Splanchnic Area Research Articles

A case of successful comprehensive treatment of necrotizing enterocolitis in a newborn child

Necrotizing enterocolitis is an inflammatory disease caused by infection and hypoxic–ischemic damage of the intestinal mucosa, which leads to generalization with the development of a systemic inflammatory response. The pathogenetic mechanisms leading to intestinal wall damage are ischemia and pain. Therefore, the use of central neuraxial blocks, which provide the analgesic effect and preganglionic blockade of the sympathetic nervous system, is pathogenetically justified.
 The aim of the work is to acquaint practitioners with the case of successful comprehensive treatment using neuraxial blocks in a newborn with necrotizing enterocolitis.
 Materials and methods. The child was treated at the Department of Anesthesiology and Intensive Care for Newborns of Zaporizhzhia City Pediatric Hospital No. 5. He underwent clinical and biochemical blood tests, microbiological, radiological and ultrasound examinations using hospital equipment.
 Results. A child was operated due to suspected intestinal perforation and pneumoperitoneum. It was found that throughout the small and large intestines had multiple hemorrhages and air bubbles in the subserosa, but no perforation sites were found. Subsequently, the child underwent conservative treatment with antibacterial therapy according to the de-escalation principle, antifungal therapy, intravenous immunoglobulins, total parenteral nutrition. In addition to this standard treatment, the child underwent caudal-epidural blocks twice a day for a week in the postoperative period for effective analgesia, improvement of microcirculation and splanchnic blood flow.
 Conclusions. Surgical intervention performed on a newborn child with the second stage of necrotizing enterocolitis (intestinal pneumatosis), when its perforation could not be excluded, did not significantly affect the course of the disease, so the positive outcome can be considered the result of successful comprehensive intensive care. In our opinion, the decisive factor that influenced the positive treatment outcomes (prevention of perforation and peritonitis) was the effect of neuraxial caudal epidural blocks, which contributed to the improvement of microcirculation in the splanchnic area, elimination of intestinal ischemia and effective anesthesia.

Differential effects of milk proteins on amino acid digestibility, post-prandial nitrogen utilization and intestinal peptide profiles in rats

ObjectiveThe aim of this study was to analyze the protein digestibility and postprandial metabolism in rats of milk protein matrices obtained by different industrial processes. Material and methodsThe study was conducted on Wistar rats that consumed a meal containing different 15N-labeled milk proteins. Four milk matrices were tested: native micellar caseins (C1), caseins low in calcium (C2 low Ca2+), a matrix containing a ratio 63:37 of caseins and whey proteins (CW2) and whey proteins alone (W). Blood and urine were collected during the postprandial period and rats were euthanized 6 h after meal intake to collect digestive contents and organs. ResultsOrocaecal digestibility values of amino acids ranged between 96.0 ± 0.2% and 96.6 ± 0.4% for C1-, C2 low Ca2+- and W-matrices, while this value was significantly lower for CW2 matrix (92.4 ± 0.5%). More dietary nitrogen was sequestered in the splanchnic area (intestinal mucosa and liver) as well as in plasma proteins after ingestion of W matrix, especially compared to the C1- and C2 low Ca2+-matrices. Peptidomic analysis showed that more milk protein-derived peptides were identified in the caecum of rats after the ingestion of the matrices containing caseins compared to W matrix. ConclusionWe found that demineralization of micellar caseins did not modify its digestibility and postprandial metabolism. The low digestibility of the modified casein-to-whey ratio matrix may be ascribed to a lower accessibility of the protein to digestive enzymes due to changes in the protein structure, while the higher nitrogen splanchnic retention after ingestion of whey was probably due to the fast assimilation of its protein content. Finally, our results showed that industrial processes that modify the structure and/or composition of milk proteins influence protein digestion and utilization.

Cardiovascular changes during phototherapy in newborns.

