Luminal Saline Research Articles

Regulation of Bicarbonate Secretion in Marine Fish Intestine by the Calcium-Sensing Receptor.

In marine fish, high epithelial intestinal HCO3− secretion generates luminal carbonate precipitates of divalent cations that play a key role in water and ion homeostasis. The present study was designed to expose the putative role for calcium and the calcium-sensing receptor (CaSR) in the regulation of HCO3− secretion in the intestine of the sea bream (Sparus aurata L.). Effects on the expression of the CaSR in the intestine were evaluated by qPCR and an increase was observed in the anterior intestine in fed fish compared with unfed fish and with different regions of intestine. CaSR expression reflected intestinal fluid calcium concentration. In addition, anterior intestine tissue was mounted in Ussing chambers to test the putative regulation of HCO3− secretion in vitro using the anterior intestine. HCO3− secretion was sensitive to varying calcium levels in luminal saline and to calcimimetic compounds known to activate/block the CaSR i.e., R 568 and NPS-2143. Subsequent experiments were performed in intestinal sacs to measure water absorption and the sensitivity of water absorption to varying luminal levels of calcium and calcimimetics were exposed as well. It appears, that CaSR mediates HCO3− secretion and water absorption in marine fish as shown by responsiveness to calcium levels and calcimimetic compounds.

Intravascular photoacoustic imaging of exogenously labeled atherosclerotic plaque through luminal blood

Combined intravascular ultrasound and intravascular photoacoustic (IVUS/IVPA) imaging has been previously established as a viable means for assessing atherosclerotic plaque morphological and compositional characteristics using both endogenous and exogenous contrast. In this study, IVUS/IVPA imaging of atherosclerotic rabbit aortas following systemic injection of gold nanorods (AUNRs) with peak absorbance within the tissue optical window is performed. Ex vivo imaging results reveal a high photoacoustic signal from localized AUNRs in regions with atherosclerotic plaques. Corresponding histological staining further confirms the preferential extravasation of AUNRs in atherosclerotic regions with compromised luminal endothelium and acute inflammation. The ability to detect AUNRs using combined IVUS and photoacoustic imaging in the presence of luminal saline and luminal blood is evaluated using both spectroscopic and single wavelength IVPA imaging techniques. Results demonstrate that AUNR detection within the arterial wall can be achieved using both methods, even in the case of imaging through luminal blood.

Dry Hot Air: Is It a Reliable Method of Disinfection for Urological Endoscopes? Preliminary Study

To evaluate dry hot air effect as a reliable method of disinfection of urological endoscopes. Two groups of urological endoscopic instruments (2 cystoscopic sheaths, 2 bridges, and 2 working elements of resectoscope and urethrotome for each group), after being sterilized by full immersion in 2% glutaraldehyde solution for 10 hours, were contaminated by immersion in suspensions of Staphylococcus saprophyticus (3 x 10(3) CFU/mL), Escherichia coli (28 x 10(2) CFU/mL), and Candida albicans (27 x 10(2) CFU/mL). Group I was exposed to disinfection by full immersion in 2% glutaraldehyde solution for 20 minutes. Group II was exposed to dry hot air obtained by using a hair dryer for 3 minutes. The surfaces and lumens of the instruments of both groups were washed with specific volumes of saline. The surface and luminal specimens were collected separately and used for culture on different media specific for these organisms. Colony-forming units were estimated. In group I, the cultures isolated from the instrument surface washes were negative but those isolated from the luminal injected saline were all positive for S. saprophyticus (60 CFU/mL), E. coli (50 CFU/mL), and C. albicans (50 CFU/mL). In group II, the cultures isolated from both the instrument surface and luminal saline washes were negative for all 3 above-mentioned microorganisms. Hot dry air by using a hair dryer is an inexpensive, rapid, easy, easily available, and effective method of disinfection compared with glutaraldehyde solution.

