Splanchnic Area Research Articles

Meta-analysis: the significance of screening for JAK2V617F mutation in Budd-Chiari syndrome and portal venous system thrombosis

It is important to evaluate whether screening for JAK2V617F mutation should be routinely performed in patients with Budd-Chiari syndrome (BCS) and portal venous system thrombosis (PVST). However, the prevalence of JAK2V617F mutation in such patients is substantially varied, and its association with development of myeloproliferative disorders (MPD) is deficiently identified. To estimate the prevalence of JAK2V617F mutation and to explore the significance of screening for JAK2V617F mutation in these patients. All observational studies regarding the prevalence of JAK2V617F mutation in patients with BCS and PVST were identified via PubMed and MEDLINE databases. Primary items were the proportions of JAK2V617F mutation and MPD. Twenty-three studies fulfilled the inclusion criteria. Regardless of underlying aetiological factors, the pooled prevalence of JAK2V617F mutation was 37% and 24% in patients with BCS and PVST respectively. After pre-existing MPD was excluded, the pooled prevalence was decreased to 26% and 19%. Heterogeneity among studies was significant for the prevalence of JAK2V617F mutation. Compared with healthy subjects and patients with thrombosis in other sites, the prevalence of JAKV617F mutation was significantly higher in patients with BCS and PVST. The prevalence of MPD was significantly higher in patients with JAK2V617F mutation than those without. JAK2V617F mutation is frequently found in patients with BCS and PVST, but there is a huge variation of prevalence among the included studies. Additionally, it is more specific to thrombosis in splanchnic areas and strongly associated with the development of MPD in these patients. Further studies are needed to evaluate whether the screening test should be widely performed in Asian countries and cirrhotic patients.

Gut-Brain Chemokine Changes in Portal Hypertensive Rats

Hepatic encephalopathy is a syndrome whose physiopathology is poorly understood; therefore, current diagnostic tests are imperfect and modern therapy is nonspecific. Particularly, it has been suggested that inflammation plays an important role in the pathogenesis of portal hypertensive encephalopathy in the rat. We have studied an experimental model of portal hypertension based on a triple partial portal vein ligation in the rat to verify this hypothesis. One month after portal hypertension we assayed in the splanchnic area (liver, small bowel and mesenteric lymph nodes) and in the central nervous system (hippocampus and cerebellum) fractalkine (CX3CL1) and stromal cell-derived factor alpha (SDF1-α) as well as their respective receptors (CX3CR1 and CXCR4) because of their key role in inflammatory processes. The significant increase of fractalkine in mesenteric lymph nodes (P<0.05) and its receptor (CX3CR1) in the small bowel (P<0.05) and hippocampus (P<0.01), associated with the increased expression of SDF1-α in the hippocampus (P<0.01) and the cerebellum (P<0.01) suggest that prehepatic portal hypertension in the rat induces important alterations in the expression of chemokines in the gut-brain axis. The present study revealed that portal hypertension is associated with splanchnic-brain inflammatory alterations mediated by chemokines.

Vasopressor Agents After Experimental Brain Death: Effects of Dopamine and Vasopressin on Vitality of the Small Gut

Background Both congenital and acquired short bowel syndrome frequently leads to the necessity for long-term parenteral nutrition, which in turn may lead to any of several complications or death. Transplantation of the small bowel from brain-dead organ donors has been successfully performed over the last years. However, systemic blood pressure and blood perfusion to the splanchnic area decrease rapidly after brain death, which comprises the vitality of the small bowel. Objective To evaluate the differences between dopamine and low-dose vasopressin on perfusion and vitality of the small bowel after brain death. Methods Fifteen pigs were randomized into 3 groups: vasopressin (n = 6), dopamine (n = 6), or control (n = 3). Brain death was induced via stepwise filling of an epidural balloon. When the hypotensive phase was achieved, vasopressin, maximum dose of 0.04 IU/kg/h, or dopamine, maximum dose of 20 μg/kg/min, was administered for 5 hours with the objective of increasing mean arterial blood pressure by 15 mm Hg. Results Target blood pressure was achieved in the vasopressin group but not the dopamine group. Vasopressin reduced cardiac output, superior mesenteric artery (SMA) blood flow and oxygen delivery, and systemic oxygen delivery and consumption, and increased oxygen extraction. Dopamine increased SMA blood flow, and had no effect on systemic oxygen delivery or consumption. Conclusions Vasopressin reversed hypotension but compromised both the systemic and SMA blood flow. Vasopressin was associated with inadequate oxygen delivery, estimated from decreased oxygen delivery and increased oxygen extraction. These adverse effects were not observed with dopamine.