Phototherapy is the most effective non-invasive method of neonatal hyperbilirubinemia treatment. Application of this method can be associated with side effects including changes in the cardiovascular system. During phototherapy, the primary effects in the cardiovascular system include cutaneous vasodilation leading to skin hyperperfusion and subsequent redistribution of blood. The increased blood flow through the skin is associated with increased transepidermal water loss. Further effects include an increase in cerebral blood flow. Redistribution of blood to the cutaneous bed is compensated by hypoperfusion in the splanchnic area (mostly postprandial) and a significant reduction of the renal blood flow. Regarding closure/reopening of the ductus arteriosus, the results suggest that that phototherapy does not affect ductal patency. During phototherapy the cardiac output can be slightly reduced due to a decreased stroke volume, especially in preterm newborns. Systemic blood pressure is decreased and heart rate is elevated in both preterm and term newborns during phototherapy. The heart rate variability is slightly reduced. Symbolic dynamics analysis of the short-term HRV showed that during phototherapy the activity of the ANS regulating the heart rate is shifted towards the dominancy of the sympathetic activity. The responses in the cardiovascular system of premature/mature newborns without other pathology confirm a well physiologically functioning control of this system, even under specific conditions of phototherapy.

Acute-phase protein synthesis: a key feature of innate immune functions of the liver.

The expression of acute-phase proteins (APP's) maintains homeostasis and tissue repair, but also represents a central component of the organism's defense strategy, especially in the context of innate immunity. Accordingly, an inflammatory response is accompanied by significant changes in the serum protein composition, an aspect that is also used diagnostically. As the main site of APP synthesis the liver is constantly exposed to antigens or pathogens via blood flow, but also to systemic inflammatory signals originating either from the splanchnic area or from the circulation. Under both homeostatic and acute-phase response (APR) conditions the composition of APP's is determined by the pattern of regulatory mediators derived from the systemic circulation or from local cell populations, especially liver macrophages. The key regulators mentioned here most frequently are IL-1β, IL-6 and TNF-α. In addition to a variety of molecular mediators described mainly on the basis of in vitro studies, recent data emphasize the in vivo relevance of cellular key effectors as well as molecular key mediators and protein modifications for the regulation and function of APP's. These are aspects, on which the present review is primarily focused.

Danger of bacterial translocation for a surgical patient.

Intestinal barrier disorder manifestation occurs in connection with surgery in conditions of shock ischemia-reperfusion of the intestine or deterioration of an already damaged barrier due to chronic disease. The result is infectious complications caused by the transport of pathogens through the venous blood, most often postoperative pneumonia and sepsis. However, amore frequent manifestation is the intensification of the postoperative systemic inflammatory response through the lymphatic transport of toxic substances, inanimate antigens and cytokines through the lymphatic system of the splanchnic area (gut-lymph axis). The problem can affect up to half of patients with abdominal surgery. Preventive measures consist of strengthening the intestinal barrier before surgery and alleviating the loss of the intestinal barrier in the perioperative period. In the treatment of infectious complications, an early recognition indication for the therapeutic administration of antibiotics based on preoperative microbial screening of patients at risk may help.

Somatostatin Infusion Inhibits Stellate Cell Activation and Collagen Deposition in the Acute Phase of “Small-for-Size” Liver Regeneration

Purpose: The development of “small-for-size” syndrome (SFSS) after extended hepatectomies is associated with dreadful consequences for the patient. Excessive portal pressure and flow in the remnant liver may cause severe endothelial injury and impairs the normal process of liver regeneration leading to postoperative liver insufficiency. Somatostatin has been described as a protective pharmacological agent to prevent this syndrome when a partial graft is transplanted for its hemodynamic effects in the splanchnic area.

