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PubMedDate not supplied

[The participation of hospital pharmacy services in enteral nutrition].

We present the results of a study done in the departments of hospital pharmacy of our country with the aim of knowing their participation in the use and clinical follow up of patients with enteral nutrition. 293 questionnaires were sent out, and 121 were filled out and returned (41.3%). The responses were classified into three groups, according to the number of hospital beds, considering > or = 1000 (large), 500-1000 (medium), and < or = 500 (small). The data were analyzed by means of a statistical program (R-Sigma Horus). 79% (68) of the small hospitals have a unitary dose drug dispensation system, and the Enteral Nutrition was distributed through this system in 53% (50) of them; only 29% (27) of them have a stock of these preparations on the wards. 93% (14) and 65% (54) of the large and small hospitals respectively, prefer the use of enteral nutrition as opposed to parenteral nutrition. 85% (11) of the large hospitals have protocols for the use of enteral nutrition, this being 62% (10) and 59% (47) in medium and small hospitals. The committees for artificial nutrition are present in 75% of the large hospitals, in addition to which, in 66% of these there is a nutritional support team. A pharmacist from the department of pharmacy participates in both multidisciplinary groups. If it is necessary to manipulate the enteral nutrition preparations, in 30% of the departments of pharmacy of the smaller hospitals, this is centralized, being done by personnel of the department itself; in 59% of them (19) there is a specific area for the elaboration, which is not the case in large hospitals. Drugs are mixed with the enteral nutrition in 25% (1), 12% (1), and 9% (4) of the large, medium and small hospitals respectively. There is great, active participation of the hospital pharmacists in the activities of the multidisciplinary nutritional support systems, although at the present time, the involvement of the departments of pharmacy in the centralization of the manipulation of the enteral nutrition is reduced. It is necessary therefore, to implement the development of enteral nutrition programs with a quality guarantee from the departments of pharmacy.

Enteral Nutrition↗

PubMed2001

Enteric co-innervation of striated muscle fibers in the esophagus: just a "hangover"?

Striated muscle of the esophagus was until recently considered to consist of "classical" skeletal muscle fibers innervated by cholinergic vagal motoneurons. The recently described co-innervation originating from enteric neurons expressing nNOS, VIP, NPY, and galanin added a new dimension of complexity. The aim of this study was to summarize current knowledge about, and to get further hints as to the possible function of enteric co-innervation of striated esophageal muscle fibers. Aldehyde fixed rat esophagi were processed for immunocytochemistry for CGRP or VAChT (to demonstrate vagal motor terminals), nNOS/NADPH-d, VIP, NPY, and galanin (to demonstrate enteric terminals), met-enkephalin, mu opiate receptor, muscarinic receptors m1-3, soluble guanylyl cyclase, and cGMP dependent kinase type I and II. Motor endplates were visualized using fluorochrome tagged alpha-bungarotoxin to label nicotinic receptors, or with AChE histochemistry. Besides light and confocal laser scanning microscopy, immuno electron microscopy was also employed. Up to 80% of motor endplates were co-innervated. In addition to nNOS, VIP, NPY, and galanin, many enteric terminals in esophageal motor endplates expressed met-enkephalin. Some appeared to stain for the muscarinic m(2) receptor. There was prominent immunostaining for the micro opioid receptor in the sarcolemma at both junctional and extrajunctional sites. Immunostaining for soluble guanylyl cyclase was prominent immediately beneath the clusters of nicotinic receptors. Enteric varicosities and vagal terminals intermingled in motor endplates often without intervening teloglial processes. During ontogeny, initially high co-innervation rates were reduced to adult levels in a cranio-caudally progressing manner. We conclude that, in addition to a possible nitrergic, VIP-, NPY-, and galaninergic modulation of neuromuscular transmission by enteric neurons, opioidergic mechanisms could play a role. On the other hand, cholinergic influence on enteric neurons may be exerted also by the nucleus ambiguus via motor endplates, in addition to the input from the dorsal motor nucleus. The observations that enteric nerve fibers contact striated muscle fibers at specialized sites, i.e., motor endplates, and that these contacts appear in an ordered cranio-caudal sequence after cholinergic motor endplates have been established point to a specific function in neuronal control of esophageal muscle rather than to be an unspecific "hangover" from the smooth muscle past of this organ.