In Vitro Examination of Interactions Between Copper and Zinc Uptake via the Gastrointestinal Tract of the Rainbow Trout (Oncorhynchus mykiss)

An in vitro gut sac technique was used to investigate whether reciprocal inhibitory effects occurred between Cu and Zn uptake in the gastrointestinal tract of the rainbow trout and, if so, whether there was regional variation among the stomach, anterior intestine, mid intestine, and posterior intestine in the phenomena. Metal accumulation in surface mucus and in the mucosal epithelium and transport into the blood space were assayed using radiolabeled Cu or Zn at environmentally realistic concentrations of 50 micromol L(-1) in the luminal saline, with 10-fold higher levels of the other metal (nonradioactive) as a potential inhibitor. Zn transport rates were generally higher than Cu transport rates in all compartments except the stomach, where they were lower. High [Zn] reduced Cu transport into the blood space in the mid and posterior intestines by 67% and 33%, respectively, whereas high [Cu] reciprocally reduced Zn transport into the blood space in these same sections by 54% and 78%. No inhibitions occurred in either the anterior intestine or the stomach. In these segments, elevated concentrations of the other metal stimulated Cu and Zn transport into the blood space and/or the mucosal epithelium by 50-100%, possibly by displacement from intracellular binding sites, thereby raising local concentrations at other transport sites. None of the treatments affected metal accumulation in surface mucus. The results indicate that one or more shared high-affinity pathways (possibly DMT1) occur in the mid and posterior intestine, which transport both Cu and Zn. These pathways appear to be absent from the stomach and anterior intestine, where other transport mechanisms may occur.

In vitro characterization of cadmium and zinc uptake via the gastro-intestinal tract of the rainbow trout ( Oncorhynchus mykiss): Interactive effects and the influence of calcium

An in vitro gut sac technique was employed to study whether Cd and Zn uptake mechanisms in the gastro-intestinal tract of the rainbow trout are similar to those at the gills, where both metals are taken up via the Ca transport pathway. Metal accumulation in surface mucus, in the mucosal epithelium, and transport into the blood space were assayed using radiolabelled Cd or Zn concentrations of 50 μmol L −1 in the luminal (internal) saline. Elevated luminal Ca (10 or 100 mmol L −1 versus 1 mmol L −1) reduced Cd uptake into all three phases by approximately 60% in the stomach, but had no effect in the anterior, mid, or posterior intestine. This finding is in accordance with recent in vivo evidence that Ca is taken up mainly via the stomach, and that high [Ca] diets inhibit Cd accumulation from the food specifically in this section of the tract. In contrast, 10 mmol L −1 luminal Ca had no effect on Zn transport in any section, whereas 100 mmol L −1 Ca stimulated Zn uptake, by approximately threefold, into all three phases in the stomach only. There was no influence of elevated luminal Zn (10 mmol L −1) on Cd uptake in the stomach or anterior intestine, or of high Cd (10 mmol L −1) on Zn uptake in these sections. However, high [Zn] stimulated Cd transport into the blood space but inhibited accumulation in the mucosal epithelium and/or mucus-binding in the mid and posterior intestine, whereas high [Cd] exerted a reciprocal effect in the mid-intestine only. We conclude that Cd uptake occurs via an important Ca-sensitive mechanism in the stomach which is different from that at the gills, while Cd transport mechanisms in the intestine are not directly Ca-sensitive. Zn uptake does not appear to involve Ca uptake pathways, in contrast to the gills. These results are discussed in the context of other possible Cd and Zn transport pathways, and the emerging role of the stomach as an organ of divalent metal uptake.