Intestinal, Hepatic, Muscle, and Renal Xenometabolite Release and Uptake in Healthy Conscious Pigs

Abstract Objectives To characterize the intestinal, hepatic, muscle, and renal release and uptake of xenometabolites (non-host derived metabolites) and endogenously modified xenometabolites by measuring their across-organ net release and uptake in a post-absorptive conscious pig model. Methods Twelve 2–3 months old female pigs (25.6 ± 2.2 kg) had surgically-implanted catheters across portal drained viscera (PDV), splanchnic area (SPL), liver, kidney, and hindquarter muscle. Ten days after catheter implantation, overnight fasted arterial and venous plasma was collected in a conscious state and stored at -80°C. Thawed samples were analyzed by liquid chromatography-mass spectrometry. Xenometabolites were identified by retention time and MS2 spectra from in-house authentic standards and expressed as peak areas. Plasma flow measurements determined with para-aminohippuric acid dilution technology. Net organ balance rate (peak area/kg body weight/min) was calculated. Significant (P < 0.05) release or uptake was determined if tissue net balance differed from zero, using the Wilcoxon Signed Rank Test. Results Forty-eight xenometabolites were structurally identified in this model. Of these, 31 had at least one tissue with a significant net release or uptake. Metabolites suggestive of intestinal origin (i.e., significant PDV net release) included 2-hydroxybenzoic acid, 4-hydroxyphenyllactic acid, acetic acid, atrolactic acid, dodecanedioic acid, hydroxycinnamic acid, p-cresol sulfate, p-cresol glucuronide, stercobilin, and several bile acids and indole derivatives. Of these, atrolactic acid, hydrocinnamic acid, indole-3-acetic acid, stercobilin, and all of the bile acids were taken up by the liver; p-cresol glucuronide was taken up by the kidneys. No xenometabolite released from the gut was taken up by muscle, but 4-hydroxyphenyllactic acid, dodecanedioic acid, and indole-3-carboxaldehyde were also released by muscle tissue. Conclusions Our study confirm gastrointestinal origins for a number of known xenometabolites. Liver and kidney are key organs for xenometabolite uptake. Other putative xenometabolites appear to have either non-gut origins or released by other tissues. Funding Sources Funding provided by the US Department of Agriculture-Agricultural Research Service.

Splanchnic and systemic circulation cross talks: Implications for hemodynamic management of liver transplant recipients.

The interaction between splanchnic and systemic circulation has many hemodynamic and renal consequences during liver transplant. In a patient with liver cirrhosis, splanchnic vasodilatation causes arterial steal from the systemic circulation into the splanchnic bed, which decreases the effective blood volume. Moreover, rapid volume loading in these patients has less impact on the cardiac output because a higher proportion of infused fluid is shifted to the splanchnic area. Thus, in dissection phase, the traditional approach of volume loading to maintain intraoperative hemodynamic stability not only seems ineffective, but it may also aggravate surgical bleeding. Two approaches of volume therapy have been mentioned to maintain hemodynamic stability during liver transplantation: splanchnic volume reduction by volume restriction with or without phlebotomy to maintain low central venous pressure (CVP), and splanchnic decongestion using splanchnic vasoconstrictors. After reperfusion, an increase in the central blood volume was thought to have a deleterious effect on the new graft function; however, the precise central venous pressure value that causes hepatic congestion after reperfusion is unknown.

Effect of dexmedetomidine on ischemia-reperfusion injury of liver and kidney tissues in experimental diabetes and hepatic ischemia-reperfusion injury induced rats

Background: Reperfusion following ischemia can lead to more injuries than ischemia itself especially in diabetic patients. The aim of this study was to evaluate the effect of dexmedetomidine on ischemia-reperfusion injury (IRI) in rats with have hepatic IRI and diabetes mellitus.

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.

Profound Changes in Net Energy and Nitrogen Metabolites Fluxes within the Splanchnic Area during Overfeeding of Yucatan Mini Pigs That Remain Euglycemic.