Is the JAK2 V617F Mutation a Hallmark for Different Forms of Thrombosis?

Background/Aims: The association between venous thrombosis outside the splanchnic area as well arterial thromboembolism and the JAK2 V617F mutation, an important marker for chronic myeloproliferative neoplasms (MPN), is not completely clear. Methods: Four hundred forty-four patients with venous thrombosis of the lower/upper limbs and/or pulmonary embolism and 60 patients with ischemic stroke were screened for the JAK2 V617F mutation, factor V Leiden, and factor II G20210A. Results: The JAK2 V617F mutation was detected in 1.4% of patients with venous thrombosis and in 3.3% of patients with ischemic stroke. Because 6 out of 2,430 control individuals with no medical history of venous thrombosis, stroke, or MPN were positive for the JAK2 V617F mutation, a significant association was observed (OR 5.53, CI 1.77–17.2, p = 0.0053 for venous thrombosis; OR 13.9, CI 2.75–70.5, p = 0.0145 for stroke). Conclusion: We provide evidence of the association between the JAK2 V617F mutation and different forms of thrombosis. This association is comparable with the association between inherited risk factors (factor V Leiden and factor II G20210A) and thrombotic events, but with a much lower prevalence of the mutation. Finally, the JAK2 V617F mutation is not absent from the general population despite being considered somatic and an acquired genetic variation.

Effect of mechanical ventilation on microvascular perfusion in critical care patients

Microvascular perfusion, pivotal for adequate tissue oxygenation is potentially linked to outcome in critical care therapy. Mechanical ventilation (MV) and positive end-expiratory pressure (PEEP) as standard concepts of respiratory management are known to have deleterious effects on regional organ perfusion especially in the splanchnic area. As these effects have been attributed to different physiologic mechanisms, the purpose of this study was to investigate the effect of positive pressure ventilation on extra-abdominal tissue perfusion in non-surgical intensive care patients. Sublingual microcirculation was evaluated in 46 severely ill patients (group 1: n=26 requiring MV and PEEP; group 2: n=20 spontaneous breathing) admitted to the intensive care unit using sidestream darkfield intravitalmicroscopy. According to current guidelines, sublingual vessels were categorized by means of size and flow in semi-quantitative categories determining microvascular flow index (MFI). Total microvascular flow index (TMFI) was calculated for each patient as mean value of flow in all vessel categories. No significant difference was observed between both groups in microvascular flow index in each vessel category and in total microvascular flow index. Patients requiring mechanical ventilation presented with more comorbidities and higher acuity of illness scores resulting in a higher ICU mortality, which however was not accompanied by microcirculatory differences at the time of measurement. Mechanical ventilation and PEEP have no general deleterious effects on microvascular perfusion of the sublingual mucosa. However, further clinical studies are required to investigate potential effects of higher levels of ventilation pressure or PEEP on microvascular perfusion.

The role of ischemia modified albumin in the evaluation of hemodynamic changes in the splanchnic area during laparoscopic cholecystectomy

GIRIS Laparoskopi, karin ici hastaliklarinin tani ve tedavisinde sik kullanilan minimal invaziv bir yontemdir. Klinik olarak oldukca faydasi olmasina ragmen, pnomoperitoneuma bagli bir takim yan etkiler gozlenebilir. Pnomoperitoneum olusturmak icin, cok cabuk absorbe olan karbondioksit gazi kullanilmaktadir. Pnomoperitoneuma bagli yukselen karin ici basinc, karin ici organlarin kan akimina etki yapmaktadir (1-8).