Animals↗

PubMed1997

Two amino acid changes at the N-terminus of transmissible gastroenteritis coronavirus spike protein result in the loss of enteric tropism.

To study the molecular basis of TGEV tropism, a collection of recombinants between the PUR46-MAD strain of transmissible gastroenteritis coronavirus (TGEV) infecting the enteric and respiratory tracts and the PTV strain, which only infects the respiratory tract, was generated. The recombinant isolation frequency was about 10(-9) recombinants per nucleotide and was 3.7-fold higher at the 5'-end of the S gene than in other areas of the genome. Thirty recombinants were plaque purified and characterized phenotypically and genetically. All recombinant viruses had a single crossover and had inherited the 5'- and 3'-halves of their genome from the enteric and respiratory parents, respectively. Recombinant viruses were classified into three groups, named 1 to 3, according to the location of the crossover. Group 1 recombinants had the crossover in the S gene, while in Groups 2 and 3 the crossovers were located in ORF1b and ORF1a, respectively. The tropism of the recombinants was studied. Recombinants of Group 1 had enteric and respiratory tropism, while Group 2 recombinants infected the respiratory, but not the enteric, tract. Viruses of both groups differed by two nucleotide changes at positions 214 and 655. Both changes may be in principle responsible for the loss of enteric tropism but only the change in nucleotide 655 was specifically found in the respiratory isolates and most likely this single nucleotide change, which leads to a substitution in amino acid 219 of the S protein, was responsible for the loss of enteric tropism in the closely related PUR46 isolates. The available data indicate that in order to infect enteric tract cells with TGEV, two different domains of the S protein, mapping between amino acids 522 and 744 and around amino acid 219, respectively, are involved. The first domain binds to porcine aminopeptidase N, the cellular receptor for TGEV. In the other domain maps a second factor of undefined nature but which may be the binding site for a coreceptor essential for the enteric tropism of TGEV.

Animals↗

PubMed1991

Screening of children for enteric bacterial pathogens in the outborn neonatal ward in Lagos, Nigeria.

Babies, on admission into a neonatal ward at the Lagos University Teaching Hospital, had their rectal swab specimens examined bacteriologically and screened for enteric bacterial pathogens over a one-year-period at two-week intervals. It was found that on the average there were 3 (9.68%) enteric bacterial pathogens out of an average of 31 admissions at each screening period. The enteric bacterial pathogens isolated included: non-typhoid salmonellae, which accounted for 55 (80.88%) isolates out of the 68 enteric bacterial pathogens, Salmonella typhi 2.94%, Shigella dysenteriae 2.94%, Shigella flexneri 4.41%, S. boydii 1.47%, S. sonnei 1.47%, Campylobacter jejuni 1.47% and Enteropathogenic Escherichia coli (EPEC) 2.94%. The main clinical conditions associated with those babies in whom the enteric pathogens were isolated included sepsis, prematurity, neonatal jaundice and tetanus. It is concluded that the enteric bacterial pathogens, even though they were not directly associated with diarrhoeal disease in the newborns in this study, might have contributed to other illnesses like sepsis and meningitis. It is also noteworthy that the enteric bacterial pathogens isolated sporadically from the babies could have been over-looked in view of the fact that it is not conventional to search for enteric bacterial pathogens in babies without diarrhoea on admission. Rectal swab investigations could provide additional information which might be of epidemiological importance in ill neonates in the clinical settings that prevail in developing countries.

Bacteria↗

PubMed1990

Origin and distribution of enteric neurones in Xenopus.

