone position on hepato-splanchnic hemodynamics, metabolism and gut mucosal energy balance. Prospective clinical study. Medical intensive care unit in a university hospital. Eleven hemodynamically stable patients with acute lung injury (ALI) requiring mechanical ventilation. Patients were studied in the supine position, after 90 min in the prone position and after 90 min of supine repositioning. In addition to global hemodynamics we measured intra-abdominal pressure (IAP, bladder), hepato-splanchnic blood flow (HSBF, steady state indocyanine green technique using a hepatic vein catheter) and gastric mucosal-arterial PCO(2) gap (PCO(2) gap, automated air tonometry). Systemic hemodynamics did not change during the whole study. Prone positioning did not significantly affect IAP. HSBF as well as splanchnic oxygen consumption remained unaltered, too. Similarly, neither liver lactate uptake nor indocyanine green extraction were influenced by positional changes. Finally, stable regional hemodynamics were accompanied by an unchanged PCO(2) gap. We conclude that if IAP and systemic hemodynamics remain unaffected, the prone position in ALI patients compromises neither hepato-splanchnic perfusion nor gastric mucosal energy balance.

Update on Vasopressors and Inotropes in Septic Shock

Vasopressors and inotropes are used in septic shock in patients who remain hypotensive despite adequate fluid resuscitation. The goal is to increase blood pressure to optimize perfusion to organs. Generally, goal-directed therapy to supra-normal oxygen transport variables cannot be recommended due to lack of benefit. Traditionally, vasopressors and inotropes in septic shock have been started in a step-wise fashion starting with dopamine. Recent data suggest that there may be true differences among vasopressors and inotropes on local tissue perfusion as measured by regional hemodynamic and oxygen transport. When started early in septic shock, norepinephrine decreases mortality, optimizes hemodynamic variables, and improves systemic and regional (eg, renal, gastric mucosal, splanchnic) perfusion. Epinephrine causes a greater increase in cardiac index (CI) and oxygen delivery (DO 2 ) and increases gastric mucosal flow, but increases lactic acid and may not adequately preserve splanchnic circulation owing to its predominant vasoconstrictive alpha (α) effects. Epinephrine may be particularly useful when used earlier in the course of septic shock in young patients and those who do not have any known cardiac abnormalities. Unlike epinephrine, dopamine does not preferentially increase the proportion of CI that preferentially goes to the splanchnic circulation. Dopamine is further limited because it cannot increase CI by more than 35% and is accompanied by tachycardia or tachydysrhythmias. Dopamine, as opposed to norepinephrine, may worsen splanchnic oxygen consumption (VO 2 ) and oxygen extraction ratio (O 2 ER). Low-dose dopamine has not been shown to consistently increase the glomerular filtration rate or prevent renal failure, and, indeed, worsens splanchnic tissue oxygen use. Routine use of concurrently administered dopamine with vasopressors is not recommended. Phenylephrine should be used when a pure vasoconstrictor is desired in patients who may not require or do not tolerate the beta (β) effects of dopamine or norepinephrine with or without dobutamine. Patients with high filling pressure and hypotension may benefit from the combination of phenylephrine and dobutamine. Investigational approaches to vasopressor-refractory hypotension in septic shock include the use of vasopressin and corticosteroids.

The effects of dopamine and epinephrine on hemodynamics and oxygen metabolism in hypoxic anesthetized piglets.

The most appropriate inotropic agent for use in the newborn is uncertain. Dopamine and epinephrine are commonly used, but have unknown effects during hypoxia and pulmonary hypertension; the effects on the splanchnic circulation, in particular, are unclear. The effects on the systemic, pulmonary, hepatic, and mesenteric circulations of infusions of dopamine and epinephrine (adrenaline) were compared in 17 newborn piglets. Three groups [control (n = 5), dopamine (n = 6) and epinephrine (n = 6)] of fentanyl anesthetized newborn piglets were instrumented to measure cardiac index (CI), hepatic arterial and portal venous blood flow, mean systemic arterial pressure (SAP), mean pulmonary arterial pressure (PAP), and arterial, portal and mixed venous oxygen saturations. Systemic, pulmonary, and mesenteric vascular resistance indices [systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI), mesenteric vascular resistance index (MVRI)], and systemic and splanchnic oxygen extraction and consumption were calculated. Alveolar hypoxia was induced, with arterial oxygen saturation being maintained at 55-65%. After 1 h of stabilization during hypoxia, each animal received either dopamine or epinephrine; randomly administered doses of 2, 10, and 32 microg kg-1 min-1 and 0.2, 1.0, and 3.2 microg kg-1 min-1 respectively were infused for 1 h at each dose. Results were compared with the 1 h hypoxia values by two-way analysis of variance. Epinephrine increased CI at all doses, with no significant effects on SAP and SVRI. Although epinephrine increased PAP at 3.2 microg kg-1min-1, it had no effect on PVRI. Dopamine had no effect on CI, SAP, and SVRI, but increased PAP at all doses and PVRI at 32 microg kg-1min-1. The SAP/PAP ratio was decreased with 32 microg kg-1min-1 dopamine, whereas epinephrine did not affect the ratio. In the mesenteric circulation, dopamine at 32 microg kg-1 min-1 increased portal venous flow and total hepatic blood flow and oxygen delivery, and decreased MVRI; epinephrine had no effect on these variables. Epinephrine increased hepatic arterial flow at 0.2 microg kg-1 min-1; dopamine had no effect on hepatic arterial flow at any dose. Despite these hemodynamic changes, there were no differences in systemic or splanchnic oxygen extraction or consumption at any dose of dopamine or epinephrine. Epinephrine is more effective than dopamine at increasing cardiac output during hypoxia in this model. Although epinephrine preserves the SAP/PAP ratio, dopamine shows preferential pulmonary vasoconstriction, which might be detrimental if it also occurs during the management of infants with persistent fetal circulation. Dopamine, but not epinephrine, increases portal flow and total hepatic flow during hypoxia.