A dysregulation of nutrient exchange between tissues (gut, liver, muscles, adipose) occurs during overnutrition and could induce obesity and metabolic diseases. We aimed to evaluate how, in overfed mini pigs, nutrients use and partition were regulated in the gut and liver. Net nutrients fluxes were assessed in the fed (PP) and post absorptive (PA) states at 1, 14 and 60 days of adaptation to overfeeding in five adult Yucatan female multicatheterized minipigs. Pigs PA glycaemia and PP-induced hyperglycemia remained unchanged over the experimental period, suggesting that the management of the excess of energy intake allowed the maintenance of glucose levels. This was associated with (1) an increased PA plasma insulin, (2) an increased gut lactate production (increased lactate net release +89%, 1 h PP, D1 vs. D60) probably from an increased glucose oxidation, (3) a shift in utilization of gluconeogenic precursor (lactate, propionate) in the liver, and (4) a reduced gut utilization of nitrogen moieties for energy purposes (glutamine), a nitrogen sparing effect at the whole body level (decreased plasma urea in PA (−24% D1 vs. D60) and PP states) and a specific increased level of AA involved in lipids handling and bile recycling in the gut lumen (taurine and glycine).

Impact of 3-week citrulline supplementation on postprandial protein metabolism in malnourished older patients: The Ciproage randomized controlled trial

Citrulline (CIT), is not extracted by the splanchnic area, can stimulate muscle protein synthesis and could potentially find clinical applications in conditions involving low amino acid (AA) intake, such as in malnourished older subjects. Our purpose was to research the effects of CIT supplementation on protein metabolism in particular on non-oxidative leucine disposal (NOLD, primary endpoint), and splanchnic extraction of amino acids in malnourished older patients. This prospective randomized multicenter study determined whole-body and liver protein synthesis, splanchnic protein metabolism and appendicular skeletal muscle mass (ASMM) in 24 malnourished older patients [80-92 years; 18 women and 6 men] in inpatient rehabilitation units. All received an oral dose of 10g of CIT or an equimolar mixture of six non-essential amino acids (NEAAs), as isonitrogenous placebo, for 3 weeks. NOLD and albumin fractional synthesis rates were not different between the NEAA and CIT groups. Splanchnic extraction of dietary amino acid tended to decrease (p=0.09) in the CIT group (45.2%) compared with the NEAA group (60.3%). Total differences in AA and NEAA area under the curves between fed-state and postabsorptive-state were significantly higher in the CIT than in the NEAA group. There were no significant differences for body mass index, fat mass (FM), lean mass (LM) or ASMM in the whole population except for a tendential decrease in FM for the citrulline group (p=0.089). Compared with Day 1, lean mass and ASMM significantly increased (respectively p=0.016 and p=0.018) at Day 20 in CIT-treated women (mean respective increase of 1.7kg and 1.1kg), and fat mass significantly decreased (p=0.001) at Day 20 in CIT-group women (mean decrease of 1.3kg). Our results demonstrate that CIT supplementation has no effect on whole-body protein synthesis or liver protein synthesis in malnourished older subjects. However, CIT supplementation was associated with a higher systemic AA availability. In the subgroup of women, CIT supplementation increased LM and ASMM, and decreased FM.

The contribution of muscle, kidney, and splanchnic tissues to leucine transamination in humans.

The first steps of leucine utilization are reversible deamination to α-ketoisocaproic acid (α-KIC) and irreversible oxidation. Recently, the regulatory role of leucine deamination over oxidation was underlined in rodents. Our aim was to measure leucine deamination and reamination in the whole body, in respect to previously determined rates across individual organs, in humans. By leucine and KIC isotope kinetics, we determined whole-body leucine deamination and reamination, and we compared these rates with those already reported across the sampled organs. As an in vivo counterpart of the "metabolon" concept, we analysed ratios between oxidation and either deamination or reamination. Leucine deamination to KIC was greater than KIC reamination to leucine in the whole body (p = 0.005), muscles (p = 0.005), and the splanchnic area (p = 0.025). These rates were not significantly different in the kidneys. Muscle accounted for ≈60% and ≈78%, the splanchnic bed for ≈15% and ≈15%, and the kidney for ≈12% and ≈18%, of whole-body leucine deamination and reamination rates, respectively. In the kidney, percent leucine oxidation over either deamination or reamination was >3-fold greater than muscle and the splanchnic bed. Skeletal muscle contributes by the largest fraction of leucine deamination, reamination, and oxidation. However, in relative terms, the kidney plays a key role in leucine oxidation.