In Xenopus, we investigated the origin of enteric neurones and their distribution in relation to the extracellular matrix (ECM) components, fibronectin (FN) and tenascin (TN). Enteric neurone precursor cells originate from the anterior trunk neural crest (NC). They migrate along the ventromedial NC pathway (between somites and neural tube/notochord) into the primitive gut (via the dorsal mesentery/lateral plate mesoderm) where they differentiate into enteric neurones. NC cells were identified during their migration and in the gut using the X. laevis - X. borealis nuclear marker system. The neuronal character of NC cells in the gut could be demonstrated immunohistochemically with a monoclonal antibody against the HNK-1 epitope. This antibody is superior to N-CAM and neurofilament antibodies which proved insufficient in Xenopus. In early tadpoles (stage 45), enteric neurones occurred frequently in the mesenchymal lining of the oesophagus, either singly or in groups of two to three cells. In more distal portions of the digestive tract, enteric neurones were rarely found. In metamorphosing tadpoles (stage 62/63), enteric neurones were scattered singly beneath the mucosa, or formed small aggregates between the inner and outer muscle layer throughout the length of the digestive tract. The neurones occurred in positions corresponding to the myenteric and submucosal plexus of higher vertebrates. The distribution of enteric neurones was studied in relation to fibronectin (FN) and tenascin (TN), glycoproteins of the ECM, which support (FN) and inhibit (TN) amphibian NC cell migration. Using immunohistochemistry, FN was found during NC cell migration in ECM spaces along the ventromedial pathway, and in the gut between the mucosa and the muscle layers, where it would be able to support adhesion and migration of NC cells. TN, in contrast, appeared much later than FN, both in the dorsal trunk and also ventrally, in the gut. In older tadpoles, TN was present in the mesenchyme and muscle layers of the digestive tract, where it might have an inhibiting influence on the migration of enteric neurones within the gut wall.

Animals↗

PubMed1990

A pharmacological analysis of the neuronal circuitry involved in distension-evoked enteric excitatory reflex.

Isolated segments of guinea-pig small intestine were set up in a partitioned bath to study the enteric excitatory reflex evoked by distension. The gut was distended by a rubber balloon inserted at the aboral end and contractions of the circular muscle were recorded at the oral end. The oral and aboral ends of the gut were separated by an intermediate compartment of the bath. Inflation of the intraluminal balloon with 0.075-0.35 ml water elicited reproducible and distension-dependent contraction. This enteric orally directed (ascending) excitatory reflex was abolished by tetrodotoxin irrespective of the compartment in which it was applied. Hyoscine (0.3 microM) almost abolished the enteric excitatory reflex when it was applied to the oral compartment. This indicates that the transmission from the final motor neurons to the circular muscle is mainly cholinergic, acting via muscarinic receptors. Hyoscine had no effect on the enteric excitatory reflex when added to the intermediate compartment. When hyoscine was added to the aboral compartment, it decreased the enteric excitatory reflex elicited by low distension stimuli to 70% of control and decreased the enteric excitatory reflex elicited by higher distension stimuli to 95% of control. This indicates that ganglionic transmission involving muscarinic receptors at the site of distension in the aboral bath contributes to the enteric excitatory reflex. Hexamethonium (100 microm) greatly depressed the enteric excitatory reflex when applied to any compartment indicating that nicotinic transmission is most important in the afferent, intermediate and efferent components of the reflex and that the reflex pathway involves a polysynaptic chain of cholinergic interneurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

Enteral feeding.

In this review, topics with scientific strength, topical interest, and controversy were selected. Over the past 50 years, malnutrition has become increasingly recognized as a cause of increased morbidity and mortality in hospital patients. From 1970 to 1980, parenteral nutrition was advocated as the most appropriate form of nutritional therapy for hospital patients. Since then, parenteral nutrition has been replaced by enteral nutrition as the best way of delivering nutrients to hospital patients. The timing of enteral nutrition has been debated. Should it be instituted early, within the first 24 hours? In addition, enteral nutrition containing immune-enhancing nutrients such as arginine, omega-3 fatty acids, glutamine, and nucleotides has been advocated for critically ill patients. The relative merits of enteral versus total parenteral nutrition continue to be debated. Questions about possible complications related to enteral nutrition have been raised. Patients are at risk of nosocomial pneumonia from aspiration and at risk of bowel ischemia because enteral nutrition increases intestinal oxygen consumption. Steroids are often used to treat Crohn disease, but because of undesirable side effects, various techniques have been used to reduce steroid dependency. Enteral nutrition has been advocated as a way of reducing steroid dependency. Finally, enteral nutrition is routinely used to feed demented patients and those in a vegetative state. It is not clear whether this practice alters outcome or quality of life.