Effect of prone position on hepato-splanchnic hemodynamics in acute lung injury

Abstract Objective. To evaluate the effects of prone position on hepato-splanchnic hemodynamics, metabolism and gut mucosal energy balance. Design. Prospective clinical study. Setting. Medical intensive care unit in a university hospital. Patients. Eleven hemodynamically stable patients with acute lung injury (ALI) requiring mechanical ventilation. Intervention. Patients were studied in the supine position, after 90 min in the prone position and after 90 min of supine repositioning. Measurements and results. In addition to global hemodynamics we measured intra-abdominal pressure (IAP, bladder), hepato-splanchnic blood flow (HSBF, steady state indocyanine green technique using a hepatic vein catheter) and gastric mucosal-arterial PCO2 gap (PCO2 gap, automated air tonometry). Systemic hemodynamics did not change during the whole study. Prone positioning did not significantly affect IAP. HSBF as well as splanchnic oxygen consumption remained unaltered, too. Similarly, neither liver lactate uptake nor indocyanine green extraction were influenced by positional changes. Finally, stable regional hemodynamics were accompanied by an unchanged PCO2 gap. Conclusion. We conclude that if IAP and systemic hemodynamics remain unaffected, the prone position in ALI patients compromises neither hepato-splanchnic perfusion nor gastric mucosal energy balance.

Hepatic and splanchnic oxygen consumption during acute hypoxemic hypoxia in anesthetized pigs.

To compare the hepatosplanchnic oxygen consumption (VO2) with the hepatic and splanchnic VO2 and to calculate the critical oxygen delivery (DO2crit) below which VO2 decreases in the hepatic, splanchnic, and hepatosplanchnic regions in a model of hypoxemic hypoxia. Prospective animal study. University research laboratory. Anesthetized and ventilated pigs (n = 7). The right carotid artery was cannulated to measure mean arterial pressure. A pulmonary artery catheter was inserted to measure mean pulmonary arterial pressure and cardiac output. After a midline abdominal incision, two flow probes were positioned around the portal vein and the hepatic artery to measure portal vein blood flow and hepatic artery blood flow. Oxygen and lactate contents in the carotid artery, the portal vein, and the hepatic vein were measured in blood samples obtained from the appropriate catheters. After a 2-hr stabilization period, hemodynamic and biological variables were recorded during acute hypoxemic hypoxia (FIO2 = 0.5, 0.4, 0.3, 0.21, 0.15, 0.10, and 0.07). VO2, DO2, and DO2crit were determined in the hepatic, splanchnic, and hepatosplanchnic regions. The hepatosplanchnic VO2 was 48 +/- 5 mL/min at high FIO2 (40% for the liver and 60% for the splanchnic organs) and decreased below FIO2 of 0.15. Lactate uptake in the whole hepatosplanchnic region remained steady at FIO2 values of 0.5 to 0.15 and then switched to a lactate release at low FIO2. However, the splanchnic region released lactate, whereas lactate was taken up by the liver. DO2crit in the hepatic, splanchnic, and hepatosplanchnic regions was 24 +/- 3, 38 +/- 2, and 49 +/- 4 mL/min, but the systemic DO2crit, below which regional VO2 became oxygen supply dependent, did not differ in the liver, splanchnic, and hepatosplanchnic regions. The variables of oxygenation and lactate flux measured in the hepatosplanchnic region summarize the metabolic changes of various organs that may vary in different ways during hypoxemic hypoxia.