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PubMed1985

Biological and pathological aspects of the mammalian small intestinal permeability to macromolecules.

The literature on the biology and pathology of mammalian small intestinal permeability to macromolecules is reviewed. In mammals, macromolecules may penetrate the epithelial layer of the small intestinal mucosa, especially in the neonatal period. The neonatal uptake and transport of immunoglobulins is important in the acquisition of passive immunity in the newborn. In the mature small intestine the uptake of macromolecules almost ceases, except in M-cells. Excessive uptake and transport of macromolecules has been demonstrated in several experimental and spontaneous gastrointestinal diseases, in which increased concentration of macromolecules in the small intestinal lumen and/or damage of one or more components of the small intestinal mucosal barrier is present. Finally, methods to study macromolecular permeation of the small intestine are discussed.

Animals↗
PubMed2000

Exclusive breast-feeding: does it have the potential to reduce breast-feeding transmission of HIV-1?

Exclusive breast-feeding is unambiguously the optimal infant feeding practice and is universally promoted in the absence of human immunodeficiency virus (HIV-1). It is associated with reduced morbidity and mortality from diarrheal and respiratory diseases. Recent findings suggest that exclusive breast-feeding may pose less risk of HIV-1 transmission than the more common practice of mixed feeding (i.e., breast-feeding concurrent with the feeding of water, other fluids, and foods), which has important infant feeding policy implications for low-resource settings. This paper reviews the biologic mechanisms associated with exclusive breast-feeding that provide protection against gastrointestinal, respiratory, and atopic diseases, and evaluates the relevance of these mechanisms for HIV-1 transmission. Potential mechanisms include reduction in dietary antigens and enteric pathogens that may maintain integrity of the intestinal mucosal barrier and limit inflammatory responses of the gut mucosa; promotion of beneficial intestinal microflora that may increase resistance to infection and modulate the infant's immune response; alteration in specific antiviral or anti-inflammatory factors in human milk that may modulate maternal hormonal or immunologic status; and maintenance of mammary epithelial integrity that may reduce viral load in breast milk.

Breast Feeding↗
PubMed2001

[Pancreatitis and nutrition. Significance of the gastrointestinal tract and nutrition for septic complications].

Septic complications are an important factor for the morbidity and mortality of acute pancreatitis. The gut has been identified as a source of infection early in the course of the disease allowing intestinal bacteria to translocate into pancreatic necrosis and other organs. Bacterial translocation is promoted by an impaired intestinal mucosal barrier which can be attributed to the reduced oxygen and substrate supply of the intestine during the early systemic response to the pancreatic injury. A rat model of severe acute pancreatitis has been used to confirm the hypothesis that an impaired mucosal barrier can be stabilized by supplying certain nutritients, vitamins and trace elements. Following a discussion of the many aspects of bacterial translocation and gut derived sepsis, the role of the gut and nutrition for the development of septic complications in acute pancreatitis is summarized as follows: Early in the course of acute pancreatitis the gut is a target organ of the primary systemic inflammatory response (SIRS) to pancreatic injury. SIRS-induced gut barrier dysfunction promoting bacterial translocation makes the gut the motor for secondary (septic) complications. As a septic focus the gut becomes a target for therapeutic measures aimed at stabilizing the impaired gut barrier. Nutritive factors demonstrated to improve impaired gut barrier function include early enteral feeding and specific factors like glutamine which are essential for enterocytes and colonocytes in stress. Experimental data are presented to underline the significance of these nutritive factors and subsequent randomized multicenter trials performed to verify the positive experimental results are introduced. The effect of other nutritive factors (e.g. omega-3-fatty acids) has not yet been systemically investigated. Thus, experimental and clinical studies need to be performed for evaluating their effect on bacterial translocation and the disease course in acute pancreatitis.

Animals↗
PubMed2004

[Induction mechanism of shock: applying the etiology in judgment of the cause of death in forensic practice].