The Association of Hemodilution and Transfusion of Red Blood Cells with Biochemical Markers of Splanchnic and Renal Injury During Cardiopulmonary Bypass

Hemodilution is the main cause of a low hematocrit concentration during cardiopulmonary bypass. This low hematocrit may be insufficient for optimal tissue oxygen delivery and often results in packed cell transfusion. Our objective in this study was to find a relationship between intraoperative hematocrit and allogeneic blood transfusion on release of postoperative injury markers from the kidneys and the splanchnic area. Fifty consecutive patients undergoing coronary artery bypass grafting with cardiopulmonary bypass were included. Systemic tissue hypoxia was assessed by lactate concentrations. Kidney and splanchnic ischemia were assessed by the measurement of N-acetyl-beta-D-glucosaminidase (NAG) and intestinal fatty acid binding protein (IFABP) in urine. Patients were retrospectively placed into groups according to their lowest hematocrit concentration on bypass (<24% or >or=24%). The intraoperative lactate and the postoperative NAG and IFABP concentrations were higher in the low hematocrit group (<24%) than in the high hematocrit group (>or=24%; P < 0.05). Low hematocrit correlated with higher lactate concentrations (R(2) = 0.150, P < 0.01) and with higher NAG concentrations (R(2) = 0.138, P < 0.01) and IFABP concentrations (R(2) = 0.107, P < 0.01) postoperatively. Transfusion of packed cells during cardiopulmonary bypass correlated with higher lactate (R(2) = 0.089, P < 0.05), NAG (R(2) = 0.431, P < 0.01), and IFABP concentrations (R(2) = 0.189, P < 0.01). The results support the concept that hemodilution below an intraoperative hematocrit of 24% and consequently transfusion of red blood cells is related to release of injury markers of the kidneys and splanchnic area.

Blood Redistribution during Exercise in Subjects with Spinal Cord Injury and Controls

During exercise, redistribution of blood takes place to enhance blood flow to exercising muscles. To examine the role of sympathetic control in blood redistribution, we assessed blood flow in inactive regions (leg-splanchnic area) during arm-crank exercise in controls and in subjects with spinal cord injury (SCI) who lack central sympathetic control. SCI with a low lesion (< or = T7; SCI-L) have no leg sympathetic control and SCI with high lesion (> or = T6; SCI-H) lack sympathetic control in the legs and splanchnic area. This enables us to compare inactive regions between subjects with (controls, SCI-L; splanchnic) and without sympathetic innervation (SCI-L: leg, SCI-H: leg-splanchnic). Before and every 5 min during a 25-min arm-crank exercise bout at 50% of the individual maximal capacity, portal vein and femoral artery blood flow were measured. Before exercise, portal vein blood flow was not different among groups. Arm-crank exercise induced a significant decrease in portal vein blood flow in subjects with splanchnic sympathetic control (able-bodied controls + SCI-L; ANOVA, P < 0.05), whereas SCI-H showed no change in portal vein blood flow. Baseline femoral artery blood was significantly lower in SCI compared with able-bodied controls. Exercise increased femoral artery blood flow in subjects with leg sympathetic control (controls; ANOVA, P < 0.05) but not in persons lacking sympathetic control in the leg (SCI). Leg vascular conductance did not change during exercise in both groups. In summary, portal vein blood flow decreases in subjects with sympathetic control of the splanchnic area, whereas exercise-induced changes in femoral artery hemodynamics did not differ between groups. These observations primarily indicate the presence of regional differences regarding the magnitude of exercise-induced blood redistribution in vivo in humans.

The gut does not contribute to systemic ammonia release in humans without portosystemic shunting