In vitro analysis of the bioavailability of six metals via the gastro-intestinal tract of the rainbow trout ( Oncorhynchus mykiss)

An in vitro gut sac technique was used to compare the uptake rates of essential (copper, zinc and nickel) and non-essential metals (silver, cadmium and lead) at 50 μmol L −1 each (a typical nutritive level in solution in chyme) in the luminal saline in four sections of the gastro-intestinal tract (stomach, anterior, mid and posterior intestines) of the freshwater rainbow trout. Cu, Zn, Cd and Ag exhibited similar regional patterns: on an area-specific basis, uptake rates for these metals were highest in the anterior intestine, lowest in the stomach, and approximately equal in the mid and posterior intestinal segments. When these rates were converted to a whole animal basis, the predominance of the anterior intestine increased because of its greater area, while the contribution of the stomach rose slightly to approach those of the mid and posterior intestines. However, for Pb and Ni, area-specific and whole organism transport rates were greatest in the mid (Pb) and posterior (Ni) intestines. Surprisingly, total transport rates did not differ appreciably among the essential and non-essential metals, varying only from 0.025 (Ag) to 0.050 nmol g −1 h −1 (Ni), suggesting that a single rate constant can be applied for risk assessment purposes. These rates were generally comparable to previously reported uptake rates from waterborne exposures conducted at concentrations 1–4 orders of magnitude lower, indicating that both routes are likely important, and that gut transporters operate with much lower affinity than gill transporters. Except for Ni, more metal was bound to mucus and/or trapped in the mucosal epithelium than was transported into the blood space in every compartment except the anterior intestine, where net transport predominated. Overall, mucus binding was a significant predictor of net transport rate for every metal except Cd, and the strongest relationship was seen for Pb.

The effects of pH and the iron redox state on iron uptake in the intestine of a marine teleost fish, gulf toadfish ( Opsanus beta)

In the marine teleost intestine the secretion of bicarbonate increases pH of the lumen (pH 8.4 –9.0) and importantly reduces Ca 2+ and Mg 2+ concentrations by the formation of insoluble divalent ion carbonates. The alkaline intestinal environment could potentially also cause essential metal carbonate formation reducing bioavailability. Iron accumulation was assessed in the Gulf toadfish ( Opsanus beta) gut by mounting intestine segments in modified Ussing chambers fitted to a pH-stat titration system. This system titrates to maintain lumen pH constant and in the process prevents bicarbonate accumulation. The luminal saline pH was clamped to pH 5.5 or 7.0 to investigate the effect of proton concentrations on iron uptake. In addition, redox state was altered (gassing with N 2, addition of dithiothreitol (DTT) and ascorbate) to evaluate Fe 3+ versus Fe 2+ uptake, enabling us to compare a marine teleost intestine model for iron uptake to the mammalian system for non-haem bound iron uptake that occurs via a ferrous/proton (Fe 2+/H +) symporter called Divalent Metal Transporter 1 (DMT1). None of the redox altering strategies affected iron (Fe 3+ or Fe 2+) binding to mucus, but the addition of ascorbate resulted in a 4.6-fold increase in epithelium iron accumulation. This indicates that mucus iron binding is irrespective of valency and suggests that ferrous iron is preferentially transported across the apical surface. Altering luminal saline pH from 7.0 to 5.5 did not affect ferric or ferrous iron uptake, suggesting that if iron is entering via DMT1 in marine fish intestine this transporter works efficiently under circumneutral conditions.

Hepatocyte growth factor ameliorates inflammatory bowel disease in a rat model.

This study was designed to investigate the benefits of administration of hepatocyte growth factor in a rat model of inflammatory bowel disease. Transfection of the HLA-B27 gene into Fisher rats induces a phenotype similar to inflammatory bowel disease. Fisher rats and HLA-B27 rats were divided into six groups: (1) Fisher, intravenous saline; (2) HLA-B27, intravenous saline; (3) HLA-B27, intravenous hepatocyte growth factor; (4) Fisher, luminal saline; (5) HLA-B27, luminal saline; and (6) HLA-B27, luminal hepatocyte growth factor. Rats received a 14-day infusion through an osmotic pump attached to a catheter positioned in either the jugular vein or the terminal ileum. Rats were evaluated for stool character, and gross and microscopic bowel inflammation. Statistics were analyzed using analysis of variance or the Kruskal-Wallis nonparametric test. A value of P<0.05 was significant. Compared to untreated HLA-B27 rats, intravenous administration of hepatocyte growth factor decreased diarrhea by 41% and microscopic inflammation by 54% (P<0.05). Luminal hepatocyte growth factor exposure decreased total bowel lesions by 53% and microscopic inflammation by 40% compared to untreated HLA-B27 rats (P<0.05), but it did not have an effect on diarrhea. Administration of hepatocyte growth factor ameliorates many of the features of bowel disease in this rat model and theoretically could have therapeutic applications in the management of inflammatory bowel disease in humans.