In the field of forensic medicine, shock has been identified as a cause of death owing to various kinds of exogenous insults. The etiology and pathogenesis of shock cannot be explained well by the usual gross appearance in medicolegal autopsies, because it is now generally established that the shock is a functional reaction of the vascular system to bodily injury, and that several organs are secondarily impaired during shock. Thus it seemed to forensic pathologists that these morphological changes in several organs after shock did not reveal any significant differences among the causes of death. We approached to the induction mechanism of shock, and we investigated what etiology induced these morphological changes after shock in order to identify shock as the cause of death. It is now generally accepted that the kidney is a target organ of shock, so we mainly investigated the cause of kidney disorder in a case of burn shock and hemorrhagic shock. 1. Consequences of bacterial translocation (BT) in the shock. The concept of BT indicates that the beginning of shock is induced by the loss of gut barrier function and consequent translocation of bacteria. In general, impaired gut barrier function can be caused either during the shock period by decreased intestinal blood flow and reduced oxygen delivery, resulting during reperfusion in a stage of increased intestinal blood flow, or at a later stage again by reduced flow. A variety of physiological stresses, such as trauma, hemorrhage, thermal injury, surgical operation, various kinds of drags and mental stress, have been shown to cause failure of the gut mucosal barrier, with translocation of bacteria/endotoxin from the gastrointestinal into the mesenteric lymph nodes, and translocation into remote organs and systemic circulation. 2. Burn shock. We designed to evaluate the BT in a burn shock rat model (following 20% full-thickness scald injury). The p38 MAPK pathway is an important stress-responsive signal molecule pathway, and it is responsible for the production and signal transduction of cytokines. This pathway is activated by the bacterial LPS or ischemia, so we examined the effects of FR167653, a specific inhibitor of p38 MAPK, on the development of renal failure after the burn-induced intestinal barrier damage. Our study demonstrated that viable bacteria reached the remote organs after burn by quantitative bacterial culture data and FR167653 blocked the burn-induced intestinal barrier damage, and the immunohistochemical data showed that FR167653 prevented the accumulation of polymorphonuclear leukocytes (PMNs) in the glomerular capillaries after burn, and blockaded the burn-induced renal failure by serum UN assay. FR167653 especially decreased the phosphorylation levels of p38 MAPK in the infant kidney after burn, and TNF-alpha and IL-1beta mRNA decreased through the p38 MAPK pathway. The above-mentioned facts do provide additional support for the hypothesis that postburn renal failure is mediated by endotoxin associated with the bacterial translocation, and we identified the pathophysiologic role of p38 MAPK pathway in the development of renal failure after the burn-induced intestinal barrier damage. 3. Hemorrhagic shock. We evaluated the role of endogenous TNF-alpha in the renal failure and gut bacterial translocation induced by mild hemorrhagic shock (16.7% bleeding of total body blood via a common carotid catheter without fluid resuscitation). FR167653, a potent inhibitor of TNF-alpha up regulation through p38 MAPK pathway, significantly inhibited these increases of TNF-alpha. Adding to this, our study demonstrated that FR167653 prevented renal failure, such as the infiltration of inflammatory cells and tubular cell necrosis after hemorrhage, and the intestinal barrier damage was also dramatically improved by FR167653 treatment. These results show that derived endogenous TNF-alpha plays a key role in renal failure through p38 MAPK activation during the early phase of mild hemorrhagic shock, including the possible participation of BT. According to these results, we hypothesized that the invading leukocytes induced these organs failures after hemorrhagic shock, so we examined the appearances of leukocytes by the immunohistochemical myeloperoxidase (MPO) staining (marker staining for PMNs). The incidences of PMNs in these organs after mild hemorrhagic shock increased significantly, and FR157653 prevented the appearance of PMNs. These results showed the possible effective role of the PMNs on the occurrence of organ failure caused by mild hemorrhagic shock. 4. Forensic practice. Six hundred and seven forensic autopsy cases in our department of forensic medicine during the past 11 years between 1992 and 2002 were analyzed with regard to the cause of death. Shock cases accounted for 18% of all forensic autopsy cases, and among them 65% of cases identified hemorrhagic shock as the cause of death. So we investigated what good grounds to clearly identify the cause of death induced by hemorrhagic shock. Our experimental hemorrhagic shock data showed PMNs activation and priming during hemorrhagic shock, and it might be closely related to BT and remote organ failure. Consequently, we used the MPO staining method, and we immunohistochemically investigated several organs of our practical autopsy cases to detect the appearance of PMNs as a marker of shock induction. We compared the hemorrhagic shock with other causes of death, such as blood loss, asphyxia, drawing and head injury (intracranial hemorrhage). In every organ, a significant appearance of PMNs was observed in the hemorrhagic shock compared to the other causes of death. Especially, the appearance of PMNs in the heart was clear than that of the other organs in the hemorrhagic shock cases. Therefore, detecting the appearance of PMNs as a marker of shock induction is a very useful and significant method forjudging the cause of death in forensic practice.