The gut is classically seen as the main source of circulating ammonia. However, the contribution of the intestines to systemic ammonia production may be limited by hepatic extraction of portal-derived ammonia. Recent data suggest that the kidney may be more important than the gut for systemic ammonia production. The aim of this study was to quantify the role of the kidney, intestines, and liver in interorgan ammonia trafficking in humans with normal liver function. In addition, we studied changes in interorgan nitrogen metabolism caused by major hepatectomy. From 21 patients undergoing surgery, blood was sampled from the portal, hepatic, and renal veins to assess intestinal, hepatic, and renal ammonia metabolism. In seven cases, blood sampling was repeated after major hepatectomy. At steady state during surgery, intestinal ammonia release was equaled by hepatic ammonia uptake, precluding significant systemic release of intestinal-derived ammonia. In contrast, the kidneys released ammonia to the systemic circulation. Major hepatectomy led to increased concentrations of ammonia and amino acids in the systemic circulation. However, transsplanchnic concentration gradients after major hepatectomy were similar to baseline values, indicating the rapid institution of a new metabolic equilibrium. In conclusion, since hepatic ammonia uptake exactly equals intestinal ammonia release, the splanchnic area, and hence the gut, probably does not contribute significantly to systemic ammonia release. After major hepatectomy, hepatic ammonia clearance is well preserved, probably related to higher circulating ammonia concentrations.

Insufficient flow reduction during LBNP in both splanchnic and lower limb areas is associated with orthostatic intolerance after bedrest

We quantified the impact of a 60-day head-down tilt bed rest (HDBR) with countermeasures on the arterial response to supine lower body negative pressure (LBNP). Twenty-four women [8 control (Con), 8 exercise + LBNP (Ex-LBNP), and 8 nutrition (Nut) subjects] were studied during LBNP (0 to -45 mmHg) before (pre) and on HDBR day 55 (HDBR-55). Left ventricle diastolic volume (LVDV) and mass, flow velocities in the middle cerebral artery (MCA flow) and femoral artery (femoral flow), portal vein cross-sectional area (portal flow), and lower limb resistance (femoral resistance index) were measured. Muscle sympathetic nerve activity (MSNA) was measured in the fibular nerve. Subjects were identified as finishers or nonfinishers of the 10-min post-HDBR tilt test. At HDBR-55, LVDV, mass, and portal flow were decreased from pre-HDBR (P < 0.05) in the Con and Nut groups only. During LBNP at HDBR-55, femoral and portal flow decreased less, whereas leg MSNA increased similarly, compared with pre-HDBR in the Con, Nut, and NF groups; 11 of 13 nonfinishers showed smaller LBNP-induced reductions in both femoral and portal flow (less vasoconstriction), whereas 10 of 11 finishers maintained vasoconstriction in either one or both regions. The relative distribution of blood flow in the cerebral versus portal and femoral beds during LBNP [MCA flow/(femoral + portal flow)] increased or reduced < 15% from pre-HDBR in 10 of 11 finishers but decreased > 15% from pre-HDBR in 11 of 13 nonfinishers. Abnormal vasoconstriction in both the portal and femoral vascular areas was associated with orthostatic intolerance. The vascular deconditioning was partially prevented by Ex-LBNP.

Methionine splanchnic uptake is increased in critically ill children.

During critical illness the splanchnic area is profoundly affected. There is no information on splanchnic uptake of amino acids in vivo, in critically ill children.Hypothesis:Methionine splanchnic uptake in critically ill children will differ from estimates in healthy adults.Methods:We studied 24 critically ill children. Eight infants (age 6±3months; wt 6±1.4 kg), eight children (age 5±2 y; wt 14±3 kg and 8 adolescents (15±1.94 y; wt 63.3±21kg), who received continuous enteral feedings, providing protein and energy intake at full maintenance needs. We conducted a simultaneous, intravenous, primed, constant, 9h tracer infusion of L‐[2H3methyl] methionine at 2.5 μmol.kg −1h1 and enteral infusion of L‐[13C] methionine at 5μmol.kg−1h1.Results:Plasma methionine fluxes obtained with the enteral 13C and the intravenous 2H3 labels were 85±13 and 30±8, 71±5 and 41±15, and 68±7 and 35±7 μmol.kg−1h−1, respectively for infants, children and adolescents. First pass disappearance of methionine tracer, respectively, was 63, 43 and 47%. The rates of intestinal methionine oxidation were 24±10, 18±6 and 23±8 μmol.kg−1h1Conclusions:Methionine splanchnic uptake is higher in critically ill infants when compared to children and adolescents (p&lt;0.05), and higher than values of about 15% reported in healthy adults. NIH DK‐62363, T32 HD‐007445, Ajinomoto 3‐ARP; USDA/ARS 25337387, Sophia Foundation for Scientific Research