The portal‐drained viscera release fibroblast growth factor 19 in humans

Fibroblast growth factor 19 (FGF19) is an ileum‐derived endrocrine factor that is produced in response to transepithelial bile salt flux. FGF19 represses bile salt synthesis in the liver. Despite the general assumption that FGF19 signals to the liver via portal blood, no human data are available to support this notion. The aim was to study portal FGF19 levels, and determined bile salt and FGF19 fluxes across visceral organs in humans. Bile salt and FGF19 levels were assessed in arterial, portal, and hepatic venous blood collected from fasted patients who underwent partial liver resection for colorectal liver metastases (n = 30). Fluxes across the portal‐drained viscera (PDV), liver, and splanchnic area were calculated. Portal bile salt levels (7.8 [5.0–12.4] μmol/L) were higher than levels in arterial (2.7 [1.7–5.5] μmol/L, P < 0.0001) and hepatic venous blood (3.4 [2.5–6.5] μmol/L, P < 0.0001). Bile salts released by the PDV (+1.2 [+0.7–+2.0] mmol kg−1 h−1, P < 0.0001) were largely taken up by the liver (−1.0 [−1.8 to −0.4] mmol kg−1 h−1, P < 0.0001). Portal levels of FGF19 (161 ± 78 pg/mL) were higher than arterial levels (135 ± 65 pg/mL, P = 0.046). A net release of FGF19 by the PDV (+4.0 [+2.1 to +9.9] ng kg−1 h−1, P < 0.0001) was calculated. There was no significant flux of FGF19 across the liver (−0.2 [−3.7 to +7.4] ng kg−1 h−1, P = 0.93). In conclusion, FGF19 levels in human portal blood are higher than in arterial blood. FGF19 is released by the portal‐drained viscera under fasted steady state conditions.

Regulation of Growth Hormone by the Splanchnic Area.

The regulation of growth hormone (GH) was traditionally thought to be under the control of two main hypothalamic neuropeptides; GH-releasing hormone and somatostatin. In 1999, with the isolation of ghrelin, as a gastric-derived peptide with potent GH-releasing activity, concept of regulation of the somatotropic axis completely changed. In addition to its GH-releasing activity, ghrelin exhibited the capacity to modulate food intake and body weight. The role of this splanchnic factor in regulating GH as a nexus of energy balance control and GH are explored in this chapter. From a physiological standpoint, a novel mechanism of GH regulation mediated by ghrelin exists, implicating the peripheral modulation of the cannabinoid receptor.

Characterization of Sarcoptes scabiei cofilin gene and assessment of recombinant cofilin protein as an antigen in indirect-ELISA for diagnosis

BackgroundScabies impairs the health of humans and animals and causes heavy economic losses. Traditional diagnostic methods for scabies are inefficient and ineffective, and so far there is no commercial immunodiagnostic or molecular based test for scabies.MethodsHere, we used recombinant Sarcoptes scabiei cofilin protein as an antigen to establish indirect ELISA. S. scabiei cofilin is highly homologous to Dermatophagoides farinae Der f 31 allergen (90 % identity). The S. scabiei cofilin gene was cloned and expressed in Escherichia coli to obtain recombinant protein. Western blotting and fluorescence immunohistochemistry were carried out, and we established an indirect ELISA method and detected 33 serum samples from scabies infected rabbits and 30 serum samples from naïve rabbits.ResultsWestern blotting demonstrated that S. scabiei cofilin possessed good immunogenicity and fluorescence immunohistochemistry showed the S. scabiei cofilin is widespread in the splanchnic area of mites. In ELISA, a cut-off value of 0.188 was determined to judge experimental positive and negative serum values. Specificity and sensitivity of the ELISA were 87.9 and 83.33 %, respectively.ConclusionsRecombinant S. scabiei cofilin showed potential value as a diagnostic antigen. The ELISA method established could be used in clinical diagnosis and provide experimental information in minimal or asymptomatic infection.