Animals↗
PubMed2003

Ontogeny and prenatal expression of trefoil factor 3/ITF in the human intestine.

BACKGROUND: Trefoil factor 3 (TFF3) or intestinal trefoil factor (ITF), a peptide normally expressed and secreted by goblet cells at the mucosal surface of the small intestine and colon, is important for the maintenance and repair of the intestinal mucosal barrier. AIM: To study the ontogeny and developmental expression of TFF3 in human intestine. SUBJECTS: We examined TFF3 expression in formalin-fixed and paraffin-embedded intestinal tissues from 24 fetuses (gestational age [GA] 12-23 weeks) and 5 adults by immunohistochemical staining. To determine whether TFF3 is excreted into the fetal intestinal tract, first-passed meconium samples were collected from 43 newborn infants (gestational age 24-41 weeks). The presence of TFF3 was examined by Western blot analysis and the relative levels of TFF3 in the meconium were quantified with a slot blot assay. RESULTS: TFF3 can be detected by immunohistochemistry in human intestine as early as 12 weeks gestation. TFF3 is present in the meconium of newborn infants; no significant difference exists in TFF3 levels in the meconium of premature infants with birth weight (BW) less than 1500 g compared to those with birth weight equal to or more than 1500 g. CONCLUSION: Premature infant's susceptibility to intestinal mucosal injury is unlikely to be explained by developmental expression of TFF3 in human intestine since secreted TFF3 is not deficient in premature infants.

Adult↗
PubMed2003

Evidence that nuclear factor-kappa B activation is critical in oxidant-induced disruption of the microtubule cytoskeleton and barrier integrity and that its inactivation is essential in epidermal growth factor-mediated protection of the monolayers of intestinal epithelia.

Using monolayers of intestinal (Caco-2) cells, we showed that oxidants disrupt the microtubule cytoskeleton and barrier integrity; epidermal growth factor (EGF) was protective via stabilization of the microtubules. Because proinflammatory conditions activate nuclear factor-kappaB (NF-kappaB), we hypothesized that oxidants disrupt barrier integrity through activation of NF-kappaB and that EGF protects by suppressing NF-kappaB. Parental cells were pretreated with EGF or NF-kappaB or inhibitory kappaBalpha (I-kappaBalpha) modulators. Other cells were stably transfected with varying levels of a dominant negative mutant for the NF-kappaB inhibitor I-kappaBalpha. Both types of cells were grown as monolayers and then exposed to oxidant (H2O2). We then monitored monolayer barrier integrity (permeability), stability of the microtubule cytoskeleton (confocal microscopy, immunoblotting), intracellular levels of the I-kappaBalpha (immunoblotting), translocation, and activity of NF-kappaB (immunoblotting, sensitive enzyme-linked immunosorbent assay). Monolayers were also fractionated and processed to assess alterations in 1) polymerized tubulin (S2; an index of cytoskeletal integrity) and 2) monomeric tubulin (S1; an index of disassembly) (polyacrylamide gel electrophoresis fractionation and immunoblotting). We found the following: 1) Oxidants caused I-kappaBalpha degradation, NF-kappaB translocation, NF-kappaB (p50 and p65 subunits) activation, tubulin disassembly ( upward arrow S1, downward arrow S2), microtubule architectural instability, and barrier disruption. I-kappaBalpha stabilizers and NF-kappaB inhibitors [e.g., carbobenzyloxy-leuleu-leucinol (MG-132), lactacystin] suppressed oxidants injurious effects. 2) EGF (10 ng/ml) stabilized I-kappaBalpha and prevented both NF-kappaB translocation and activation while protecting monolayers against oxidants. 3) In stably transfected cells, transfection-induced stabilization of I-kappaBalpha by itself led to EGF-like protective effects. In these mutant cells, protection was not potentiated by EGF (10 ng/ml). Conclusions are 1) oxidants induce disruption of the cytoskeleton and intestinal barrier integrity, in part, through I-kappaBalpha degradation and subsequent NF-kappaB activation, 2) I-kappaBalpha stabilization is by itself protective, mimicking EGF, and 3) EGF protects cell monolayers through I-kappaBalpha stabilization and NF-kappaB inactivation. To our knowledge, this is the first report that NF-kappaB can affect the dynamics of cytoskeletal assembly and intestinal barrier integrity.