Pharmacology, clinical efficacy and safety of terlipressin in esophageal varices bleeding, septic shock and hepatorenal syndrome

Terlipressin, a vasopressin agonist, is a commonly used drug with different indications, particularly in patients with end-stage liver disease. As a V1 receptor agonist, it increases systemic vascular resistance, particularly in the splanchnic area, resulting in a decrease of portal pressure. Besides the approved use for variceal bleeding, terlipressin also has beneficial effects in the treatment of hepatorenal syndrome and norepinephrine-resistant septic shock. In patients with cirrhosis and variceal bleeding, the use of terlipressin reduces the portal vein pressure and decreases the pressure in esophageal varices. This can save lives when skilled endoscopists are not immediately available. Hepatorenal syndrome is associated with vasodilation in the mesenteric circulation with arterial underfilling and consecutive renal vasoconstriction. Restoration of an effective arterial blood volume can be achieved by the combination of terlipressin and volume expansion. In some cases, a success rate of up to 75% is reported. The early use of terlipressin in catecholamine-resistant shock can improve organ perfusion.

Prognostic Factors in Noncirrhotic Patients With Splanchnic Vein Thromboses

Splanchnic vein thrombosis (SVT), not associated with cancer or liver cirrhosis, is a rare event and scanty data are available on its natural history, long-term prognosis, and treatment. In this study 121 SVT patients consecutively seen from January 1998 to December 2005 were included and 95 of them were followed up for a median time of 41 months. Screening for thrombophilic factors was performed in 104 patients. New thrombotic or bleeding episodes were registered and anticoagulant therapy was performed according to preestablished criteria. SVT was an incidental finding in 34 (28.1%) patients; 34 (28.1%) presented with abdominal infarction; 39 (32.2%) had bowel ischemia or acute portal vein thrombosis; 14 (11.6%) had bleeding from portal hypertensive sources. Survival rates at 1, 3, and 7 yr were 95%, 93.3%, and 89.6%, respectively; 87.5% of deaths occurred at onset of SVT as complications of intestinal infarction. Patients with isolated portal vein thromboses had symptoms and intestinal infarction in 16/41 (39%) and 0/41 (0%) of the cases, respectively, whereas superior mesenteric vein thromboses, isolated or not, were associated with symptoms and intestinal infarction in 69/75 (92%) and 34/75 (45%), respectively. During the follow-up 14 (14.7%) suffered from 39 episodes of gastrointestinal bleeding with no deaths. A previous gastrointestinal bleed was associated with new hemorrhagic events during follow-up. New venous thrombotic episodes occurred in 10 of 95 patients (10.5%), of which 73% were in the splanchnic area. Seven out of these 10 patients had a chronic myeloproliferative disease (MPD) and none was on anticoagulation. Anticoagulant therapy was effective to obtain recanalization of acute SVT in 45.4% of patients and preserved patients from recurrent thrombosis when given lifelong.

Management of Uncontrolled Hemorrhagic Shock

Management of Uncontrolled Hemorrhagic Shock

Optimal spacing between transmitting and receiving optical fibres in reflectance pulse oximetry

Splanchnic ischaemia can ultimately lead to cellular hypoxia and necrosis, and may well contribute to the development of multiple organ failures and increased mortality. Therefore, it is of utmost importance to monitor abdominal organ blood oxygen saturation (SpO2). Pulse oximetry has been widely accepted as a reliable method for monitoring oxygen saturation of arterial blood. Animal studies have also shown it to be effective in the monitoring of blood oxygen saturation in the splanchnic region. However, commercially available pulse oximeter probes are not suitable for the continuous assessment of SpO2 in the splanchnic region. Therefore, there is a need for a new sensor technology that will allow the continuous measurement of SpO2 in the splanchnic area pre-operatively, operatively and post-operatively. For this purpose, a new fibre optic sensor and processing system utilising the principle of reflectance pulse oximetry has been developed. The accuracy in the estimation of SpO2 in pulse oximetry depends on the quality and amplitude of the photoplethysmographic (PPG) signal and for this reason an experimental procedure was carried out to examine the effect of the source-detector separation distance on the acquired PPG signals, and to ultimately select an optimal separation for the final design of the fibre-optic probe. PPG signals were obtained from the finger for different separation distances between the emitting and detecting fibres. Good quality PPG signals with large amplitudes and high signal-to-noise ratio were detected in the range of 3mm to 6mm. At separation distances between 1mm and 2mm, PPG signals were erratic with no resemblance to a conventional PPG signal. At separation distances greater than 6mm, the amplitudes of PPG signals were very small and not appropriate for processing. This investigation indicates the suitability of optical fibres as a new pulse oximetry sensor for estimating blood oxygen saturation (SpO2) in the splanchnic region.