Microbial growth in saline breast implants and saline tissue expanders.

The subject of microbial growth within the saline medium of prosthetic breast implants has been one of great controversy in recent years. Although several articles have described microbial growth within the tissue surrounding implanted breast prostheses, few have attempted to determine the possibility of such contamination of the luminal saline. The authors studied the intraluminal saline medium of a series of explanted breast prostheses with the objective of identifying any microbial contamination. Over a 6-month period, a consecutive series of saline-filled breast implants and tissue expanders were removed from 37 patients. Under the supervision of a microbiologist, saline extracted from each implant was subjected to bacterial and fungal cultures, Gram staining, and acid-fast staining. A total of 24 saline-filled breast implants were removed from 15 patients, and 32 saline-filled tissue expanders were removed from 22 patients. The average length of implantation was 28.1 months for the implants and 7.1 months for the expanders. None of the saline within the implants or expanders within our series displayed any evidence of microbial contamination. These results suggest that microbial contamination of the luminal saline of prosthetic breast implants is an extremely unlikely event.

Reversal and protection against indomethacin-induced blood stasis and mucosal damage in the rat jejunum by a beta3-adrenoceptor agonist.

In the rat, indomethacin causes jejunal villous shortening, microvascular distortion, and blood stasis prior to ulceration. The beta3-adrenoceptor agonist CL316,243 (CL) prevents both the early histological changes and ulceration. To test the hypothesis that the beta3-adrenoceptor agonist CL316,243 exerts its protective effect by prevention and/or reversal of blood flow changes in the rat jejunum exposed to indomethacin. In anaesthetized rats, jejunal villous blood flow was measured in surface capillaries using fluorescence microscopy. Stasis of superficial capillary blood flow was induced by combined topical and i.v. indomethacin (100 microg/mL, 2.8 x 10(-4) M). To examine the effect of CL on blood stasis, CL was applied either i.v. (1 mg/kg) or luminally (100 microg/mL, 2.5 x 10(-5)M) at the onset of stasis. Prophylactic protection was assessed by giving i.v. CL simultaneously with indomethacin. Results were compared with controls which received luminal saline applied at blood stasis. The effect of i.v. CL (1 mg/kg) alone, or luminal CL (100 microg/mL) alone on basal villous blood flow was also examined. The small intestines were perfusion-fixed with 10% formol saline, and removed for histology, n = 5 for all groups. Luminal CL given at stasis reversed indomethacin-induced stasis within 10 min, whereas i.v. CL did not. Pretreatment with i.v. CL prevented the onset of stasis. Basal blood flow was raised slightly only by luminal CL. The beta-adrenoceptor agonist CL316,243 can protect against indomethacin-induced blood stasis in rat jejunal villi.