Biological Transport↗
PubMed1991

A comparison of heterotopic and orthotopic intestinal transplantation in rats.

Two surgical techniques are commonly used for small intestinal transplantation: heterotopic (accessory) intestinal grafting (HIT), where the small bowel is initially defunctioned with restoration of intestinal continuity at a later date, and orthotopic (in continuity) intestinal grafting (OIT), where the small bowel is immediately anastomosed to the native intestine. The present experiments were undertaken to compare the advantages and disadvantages of these two surgical models. Graft barrier function (intestinal permeability), intestinal histology, and graft survival were evaluated after heterotopic and orthotopic intestinal transplantation in the following groups of rats: group 1: isografts, group 2: untreated allografts, group 3: low-dose cyclosporine-treated allografts (subcutaneous CsA 2 mg/kg/day), and group 4: high-dose CsA-treated allografts (subcutaneous CsA 4 mg/kg/day). Intestinal permeability was consistently higher after HIT than OIT in all of the groups (ANOVA; P less than 0.01). Histological evidence of rejection appeared earlier after HIT than OIT (HIT 5th postoperative day (POD); OIT 7th POD; P less than 0.05). The mean survival of untreated allografts was longer after HIT than OIT (HIT 15.7 +/- 6 days, OIT 9.2 +/- 1 days, P less than 0.05). The rats treated with low-dose CsA after OIT lost weight and died of rejection after a mean survival time of 17.7 +/- 2 days, while the rats treated with low-dose CsA after HIT remained well until sacrifice on POD 28 (P less than 0.01). The rats with isografts and rats with allografts treated with high-dose CsA remained well after HIT and OIT until sacrifice on the 28th POD. These data suggest that nutrients and other factors in the succus entericus may improve gut barrier function and delay the onset of rejection after OIT. However, rejection of the orthotopic intestinal graft is usually fatal, while rejection of the heterotopic graft is often surprisingly well tolerated. These factors must be taken into consideration when choosing a surgical technique for intestinal transplantation in humans.

Animals↗
PubMed1984

Identification of amylase isoenzymes in intestinal contents.

Samples of intestinal contents were obtained from 16 patients: 5 from the midjejunum, 10 from the distal ileum, and 1 from the cecum. The presence of pancreatic and nonpancreatic isoamylases in these fluids was evaluated by an inhibitor assay (Pharmacia Corporation) and by polyacrylamide gel electrophoresis. In every sample the inhibitor assay detected the presence of pancreatic-type isoamylase but not salivary-type isoamylase. Electrophoresis confirmed that salivary-type isoamylase was totally absent. Therefore, in intestinal disorders which disrupt the intestinal mucosal barrier (such as ischemia, perforation, ulceration, or obstruction), the amylase which escapes from the intestinal lumen and is reabsorbed into the circulation is likely to consist entirely of pancreatic-type isoamylases. In these circumstances, measurement of serum amylase isoenzymes will not distinguish acute pancreatitis from an acute intraabdominal catastrophe requiring surgery.

Amylases↗
PubMed1997

Effects of epidermal growth factor and Clostridium difficile toxin B in a model of mucosal injury.