Journal Article↗

PubMed1993

Regional differences between various axial segments of the avian neural crest regarding the formation of enteric ganglia.

The vagal neural crest adjacent to somites 1-7 gives rise to the enteric ganglia along the entire digestive tract. It is generally assumed that formation of enteric ganglia in preumbilical gut is independent of the axial segment from which the neural crest originates. In post-umbilical gut, however, there is evidence that the axial segment of origin of the neural crest might be relevant to neural differentiation. In this part of the gut, we previously identified a subpopulation of HNK-1-immunoreactive cells within the enteric mesenchyme. This immunoreactivity disappeared upon formation of the enteric nervous system. We studied the interaction between various axial segments of quail neural crest and the microenvironment in a neural chicken hindgut using chorioallantoic membrane cocultures. We found that neural crest cells from various axial segments could migrate into the gut and home to the correct sites. However, whereas vagal neural crest cells differentiated into enteric neurons, neural crest cells from truncal segments mainly differentiated into melanocytes. The HNK-1-immunoreactivity within the enteric mesenchyme only disappeared when neural crest cell colonization was followed by differentiation into enteric neurons and subsequent formation of enteric ganglia. To determine whether differentiation of neural crest cells in chorioallantoic membrane cocultures was influenced by the prolonged presence of the neural tube and notochord, we developed a new coculture system, using neural crest cells cultured in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Development of the enteric nervous system in chick embryonic duodenum in terms of the distribution of tubulin.

An immunohistochemical method that uses anti-tubulin was utilized to observe the development of the enteric nervous system in chick embryonic duodenum. Neural crest cells, and enteric neuroblasts, or enteric ganglia, which derive from neural crest cells were clearly shown as sharp immunoreactive regions of tubulin. The distributions of enteric neuroblasts and enteric ganglia in chick duodena were in agreement with results of previous reports in which different techniques were used. The initial stage at which cells of neural crest origin were present in the duodenal walls (4-day-old embryos) was earlier than the initial stage (about 6-day-old embryos) reported earlier. This was verified by transmission electron microscopy. Also, the tubulin that is a component of the enteric nervous system was shown to be stable at a low temperature. This tubulin-immunostaining method provides a useful histochemical technique with which to study the development of the enteric ganglion and the function of tubulin as a component of the enteric nervous system.

Animals↗

PubMed1992

Indications for enteric conversion after pancreas transplantation with bladder drainage.

BACKGROUND: Bladder drainage has become the procedure of choice for 94% of transplant centers in North America. Bladder drainage is superior to other techniques as far as graft survival and technical success are concerned; however, the procedure is associated with significant urologic problems that might necessitate conversion to enteric drainage. This review summarizes the indications and results for enteric conversion at this institution. METHODS: Between June 1982 and January 1992 a total of 240 pancreas transplantations were performed at our center. In 229 cases exocrine secretions were drained into the bladder. These cases were reviewed, and those with enteric conversions were further analyzed to delineate indications, complications, and results. RESULTS: Sixteen (7%) were converted to enteric drainage (side-to-side duodenojejunostomy). The reasons for conversion were urethral disruption (six), recurrent urine leaks (five), bleeding (four), and chronic urinary tract infection (one). Enteric conversions were performed between 1 1/2 and 32 months after the initial transplantation. With the exception of one anastomotic leak resulting in an intraabdominal abscess, no complications occurred. All patients undergoing enteric conversions had resolution of their problems and, in addition, were able to discontinue use of oral bicarbonate. CONCLUSIONS: We conclude that enteric conversion after pancreas transplantation with bladder drainage is safe and effective in the correction of urologic problems. Based on our experience, we recommend early enteric conversion if urologic problems do not resolve after an appropriate period of conservative therapy.

Duodenum↗

PubMed2000

Early versus delayed initiation of progressive enteral feedings for parenterally fed low birth weight or preterm infants.