Enhancement of intestinal adaptation by hepatocyte growth factor

Background/Purpose: Hepatocyte growth factor (HGF) was originally shown to enhance hepatocyte DNA synthesis. Recently, the expression of HGF and its receptor (c-met) were observed in the intestinal tract. In a previous study, we demonstrated that HGF can increase normal rat intestinal epithelial mass and function in vivo. This study was designed to determine if HGF, given either systemically or luminally, can enhance intestinal epithelial mass and function beyond the normal adaptive response after massive small bowel resection. Methods: Twenty young adult male Sprague-Dawley rats underwent an 80% small bowel resection. Seven days after resection, systemic infusion (via the jugular vein) or luminal perfusion (via the jejunum) were performed using subcutaneously placed osmotic minipumps. The rats were divided into four groups: group 1, systemic saline, (control, n = 5); group 2, systemic HGF at 150 μg/kg/d (n = 5); group 3, luminal saline, (control, n = 5); and group 4, luminal HGF at 75 μg/kg/d (n = 5). After a 14-day infusion, [C 14] galactose and [C 14] glycine absorption (μmol/cm 2 intestine), mucosal DNA content (μg/mg mucosa) and protein content (μg/mg mucosa) were measured in the remaining small intestine of each rat. Results: Systemic infusion of HGF increased galactose absorption 68% ( P < .05), glycine absorption 57% ( P < .05), DNA content 17% ( P < .01), and protein content 57% ( P < .01), when compared with the appropriate control. Luminal perfusion of HGF also increased galactose absorption 114% ( P < .01), glycine absorption 126% ( P < .01), DNA content 32% ( P < .01), and protein content 45% ( P < .01), when compared with the appropriate control. Conclusions: These data demonstrate for the first time that HGF can significantly enhance intestinal epithelial cell function and mucosal mass beyond the normal adaptive response. Luminal administration appeared to produce a greater response when compared with systemic administration but was significant only for galactose absorption ( P < .05). HGF may be clinically useful in patients with short bowel syndrome.

Human esophageal secretion: Mucosal response to luminal acid and pepsin

Background/Aims: Although esophageal histology in humans reveals numerous submucosal mucous glands, their secretion has never been explored. Therefore, we have studied the chemical composition and physical characteristics of esophageal secretion under the impact of luminal saline, acid, and acid/pepsin solutions. Methods: The esophageal lumen in 21 healthy volunteers was continuously perfused with saline, HCl, or HCl/pepsin. Perfusates were assayed for mucin, protein, and viscosity. In addition, analysis of amino acid and sugar composition of purified esophageal mucin was performed. Results: Esophageal perfusion with saline resulted in luminal release of mucin at the rate of 0.23 ± 0.03 mg·cm−2 min−1. Acid/pepsin solution significantly enhanced luminal release of mucin (0.32 ± 0.03 mg·cm−2·min−1; P < 0.01). HCl/pepsin solution also significantly increased the luminal output of protein (P < 0.01) and significantly impaired the viscosity of the esophageal perfusate (P < 0.05). Threonine, serine, and proline were the major amino acids within the esophageal mucin, whereas galactose was the predominant carbohydrate. Conclusions: Luminally released esophageal mucin, shown for the first time in humans, contributes significantly to maintaining the high viscosity of esophageal secretions. Significant increase in the luminal release of mucin under the impact of acid and pepsin, with subsequent decline of the perfusate viscosity, may indicate that mucin is the major target for gastric acid and pepsin, absorbing the deleterious impact of the gastroesophageal refluxate.

Adenosine is a mediator of ethanol-induced gastric vasodilation in dogs.

The purpose of this study was to assess the role of histamine, adenosine, and prostaglandins as mediators of ethanol-induced gastric vasodilation. In an ex vivo segment of canine stomach, vasodilation occurred within the first minute of replacing luminal saline with ethanol (40% vol/vol). Ethanol caused vascular resistance to progressively decrease by approximately 53% compared with control values. In other experiments, intra-arterial infusion of histamine (300 ng/ml) or adenosine (30 micrograms/ml) to the gastric segment produced similar degrees of vasodilation as observed with ethanol. The response to these vasodilators could be markedly attenuated with specific antagonists of these substances (histamine: pyrilamine plus cimetidine; adenosine: 8-phenyltheophylline). In our final experiments, indomethacin or histamine- or adenosine-receptor antagonists were given before application of topical ethanol. Indomethacin or histamine antagonists had no significant effect on the time course or magnitude of ethanol-induced vasodilation. In contrast, pretreatment with 8-phenyltheophylline significantly reduced changes in vascular resistance during exposure to luminal ethanol. These results suggest that locally released adenosine is an important mediator of ethanol-induced vasodilation in the canine stomach under these conditions.