Numerous factors have been advocated as being paramount to the development of necrotizing enterocolitis (NEC) including hypoxia, abnormal bacterial flora, and by products of enteral feedings. In an effort to better understand mechanisms involved at the level of the intestinal mucosal barrier the authors have chosen the CACO-2 cell line to model the neonatal intestinal epithelium. By growing CACO-2 cells in transwell inserts, the authors have investigated the ability of Clostridium difficile toxin B, epidermal growth factor (EGF), and a model of mechanical injury to alter transepithelial resistance of CACO-2 monolayers. The findings show that toxin B diminishes resistance in this setting, and EGF can alter that resistance drop.

Analysis of Variance↗
PubMed2003

Adaptive responses of Salmonella enterica serovar Typhimurium DT104 and other S. Typhimurium strains and Escherichia coli O157 to low pH environments.

AIMS: Cattle are a known main reservoir for acid-resistant Escherichia coli O157 and Salmonella enterica serovar Typhimurium DT104. We studied the response of S. Typhimurium DT104 to extreme low pH environments and compared their response to that of acid-resistant E. coli O157 and other S. Typhimurium phage types. METHODS AND RESULTS: Bacteria were grown in nutrient-rich medium and subsequently acid challenged at pH 2.5. We found that stationary phase cultures of various S. Typhimurium strains were able to survive a challenge for 2 h at pH 2.5. As in E. coli, the ability of S. Typhimurium to survive at pH 2.5 was shown to be dependent on the presence of amino acids, specifically arginine. The amount of proton pumping H+/ATPase, both in E. coli O157 and S. Typhimurium strains, was lower when grown at pH values <6 than after growth at pH 7.5. Cyclo fatty acid content of membranes of bacteria grown at pH values <6 was higher than that of membranes of bacteria grown at pH 7.5. CONCLUSIONS: Various S. Typhimurium strains, both DT104 and non-DT104, are able to survive for a prolonged period of time at pH 2.5. Their response to such low pH environment is seemingly similar to that of E. coli O157. SIGNIFICANCE AND IMPACT OF THE STUDY: Food-borne pathogens like S. Typhimurium DT104 and E. coli O157 form a serious threat to public health since such strains are able to survive under extreme low pH conditions as present in the human stomach. The emergence these acid-resistant strains suggests the presence of a selection barrier. The intestinal tract of ruminants fed a carbohydrate-rich diet might be such a barrier.

Adaptation, Physiological↗
PubMed2003

Effect of estradiol administration on splanchnic perfusion after trauma-hemorrhage and sepsis.

PURPOSE OF REVIEW: This review focuses on the latest mechanistic understanding of the effects of estradiol on the splanchnic circulation and the possibility of estradiol treatment as an adjunct for the treatment of trauma-hemorrhage and sepsis. RECENT FINDINGS: Systemic hypotension induced by shock accompanies marked alterations in blood flow to various organs. Decreased splanchnic perfusion is frequently observed after insults, such as severe hemorrhage or sepsis, which leads to the destruction of the intestinal mucosal barrier and hepatic dysfunction. Studies suggest that estradiol acts as a facilitator of the intestinal blood flow via the increased production of nitric oxide, decreased production of vasoconstrictors, attenuated neutrophil adhesion, and decreased formation of oxygen free radicals. SUMMARY: Trauma-hemorrhage results in decreased circulating blood volume. In contrast, sepsis is an inflammatory state mainly mediated by bacterial products. However, these divergent insults show similar pathophysiologic alterations in terms of the splanchnic circulation. Because estradiol effectively protects the organs from circulatory failure after various adverse circulatory conditions, many studies are being performed to clarify the molecular mechanism of estradiol action with regard to tissue circulation. Estradiol improves the macro- and microcirculation of the splanchnic organs by multiple mechanisms. Nonetheless, it remains unclear which mechanism plays the most important role in the treatment of trauma-hemorrhage and sepsis. Additional studies are required to elucidate the precise mechanism of estradiol action and to determine the usefulness of estradiol treatment for severe hemorrhage and sepsis in patients.

Animals↗
PubMed1983

Selected bacterial antibodies in Crohn's disease and ulcerative colitis.