Evidence for gut factor in K+ homeostasis

We tested the hypothesis that K(+) intake is sensed by putative K(+) sensors in the splanchnic areas, and renal K(+) handling is regulated by this signal. K(+) was infused for 2 h into overnight-fasted rats via the jugular vein (systemic infusion), hepatic portal vein (intraportal infusion), or stomach (intragastric infusion) (n = 5 each), and plasma K(+) concentration ([K(+)]) and renal K(+) excretion were measured during the 2-h preinfusion, 2-h K(+) infusion, and 3-h washout periods. During systemic K(+) infusion, plasma [K(+)] increased by approximately 1.3 mM (P < 0.05), and, on cessation of the K(+) infusion, plasma [K(+)] fell to the preinfusion level within 1-2 h. Renal K(+) excretion changed in proportion to the changes in plasma [K(+)]. During intraportal or intragastric K(+) infusion, plasma [K(+)] and renal K(+) excretion profiles were similar to those with systemic infusion. The effects of K(+) infusions via the different routes (n = 5 or 6 each) were also studied during simultaneous feeding of overnight-fasted rats with a K(+)-deficient diet. During the meal, intraportal infusion resulted in increases in plasma [K(+)] similar to those with the systemic K(+) infusion, while intragastric K(+) infusion did not significantly increase plasma [K(+)]. Thus, when the intragastric K(+) infusion was combined with a meal, there was marked enhancement of clearance of the K(+) infused, which was associated with an apparent increase in renal efficiency of K(+) excretion. These data suggest that there may be a gut factor that enhances renal efficiency of K(+) excretion during meal (or dietary K(+)) intake.

Increased splanchnic arterial vascular resistance in oldest old patients

The aim of this study was to evaluate possible age-related changes in mesenteric artery and portal venous blood flow dynamics in relation to systemic haemodynamics in order to delineate putative haemodynamic changes relevant for postprandial hypotension in the elderly. Studies were performed over a wide age-range and for the first time in over 85-year-old patients. Superior mesenteric artery (SMA) parameters (diameter, peak systolic velocity, end diastolic velocity, pulsatility index, volume flow) and portal vein (PV) parameters (diameter, portal vein velocity, volume flow) were measured by duplex ultrasound (General Electrics, Vivid 3) in 98 fasting subjects aged from 21 to 96 years. Systemic vascular parameters such as blood pressure, heart rate and cardiac output (echocardiography) were also determined. Excluded were patients with severe heart failure, liver cirrhosis, sepsis and those with mesenteric artery stenosis. Pulsatility index (PI) was positively correlated with age (r=0.33, p=0.015). In patients over 85 years, PI was significantly increased (p=0.002) as compared to younger controls. Cardiac output was negatively correlated with age (r=-0.247, p=0.005). The other haemodynamic parameters did not show age-dependent alterations. The increase of PI in the SMA in patients over 85 years represents an increase of vascular resistance in the splanchnic area, because PI is sensitive to resistance changes of small arterial vessels. The pulsatility index in the splanchnic area seems to rise steeply in oldest old patients, probably as an attempt to compensate diminutions in cardiac output seen in this age group. These findings indicate that the splanchnic vascular bed is already used in the fasting state to guarantee systemic haemodynamics. Vasodilatation of this vascular bed as physiologically seen postprandially may therefore easily induce postprandial hypotension in the oldest old.