BACKGROUND: Enteral feedings in very-low-birth-weight or sick preterm infants are often delayed for several days or weeks after birth even though delayed enteral feeding could diminish the functional adaptation of the gastrointestinal tract and result in feeding intolerance later. Early initiation of feedings, if well-tolerated, may promote growth and shorten the duration of parenteral nutrition and hospital stay without increasing the risk for necrotizing enterocolitis (NEC). OBJECTIVES: For parenterally fed low-birth-weight infants, to assess the effects of early enteral feedings initiated shortly after birth compared to delayed enteral feedings (with similar schedules for advancing feedings in each group). SEARCH STRATEGY: Searches were performed of the Oxford Database of Perinatal Trials, the Cochrane Neonatal Review Group registry, MEDLINE, abstracts and conference proceedings, references from relevant publications in the English language, and studies identified by personal communication. SELECTION CRITERIA: Only randomized or quasi-randomized clinical trials were considered. Trials were included if 1) they enrolled low birth weight or preterm infants who were all given parenteral nutrition; 2) the infants were randomly assigned to either early enteral feedings (mean or median age <=4 days) or late enteral feedings (>4 days) of formula or breast milk; 3) except when feeding intolerance developed, the feedings were progressively advanced starting within 72 hours after initiating feedings; and 4) the goals for total nutrient intake were similar for both groups. (We did not require the duration or total intake of parenteral nutrients to be similar for both groups because these variables may be affected by the age at which feedings are initiated.) DATA COLLECTION AND ANALYSIS: The two reviewers reached consensus for inclusion of trials. Data regarding clinical outcomes were extracted and evaluated by two reviewers (JET and KAK) independently. Authors were contacted as needed and feasible to clarify or provide missing data. The specific data that were needed were requested in writing and by telephone. MAIN RESULTS: Only two small studies were identified (one with 60 patients and one with 12 patients). Five randomized trials were excluded because parenteral nutrition was not provided or because the groups were assigned to receive different parenteral intakes as well as different enteral intakes. An additional unpublished small trial was excluded because both groups were fed "late" according to our categorization. Because there were no clinical outcomes which were reported in both of the included studies, no meta analysis of the results was performed. Based on the results of the individual studies, early feedings had no significant effect on weight gain, necrotizing enterocolitis, mortality, or age at discharge, although important effects cannot be excluded with the small number of patients studied. Some benefits of early feedings were noted in the larger trial (Davey) -- fewer days on parenteral nutrition, fewer infants who were treated with gastric suction and interruption of feedings, fewer infants with sepsis evaluations, and fewer infants with percutaneous central venous catheters. REVIEWER'S CONCLUSIONS: The benefits and hazards of early and delayed feedings have received very little study in clinical trials, and the effects on major clinical outcomes, including necrotizing enterocolitis and death, remain uncertain. With the availability of parenteral nutrition in contemporary neonatal units, it is unclear whether high-risk infants should receive early or delayed feedings.

Enteral Nutrition↗

PubMed1998

A single rostrocaudal colonization of the rodent intestine by enteric neuron precursors is revealed by the expression of Phox2b, Ret, and p75 and by explants grown under the kidney capsule or in organ culture.