Complement C5a inhibition improves late hemodynamic and inflammatory changes in a rat model of nonocclusive mesenteric ischemia

Nonocclusive mesenteric ischemia (NOMI) can evolve in a variety of low-flow states. Although the mechanisms leading to NOMI-related intestinal necrosis are largely unknown, circumstantial evidence suggests that excessive vasoconstriction and complement activation both play important roles in this process. Because targeting of the circulatory malfunction of the splanchnic area could be of therapeutic relevance, we set out to investigate the long-term effects of treatment with a complement C5a antagonist in a rat model of partial aortic occlusion (PAO)-induced transient mesenteric hypoperfusion. The mean arterial pressure of the splanchnic area was kept between 30 and 40 mm Hg by 60 minutes of PAO in anesthetized male Sprague-Dawley rats. C5a inhibitor acetyl-peptide-A (AcPepA; 4 mg kg(-1) intravenously) or vehicle administration was initiated at the 45th minute of PAO. After 24 hours, the animals were reanesthetized to record the macrohemodynamics and ileal microcirculation, and plasma and tissue samples were taken for determination of high-mobility group box protein-1 (HMGB-1), endothelin-1, tumor necrosis factor (TNF)-α levels, and small intestinal leukocyte infiltration. Epithelial structural changes were visualized by in vivo confocal laser scanning endomicroscopy. At 24 hours after PAO, mean arterial pressure, heart rate, and cardiac output were significantly greater, the intestinal intramural microcirculation was significantly impaired, and plasma HMGB-1, endothelin-1, TNF-α levels, the degree of epithelial damage and leukocyte infiltration was increased. The AcPepA treatment moderated the hemodynamic and microcirculatory changes, and decreased inflammatory activation and histologic signs of mucosal damage. C5a inhibition ameliorated the potentially harmful local mesenteric hypoperfusion and global long-term inflammatory consequences of PAO. This approach is of promise for use in NOMI-associated situations.

Hepatic Uptake of Rectally Administered Butyrate Prevents an Increase in Systemic Butyrate Concentrations in Humans1–3

Background: Short-chain fatty acids (SCFAs), fermentation products of undigested fibers, are considered beneficial for colonic health. High plasma concentrations are potentially harmful; therefore, information about systemic SCFA clearance is needed before therapeutic use of prebiotics or colonic SCFA administration.Objective: The aim of this study was to investigate the effect of rectal butyrate administration on SCFA interorgan exchangeMethods: Twelve patients (7 men; age: 66.4 ± 2.0 y; BMI 24.5 ± 1.4 kg/m2) undergoing upper abdominal surgery participated in this randomized placebo-controlled trial. During surgery, 1 group received a butyrate enema (100 mmol sodium butyrate/L; 60 mL; n = 7), and the other group a placebo (140 mmol 0.9% NaCl/L; 60 mL; n = 5). Before and 5, 15, and 30 min after administration, blood samples were taken from the radial artery, hepatic vein, and portal vein. Plasma SCFA concentrations were analyzed, and fluxes from portal-drained viscera, liver, and splanchnic area were calculated and used for the calculation of the incremental area under the curve (iAUC) over a 30-min period.Results: Rectal butyrate administration led to higher portal butyrate concentrations at 5 min compared with placebo (92.2 ± 27.0 μmol/L vs. 14.3 ± 3.4 μmol/L, respectively; P < 0.01). In the butyrate-treated group, iAUCs of gut release (282.8 ± 133.8 μmol/kg BW · 0.5 h) and liver uptake (−293.7 ± 136.0 μmol/kg BW · 0.5 h) of butyrate were greater than in the placebo group [−16.6 ± 13.4 μmol/kg BW · 0.5 h (gut release) and 16.0 ± 13.8 μmol/kg BW · 0.5 h (liver uptake); P = 0.01 and P < 0.05, respectively]. As a result, splanchnic butyrate release did not differ between groups.Conclusion: After colonic butyrate administration, splanchnic butyrate release was prevented in patients undergoing upper abdominal surgery. These observations imply that therapeutic colonic SCFA administration at this dose is safe. The trial was registered at clinicaltrials.gov as NCT02271802.