Anti‐inflammatory agents and substance P depletion in experimental ileitis

To understand the interactions between substance P and gut inflammation, changes in substance P levels were evaluated in a chronic model of ileitis in response to three anti-inflammatory agents with distinct mechanisms of action. The agents were the prostaglandin E1 analogue misoprostol (30 μg/kg, s.c., b.i.d.), the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 100 μg/ml in drinking water) and the leumedin, N-(fluorenyl-9-methoxycarbonyl)-L-leucine (NPC 15199, 10 mg/kg, s.c.). Ileitis was induced by a transmural injection of trinitrobenzene sulphonic acid (TNBS 30 mg/kg in 50% ethanol) into the distal ileum of guinea-pigs. All anti-inflammatory therapies were introduced after TNBS administration and continued until day 7, when guinea-pigs were killed. Ileal substance P levels were measured by radioimmunoassay, and granulocyte infiltration was quantified by myeloperoxidase (MPO) activity. Protein and nitrite (an index of nitric oxide formation) levels in a luminal saline lavage were quantified in all groups. TNBS ileitis caused a marked reduction in ileal substance P content and increased MPO activity, protein and nitrite secretion. The nitric oxide synthase inhibitor, L-NAME, completely restored all parameters to baseline. Misoprostol attenuated the granulocyte infiltration and exacerbated protein leak but had no effect on substance P levels. In contrast, NPC 15199 had no effect on granulocyte infiltration but normalized substance P levels and protein leak. Only L-NAME and NPC 15199 blocked the TNBS induced increase in nitrite levels. These results suggest that the regulation of granulocyte infiltration in this model is unrelated to changes in substance P levels. Inhibition of nitric oxide synthase was the most effective therapeutic strategy in TNBS ileitis but the precise interactions between nitric oxide and the enteric nervous system during inflammatory states remain to be defined.

Comparative duodenal, jejunal and ileal responses to luminal saline load

Intestinal ionic exchanges were studied in rat duodenal, jejunal and ileal ligated loops in response to different luminal saline loads: NaCl concentration varied from 150-0 mM, solutions being made isoosmotic with mannitol. The contact delay was 60 min. An exponential relationship was found between water, Na and Cl movements and the initial saline concentration. Maximal absorption was obtained with 150 mM NaCl, and was significantly higher in the duodenum than in the jejunum and ileum. The NaCl concentration for which water, Na, and Cl movements were null was approximately 70 mM NaCl in the duodenum and jejunum, 41 mM for Na and 18 mM for Cl in the ileum. The water efflux induced by the 0-mM NaCl test solution was maximal in the duodenum (1.5 +/- 0.2 ml/h) and decreased in the jejunum (0.8 +/- 0.1 ml/h) and ileum (0.3 +/- 0.1 ml/h) as did sodium, chloride and non-chloride anion efflux. These data support the functional heterogeneity of the small intestine regulating the water and ion exchange in response to luminal saline load, the main difference being connected with the efflux capacity of the mucosa, decreasing from the duodenum to the jejunum and ileum.

Antidiuretic action of cyclic AMP, corpus cardiacum, and ventral ganglia on fluid absorption across locust ileum in vitro

Locust ileal fluid transport (3.0–3.5 μL/h per ileum) and tissue volume were nearly constant after the 1st hour of incubation in physiological saline. Inhibition of absorption by KCN + iodoacetic acid and by azide indicated metabolic dependence of fluid transport. Fluid absorption occurred against osmotic concentration differences of up to 600 mosmol (luminal osmolarity &gt; hemocoel osmolarity). Fluid absorption was stimulated by cyclic AMP, by both nervous and glandular lobes of the corpus cardiacum, and by the fifth ventral ganglion in a dose-dependent manner. All stimulants caused ilea to absorb against larger osmotic concentration differences. Stimulants in corpus cardiacum and fifth ventral ganglion extracts increased the osmotic permeability of the ileal wall at low osmotic concentration differences, whereas cyclic AMP had a much smaller effect on osmotic permeability. The absorbate remained hyperosmotic to the luminal saline under all conditions, and stimulants increased absorbate osmolarity.