The colonization of the rodent gastrointestinal tract by enteric neuron precursors is controversial due to the lack of specific cellular markers at early stages. The transcription factor, Phox2b, is expressed by enteric neuron precursors (Pattyn et al. Development 124, 4065-4075, 1997). In this study, we have used an antiserum to Phox2b to characterize in detail the spatiotemporal expression of Phox2b in the gastrointestinal tract of adult mice and embryonic mice and rats. In adult mice, all enteric neurons (labeled with neuron-specific enolase antibodies), and a subpopulation of glial cells (labeled with GFAP antibodies), showed immunoreactivity to Phox2b. In embryonic mice, the appearance of Phox2b-immunoreactive cells was mapped during development of the gastrointestinal tract. At Embryonic Days 9.5-10 (E9.5-10), Phox2b-labeled cells were present only in the stomach, and during subsequent development, labeled cells appeared as a single rostrocaudal wave along the gastrointestinal tract; at E14 Phox2b-labeled cells were present along the entire length of the gastrointestinal tract. Ret and p75 have also been reported to label migratory-stage enteric neuron precursors. A unidirectional, rostral-to-caudal colonization of the gastrointestinal tract of embryonic mice by Ret- and p75-immunoreactive cells was also observed, and the locations of Ret- and p75-positive cells within the gut were very similar to that of Phox2b-positive cells. To verify the location of enteric neuron precursors within the gut, explants from spatiotemporally defined regions of embryonic intestine, 0.3-3 mm long, were grown in the kidney subcapsular space, or in catenary organ culture, and examined for the presence of neurons. The location and sequence of appearance of enteric neuron precursors deduced from the explants grown under the kidney capsule or in organ culture was very similar to that seen with the Phox2b, Ret, and p75 antisera. Previous studies have mapped the rostrocaudal colonization of the rat intestine by enteric neuron precursors using HNK-1 as a marker. In the current study, all HNK-1-labeled cells in the gastrointestinal tract of rat embryos showed immunoreactivity to Phox2b, but HNK-1 cells comprised only a small subpopulation of the Phox2b-labeled cells. In addition, in rats, Phox2b-labeled cells were present in advance of (more caudal to) the most caudal HNK-1-labeled cells by 600-700 microm in the hindgut at E15. We conclude that the neural crest cell population that arises from the vagal level of the neural axis and that populates the stomach, midgut, and hindgut expresses Phox2b, Ret, and p75. In contrast, the sacral-level neural crest cells that populate the hindgut either do not express, or show a delayed expression of, all of the known markers of vagal- and trunk-level neural crest cells.

Animals↗

PubMed1998

Bioavailability of ciprofloxacin after multiple enteral and intravenous doses in ICU patients with severe gram-negative intra-abdominal infections.

BACKGROUND: Few data are available on the pharmacokinetics of multiple enteral dosing of ciprofloxacin in critically ill intensive care patients and none for those with severe gram-negative intra-abdominal infections (GNIAI). OBJECTIVE: To determine the bioavailability of enteral ciprofloxacin in tube-fed intensive care patients with severe GNIAI. DESIGN: A randomized crossover study. SETTING: University-based medical center. PATIENTS: 5 critically ill intensive care patients with GNIAI and an estimated creatinine clearance > 25 ml/ min who received continuous tube feeding. INTERVENTIONS: Multiple doses of enteral 750 mg b.i.d. versus 400 mg b.i.d.i.v. ciprofloxacin. MEASUREMENTS: The calculated 12-h area under the serum concentration versus time curve after 750 mg b.i.d. enteral dosing was equivalent to that after 400 mg b.i.d.i.v. The mean bioavailability of enteral dosing was 53.1% [95% confidence interval (CI) 43.5-62.8]. In seven additional patients, the mean serum steady-state concentration at 2 h after enteral administration was 3.9 microg/ml (95% CI 1.9-5.9), not significantly different from that found in the crossover study (p = 0.4). CONCLUSIONS: In tube-fed intensive care patients with severe GNIAI, the bioavailability of enteral ciprofloxacin is adequate.

Adult↗

PubMedDate not supplied

Effects of very low dose and enteric-coated acetylsalicylic acid on prostacyclin and thromboxane formation and on bleeding time in healthy subjects.