Agglutinins to four strains of anaerobic gram-positive coccoid rods (species of Eubacterium, Peptostreptococcus and Coprococcus) were found in significantly higher frequency in Crohn's disease (CD) than in ulcerative colitis (UC) and in other diseased control subjects and were virtually absent in apparently healthy subjects. When the posterior probability of having CD was calculated on the basis of these agglutination reactions, 64% of patients with CD and 34% of patients with UC but only 10% of diseased controls and none of the healthy controls were regarded as 'probable' or 'definite' cases of CD. However, the posterior probability of CD did not sharply differentiate between CD and UC but indicated chronic inflammatory bowel disease. Factors contributing to the appearance of these agglutinins in CD were also evaluated. The findings would indicate the importance of a damaged intestinal mucosal barrier for the production of these agglutinins, provided the antigens are present in the intestine. No significant differences were observed between the occurrence of antibodies to pseudomonas-like organisms (PLO) in CD and the various control groups. The study could not add further evidence to the hypothesis of a possible aetiopathogenic role of PLO in CD.

Antibodies, Bacterial↗
PubMed1994

The effect of nutrition on gastrointestinal barrier function.

The tightly adherent monolayer of epithelial cells that line the luminal side of the intestine provides a dynamic and highly regulated barrier to the passive transport of macromolecules. The presence of both nutrients and microbes within the gastrointestinal lumen impose a dichotomous task to this epithelial barrier. Several lines of evidence suggest that conditions created in modern intensive care units (ICUs) dysregulate the discriminatory function of the epithelial barrier. Alterations in intestinal barrier function may result in permeation of autotoxic macromolecules of immense size and diversity that normally reside in the gut lumen. It is becoming increasingly recognized that artificial nutritional support of the critically ill patient may result in significant alterations in epithelial barrier function. The causes and consequences of diet-induced alterations in the gastrointestinal barrier will be discussed. Future strategies in the development of more physiological diets for the critically ill will likely involve the addition of neural, hormonal, and growth factors as stimulants for enhancement of barrier function.

Animals↗
PubMed2003

Intestinal adherent bacteria and bacterial translocation in breast-fed and formula-fed rats in relation to susceptibility to infection.

The barrier function of the intestinal mucosa is immature in the newborn mammal, and is strengthened by breast milk. We investigated this effect of breast milk by comparing the susceptibility to infection assessed in terms of adherent bacterial colonization of the intestinal tissue (AdC) and bacterial translocation (BT) between breast-fed and formula-fed newborn rats. Three-day-old rat pups were assigned to one of three groups: mother-reared (MR), pseudo-cannulated (sham), and artificially reared (AR). AR rats were infused with formula through an intragastric cannula, under the control of a computer-regulated pumping machine. MR and sham rat pups were reared with their respective dams and received breast milk until weaning in a specially designed cage. In 10-d-old rats, there was no significant difference in the fecal or cecal flora between the AR and MR groups, whereas the AdC and the BT to the liver were greater in the AR than MR group. Enterobacteriaceae, Streptococcus and/or Enterococcus, and Staphylococcus were dominantly detected as microorganisms in AdC flora and BT. The AdC flora did not directly reflect the bacterial colonization flora. These findings suggest that AR rat pups mature normally, although there is a greater colonization of Enterobacteriaceae and BT in AR than MR pups. Consequently, the intestinal barrier function of the pups reared by artificial feeding may become susceptible to BT, and AdC may be more indicative than bacterial colonization of the susceptibility to BT.

Animals↗
PubMed1992

Intestinal permeability in the critically ill.

Alterations in intestinal permeability reflect one component of intestinal epithelial barrier function. The objective of this study was to assess the degree of derangement of intestinal permeability in critically ill patients and to investigate the relationship of this to markers of disease severity and sepsis. Sixteen patients admitted to the intensive care unit for a variety of problems were studied with the severity of illness and degree of sepsis recorded daily. A differential sugar absorption test, using lactulose and mannitol as markers, was performed, and in 10 patients this was repeated after an interval of between 4-11 days. The use of the lactulose/mannitol (L/M) ratio corrects for variables unrelated to permeability such as gastric emptying. The L/M ratio was significantly higher in patients (median 0.98) compared to normal controls (median 0.008). The ratios showed no relation to disease severity or sepsis. These results establish that increased intestinal permeability occurs in the general ICU patient but that it is not uniquely related to sepsis. The extent of this abnormality suggests that further study is required to show the various influences on this process.