Advances data aboute microcirculatory distress in pediatric sepsis and novel ability of intensive care wiyh L-arginine infusion

Aim. To analyze contemporary sources that contain information on the problems of microcirculation distress in sepsis, including children. The promising directions in intensive care are determined. Develop new approaches to intensive care of microcirculation distress in sepsis for children in light of the scientific data.Methods. To achieve this aim we used scales SOFA, Glasgow, PRISM Murrey. Applied determination of central and organ hemodynamics by Doppler ultrasound were studied ABB parameters of central venous, arterial blood, electrolytes, creatinine, urea, alanine transaminase, lactate, endothelin, serum metabolites of nitric oxide in children with sepsis who received standard care and its modification using infusion of L-arginine.Results. The results of the study gave reason to confirm that disorders of organ blood flow in the pulmonary, splanchnic circulation area are happened in sepsis of children. They are associated with a relative deficiency of nitric oxide and endothelin excess. Add to a goal-oriented therapy of septic conditions infusion of 4.2% solution of arginine helps eliminate pathological vasoconstriction of the renal vessels and the pulmonary circulation, leading to improve the kidney function. Change of hepatic blood flow characterized by a certain tendency to arterial vasodilation.Conclusions. Infusion of 4.2 % solution of arginine in children with sepsis does not cause adverse impact on central hemodynamics, whereas improve perfusion of vital organs. The proposed intensive care contributes significant reduction in mortality compared to the predicted (p&lt;0,001), (95 % CI 0.37-0.03)

Cerebral and somatic NIRS-determined oxygenation in IUGR preterm infants during transition

Background: Fetal growth restriction (intra-uterine growth restriction [IUGR]) has a considerable impact on perinatal morbidity. Preterm IUGR infants are prone to impaired intestine function. Near-infrared spectroscopy (NIRS) has been used to monitor oxygenation status of the brain and of the intestine.Patients and methods: We conducted a prospective case–control study at our NICU in 20 preterm infants of whom 10 infants complicated by compared with 10 non-IUGR preterm infants. Splanchnic and cerebral regional oximetry values were measured with NIRS. Three hours of consecutive recordings were performed in the first 24 h of life, T0, and during the transitional period, T1. The cerebral/splanchnic oxygenation ratio, CSOR, (cerebral regional saturations [rScO2]/splanchnic regional saturations [rSsO2]) was also calculated.Results: Both in the IUGR and the non-IUGR infants, at T0 and T1 monitoring time-points, the rSO2 values were higher in the cerebral district when compared to those of the splanchnic area. Comparison of the NIRS parameters between the IUGR and non-IUGR infants at T0 showed no difference in rScO2, while rSsO2 was significantly lower in the IUGR group. At T1, rScO2 was significantly lower and rSsO2 higher in the IUGR group.Conclusions: Cerebral/splanchnic vascular adaptation of IUGR infants to the extra-uterine environment is characterized by a postnatal persistence of the brain sparing effect with reperfusion in the transitional period.