Supplementation of soy protein with branched-chain amino acids alters protein metabolism in healthy elderly and even more in patients with chronic obstructive pulmonary disease

Background:It is often suggested that chronic wasting diseases [eg, chronic obstructive pulmonary disease (COPD)] may benefit from branched-chain amino acid (BCAA) administration via improved protein metabolism.Objective:The aim was to examine whether adding BCAAs to a soy protein meal would enhance protein anabolism in COPD patients and in healthy elderly persons.Design:Eight normal-weight COPD patients and 8 healthy control subjects were examined on 2 test days. Simultaneous continuous intravenous infusion of l-[ring-2H5]phenylalanine (Phe) and l-[ring-2H2]tyrosine tracers was done postabsorptively and at 2 h of ingestion of a maltodextrin soy or maltodextrin soy + BCAA protein meal (rate of ingestion: 0.02 g protein·kg body weight−1·20 min−1) in a crossover design. Together with the meal, oral ingestion of 1-[13C]Phe was performed to measure first-pass Phe splanchnic extraction (SPEPhe). The endogenous rate of Phe appearance [reflecting whole-body protein breakdown (WbPB)], whole-body protein synthesis (WbPS), and net WbPS (WbPS − WbPB) were calculated. Arterialized venous blood was sampled for amino acid enrichment and concentration analyses.Results:Soy feeding induced a reduction in WbPB and an increase in WbPS. BCAA supplementation of soy protein resulted in a significantly higher (P< 0.05) increase in WbPS than did soy protein alone in COPD patients but not in the healthy elderly. BCAA supplementation did not significantly alter the change in WbPB or net WbPS. Furthermore, BCAA supplementation decreased (absolute) SPEPhe(P< 0.05) but did not change the percentage Phe hydroxylation in the splanchnic area, which indicates a BCAA-related reduction in splanchnic protein synthesis.Conclusion:BCAA supplementation to soy protein enhances WbPS in patients with COPD and alters interorgan protein metabolism in favor of the peripheral (muscle) compartment in healthy elderly and even more in COPD patients.

Minimal anhepatic technique for living donor liver transplantation using right liver graft

Minimal anhepatic technique for living donor liver transplantation using right liver graft

LYMPHATIC DRAINAGE BETWEEN THORAX AND ABDOMEN: PLEASE TAKE GOOD CARE OF THIS WELL-PERFORMING MACHINERY…

Introduction: Patients with sepsis often receive large amounts of fluids and the presence of capillary leak, trauma or bleeding results in ongoing fluid resuscitation. This increases interstitial and intestinal edema and finally leads to intra-abdominal hypertension (IAH), which in turn impedes lymphatic drainage. Patients with IAH often develop secondary respiratory failure needing mechanical ventilation with high intrathoracic pressure or PEEP that might further alter lymphatic drainage. This review will try to convince the reader of the importance of the lymphatics in septic patients with IAH.Methods: A Medline and PubMed literature search was performed using the terms “abdominal pressure”, “lymphatic drainage” and “ascites formation”. The references from these studies were searched for relevant articles that may have been missed in the primary search. These articles served as the basis for the recommendations below.Results: Induction of sepsis with lesion of the capillary alveolar barrier results in an increased water gradient between the capillaries and the interstitium in the lungs. The drainage flow to the thoracic duct is initially increased in order to protect the lung and maintain the pulmonary interstitium as dry as possible, however this results in increased intrathoracic pressure. Sepsis also increases the permeability of the capillaries in the splanchnic beds. In analogy to the lungs the lymphatic flow in the splanchnic areas increases together with the pressure inside as a physiological response in order to limit the increase in IAP. At a critical IAP level (around 20 cmH2O) the lymph flow starts to decrease and the splanchnic water content progressively increases. The lymph flow from the abdomen to the thorax is progressively decreased resulting in increased splanchnic water content and ascites formation. The presence of mechanical ventilation with high PEEP reduces the lymph drainage further which together with the increase in IAP decreases the lymphatic pressure gradient in the splanchnic regions, with a further increase in water content and IAP triggering a vicious cycle.Conclusion: Although often overlooked the role of lymphatic flow is complex but very important to determine not only the fluid balance in the lung but also in the peripheral organs. Different pathologies and treatments can markedly influence the pathophysiology of the lymphatics with dramatic effects on endorgan function.