OBJECTIVE: Low dose acetylsalicylic acid (ASA) is widely used as an anti-aggregatory agent in the primary and secondary prevention of cardiovascular diseases. In an effort to spare prostacyclin formation and to reduce gastrointestinal side-effects, both very low doses and enteric-coated formulations of ASA have been introduced. However, it still remains unclear whether these different formulations and dosages are equally effective with respect to inhibition of platelet aggregation and thromboxane A2 (TXA2) formation. METHODS: In a randomized study, we therefore investigated the effects of 100 mg ASA plain (p), 100 mg ASA enteric-coated (ec) and 40 mg ASA (p) to 36 healthy male subjects given for 7 days on platelet aggregation and endogenous prostanoid formation rates. Platelet aggregation and platelet TXB2 release in platelet rich plasma (PRP) and serum TXB2 and 6-keto-PGF1alpha levels were determined at baseline and after 7 days of each medication. The urinary metabolites of TXA2 (2,3-dinor-TXB2) and prostacyclin (2,3-dinor-6-keto-PGF1alpha) were measured by gas chromatography/tandem mass spectrometry in 24-h-urines at baseline and on day 7 of each medication. RESULTS: Collagen-induced platelet aggregation was 73.1+/-1.6% of maximal aggregation at baseline. It was inhibited by 68.9%, 58.6% and 24.0% by ASA 100 mg plain, 100 mg enteric-coated, and 40 mg plain on day 7, respectively. Platelet TXB2 release was 11592.0+/-367.5 pg x ml(-1) PRP. It was inhibited by 90.1%, 86.5%, and 55.2% by ASA 100 mg plain, 100 mg enteric-coated, and 40 mg plain, respectively. Serum TXB2 was almost completely reduced on day 7 by 100 mg ASA, but not by 40 mg ASA; serum 6-keto-PGF1alpha was slightly, but significantly reduced in all three groups. Urinary 2,3-dinor-TXB, excretion was 196.0+/-41.5 pg x mg(-1) creatinine at baseline. It was reduced by 80.3% and 79.1% by ASA 100 mg plain and enteric-coated, respectively (each P < 0.05 versus baseline), but only by 55.4% by ASA 40 mg plain (P < 0.05 versus both formulations of ASA 100 mg). CONCLUSIONS: Our present data show that the plain and enteric-coated formulations of 100 mg ASA are equally effective in inhibiting platelet aggregation, platelet thromboxane production, and urinary 2,3-dinor-TXB2 excretion rates. In contrast, a very low dose of 40 mg ASA was significantly less effective in inhibiting these indices of platelet activation in healthy human subjects. ASA enteric-coated 100 mg may be a useful alternative to 100 mg ASA (p) in patients with gastrointestinal side-effects, whereas 40 mg ASA (p) may be too low to inhibit sufficiently platelet activity in patients with cardiovascular diseases in whom platelet activity is increased.

Adult↗

PubMed2002

Development of neuromuscular junctions in the mouse esophagus: focus on establishment and reduction of enteric co-innervation.

The development of vagal and enteric innervation of esophageal motor endplates was examined in perinatal and adult BALB/c and NMRI mice using immunocytochemistry and confocal laser scanning microscopy. Nicotinic acetylcholine receptors were demonstrated with fluorochrome-tagged alpha-bungarotoxin, vagal motor terminals with antisera against vesicular acetylcholine transporter and calcitonin gene-related peptide, and enteric nerve terminals with antisera against neuronal nitric oxide synthase, vasoactive intestinal peptide and galanin. Results demonstrated that enteric and vagal innervations of striated esophageal muscle fibers develop in close spatiotemporal relationship, but with different courses. Connections between VAChT-positive vagal nerve terminals and growing acetylcholine receptor clusters were established from E17 to reach 100% motor endplate innervation at P14 and were maintained throughout adult life. CGRP immunoreactivity developed with a delay of several days after the appearance of VAChT in vagal terminals. From P14 to adulthood CGRP was colocalized with VAChT in almost all motor endplates. In contrast, enteric co-innervation rates increased from E17 to a maximum of 70-80% at P4, while their incidence at motor endplates progressively declined over the following 5 months to lower levels maintained throughout adulthood. Whereas adult enteric co-innervation rates in BALB/c and NMRI mice differed significantly (approximately 30% versus approximately 10%, respectively), their increase and reduction, respectively, during development showed an identical time course. These results suggest a well-ordered sequence of attraction of enteric nerve fibers to, and removal from motor endplates in the developing mouse esophagus. Thus, enteric co-innervation may subserve a functional role in the development and control of perinatal striated esophageal muscle rather than representing an unspecific "hangover" from the smooth muscle past of this organ.

Animals↗

PubMed2004

Transient expression of NOS-II during development of the murine enteric nervous system.