Adult↗
PubMed1997

Anisodamine restores bowel circulation in burn shock.

In a group of eight burn patients with a mean of 65.3 +/- 17.4 per cent TBSA burn injury (range 50-90 per cent TBSA), accompanied by a mean of 43.5 +/- 18.9 per cent TBSA full-thickness injury, it was shown that the evidence of global hypovolaemia had disappeared at 12 h after the injury following aggressive fluid resuscitation, while there was still a subnormal pHi of stomach at 48 h. As a prolonged period of inadequacy of oxygen delivery to the intestine might result in impairment of the intestinal mucosal barrier function, and then endogenous endotoxaemia might ensue, it seems to be important to correct intestinal hypoxia as early as possible. Since the inadequate perfusion to the gut wall is due to selective vasoconstriction of the mesenteric vasculature, logic dictates that the use of a vasodilator is in order. Anisodamine, an anticholinergic drug, was then given in six burn patients with comparable burn size and amount of fluid replenishment with the eight patients in the control group. It was clearly demonstrated that gastric pHi returned to normal before 48 h after injury. Plasma endotoxin and TNF contents were measured, and they were significantly lower than control values after 72 h. In conclusion, it is believed that anisodamine might be a valuable adjunct to the resuscitation regime of burn shock, and, therefore, a promising drug to abate endogenous endotoxaemia subsequent to splanchnic vasoconstriction due to hypovolaemia. The shortcomings of the drug were a mild abdominal distention and tachycardia after its administration.

Adult↗
PubMedDate not supplied

Human breast milk and facilitation of gastrointestinal development and maturation.

Breast milk feedings make important contributions to optimal infant intestinal maturation. The current literature provides support for many important benefits attributable to breastfeeding. Breast milk feedings encourage helpful intestinal bacterial colonization and assist in development of the intestinal mucosa barrier. More importantly, breastfeeding provides immunologic properties that are delivered directly to the infant's intestinal mucosa. Breastfeeding also seems to have a protective effect in preventing allergic conditions.

Breast Feeding↗
PubMed1995

Epithelial barrier and ion transport in coeliac sprue: electrical measurements on intestinal aspiration biopsy specimens.

Epithelial barrier function and ion transport was studied in coeliac sprue using a miniaturised Ussing device for measurements on diagnostic aspiration biopsy specimens from the jejunum of untreated or gluten free nourished sprue patients, or from healthy controls. Pure epithelial resistance (Re) indicating epithelial barrier function was determined by transmural alternating current impedance analysis. It was reduced by 56% in acute sprue mean (SEM) (9 (1) omega.cm2) compared with controls (20(2) omega.cm2). In gluten free nourished sprue patients Re was only partly recovered (15 (1) omega.cm2). Subepithelial resistance (Rsub) was also changed from 28 (1) omega.cm2- in control to 17 (1) omega.cm2 in acute sprue because of the change in mucosal architecture, but was unchanged in gluten free nourished sprue patients (29 (4) omega.cm2). In acute sprue, unidirectional Na+ and Cl- fluxes were increased in both directions as a consequence of the decreased resistance. However, short circuit current (ISC) as well as Na+ and Cl- net fluxes were not significantly different from control. Subsequently, the electrogenic Cl- secretory system was investigated. After maximal stimulation with theophylline and prostaglandin E1, a Cl(-)-dependent increase in ISC was obtained in the sprue mucosa and control jejunum. It showed saturation characteristics and was blockable by serosal bumetanide. When compared with control, neither Km nor Vmax of this electrogenic Cl- secretion was significantly changed in coeliac sprue. In conclusion, a miniaturised Ussing device was used for transport measurements on intestinal biopsy specimens. In acute coeliac disease, the epithelial barrier of the jejunum was seriously disturbed. The active electrogenic Cl- secretory transport system was present in the sprue mucosa, but was not activated in the Ussing chamber in vitro when compared with control jejunum.

Acute Disease↗