In the enteric nervous system, nitric oxide (NO) is regarded as an important messenger for the non-adrenergic and non-cholinergic neurotransmission. Synthesized mainly by the constitutive nitric oxide synthase (NOS) isoforms NOS I and NOS III, this molecule exerts prejunctional inhibitory effects in the submucosal plexus as well as relaxation of enteric smooth muscles. In order to elucidate the role for NO during enteric development, we looked for the expression of all three NOS-isoforms in the enteric nervous system during mouse development from E8 to E20 using immunohistochemistry. Starting around midgestation, a transient expression of the NOS-II isoform during the very early development of enteric neurones was detected in parallel to that of HNK-1 exclusively in the myenteric plexus. Similar to findings for other neuronal systems, NOS-I and NOS III isoforms could be traced starting significantly later to increase toward the end of embryonic development when NOS II immunoreactivity faded and a strong expression of the vasointestinal peptide could be detected. In contrast to the NOSII expression, the constitutive isoforms can also be detected in the submucosal plexus. Altogether, these findings suggest NOS-II to be exclusively involved during early steps of enteric nervous system development. Absence of downstream signalling elements, such as sGC and cGMP both in neurons and in enteric muscle until the end of the second third of gestation, may indicate different effects executed by NO during development, expressed by Ca(2+) -dependent and Ca(2+) -independent NOS isoforms.

Animals↗

PubMed1994

Experience with enteral nutrition in a hospital population of acutely ill patients.

Enteral feeding has unique metabolic and immune advantages. This article describes the successful use of enteral nutrition, alone or in combination with parenteral feeding, in a tertiary-care hospital. Study participants were 89 patients who received enteral feeding during a 6-month period. These critically ill patients (ranging in age from 55 to 71 years) had severity of illness levels of 7 to 25 according to the Acute Physiologic and Chronic Health Evaluation (APACHE II) system and lengths of hospital stay from 27 to 73 days. Mortality was as high as 50% in patients with liver disease (nonmalignant), 35% in patients with cardiothoracic and vascular diseases, and 17% in patients with cancer and other diseases. Despite the severity of illness, patients met their energy and protein intake goals through enteral or combined feeding with total parenteral nutrition. Serial weights (ie, obtained weekly) and serum albumin concentrations did not improve during hospitalization. Complications related to enteral feeding were minimal (< 17% incidence). Differences were noted between survivors and nonsurvivors: nonsurvivors had lower serum albumin concentrations at the time of admission, had longer hospitalizations, and required total parenteral nutrition for more days than the survivors. Nonetheless, even with extremely sick patients, provision of enteral nutrition can be successful using the administration techniques we describe. Enteral nutrition could best be provided by beginning at a slow rate (10 c3/hour), inserting the feeding tube past the pylorus, and feeding according to sensible energy goals (25 kcal/kg of body weight), and using elemental then polymeric formulas.

Acute Disease↗

PubMed2005

The effectiveness of caloric value of enteral nutrition in patients with major burns.

UNLABELLED: Enteral nutrition as an important component of modern treatment is mandatory for patients suffering from major burns. Regardless of the initial estimation of caloric requirements, actual daily volume of energy consumption may vary depending on the general condition of the patient and the side effects of enteral nutrition. The aim of our study was to investigate the relation between caloric value of enteral nutrition and treatment course. METHODS: The prospective study involved 103 adult patients treated in the Hospital of Kaunas University of Medicine for 2 degrees -3 degrees burns of 10-80% body surface area from 1 January 2001 till 31 December 2003. All patients received enteral nutrition during the acute phase. After the completion of the treatment, caloric value of enteral nutrition was estimated, and patients were divided into two groups: group A received more than 30 kcal/(kg 24 h); and group B, received less than 30 kcal/(kg 24 h). We compared patients' mortality, complication rate, and hospital stay time. RESULTS: The mortality of patients, who enterally received less than 30 kcal/(kg 24 h), was 32.6%, comparing to 5.3% mortality in patients who received 30 or more kcal/(kg 24 h) (p < 0.01). The caloric value of less than 30 kcal/(kg 24 h) increased the frequency of pneumonia by 2.0 times, and the frequency of sepsis by 1.8 times (p < 0.05). The duration of the treatment of survivors in this group was by 12.6 days longer (p = 0.01). CONCLUSIONS: The caloric value of enteral nutrition seems to be associated with patient mortality, complication rate, and treatment duration. The results of the treatment of patients who received more or 30 kcal/(kg 24 h) were much better. Because determined relationship may not be directly causal, further study is needed to determine whether active intervention to improve nutrition could improve outcomes.

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