Effect of corpus cardiacum, ventral ganglia, and proline on absorbate composition and fluid transport by locust hindgut

Extracts of corpus cardiacum and fifth ventral ganglion stimulated transport of K+, Cl−, and fluid across everted rectal sacs exposed luminally to either high-NaCl or high-KCl saline, whereas there was little or no increase in Na+ absorption. These results contrast with the large increase in Na+ absorption across the ileum caused by the same extracts. Moreover, proline transport across the two hindgut segments differs: a large net proline flux occurs across the rectum but not the ileum under similar conditions. Not surprisingly, therefore, increasing proline concentrations in the bathing saline had no effect on ileal fluid transport. However, changing the external proline concentration from 1 to 80 mM caused a substantial increase in fluid transport across everted rectal sacs, and this persisted when external Na+, K+, and Cl− were absent, and when the osmolarity of the luminal saline was increased.

Luminal and metabolic regulation of jejunal amino acid absorption in the rat

Studies were carried out to determine the role of luminal amino acids and metabolic balance in in vivo amino acid absorption. Previous in vitro studies have shown that adaptation of amino acid transport is a complex phenomenon. In the first series of experiments, parenterally nourished rats received a 7-day jejunal infusion of either 3% aspartic acid, glutamine, lysine, valine, or mixed amino acids. A single-pass perfusion was performed to determine the effects of infusates on 5 mM valine, aspartic acid, and lysine absorption. Compared with controls receiving luminal saline, prior glutamine infusion increased valine absorption; prior valine, glutamine, and aspartic acid infusion significantly increased aspartic acid absorption; and prior valine and lysine infusion significantly increased lysine absorption. The mixed amino acid solution had no effect. The effects of metabolic balance were examined by comparing fasted rats with parenterally fed and orally fed rats. Within 24 h fasting significantly increased valine and aspartic acid absorption, despite a significant decrease in intestinal mass.

Nonspecific adaptation of jejunal amino acid uptake in the rat

Luminal nutrients are a major effector of intestinal adaptation. Amino acids are trophic to the intestine, but their role in regulating amino acid transport is not well documented. The presence of several distinct amino acid transport systems raises the question of whether adaptation is class-specific. Studies were carried out in parenterally nourished rats receiving a 7-day jejunal infusion of a 3% solution of either aminoisobutyric acid, aspartic acid, glutamine, histidine, lysine, or valine. While all amino acids were trophic to the intestine, their effects on the in vitro uptake of 0.1, 1.0 and 10.0 mM aspartic acid, lysine, and valine (representative acid, basic, and neutral amino acids) were variable and nonspecific. Compared to controls receiving either total parenteral nutrition alone or total parenteral nutrition plus luminal saline, prior lysine and aspartic acid infusion significantly increased in vitro uptake of all three amino acids tested, whereas valine had little effect on trarisport. No effect on transport was seen with glutamine (actively metabolized by the intestine as is aspartic acid), aminoisobutyric acid (a nonmetabolizable amino acid congener), or histidine (the most trophic amino acid). In conclusion, while individual amino acids cause an adaptation of amino acid Uptake, the effects are nonspecific and independent of their metabolic or trophic potential.

Displacement of endogenous enterokinase into portal venous blood and bile following luminal perfusion of proximal small intestine in guinea pigs.

The displacement of endogenous enterokinase into portal venous blood or bile was studied in conscious guinea pigs both with the small intestine undisturbed and during gentle, intermittent luminal perfusion of a 25-cm segment of duodenum and proximal jejunum. Perfusates tested included water, 150 mM saline, 5% (v/v) ethanol, 0.2% (w/v) lysolecithin, and mixtures of ethanol and lysolecithin. Enterokinase activity was absent from portal venous blood of control guinea pigs with the intestine undisturbed but perfusion with luminal saline or water was consistently associated with substantial levels of active enterokinase in portal venous blood. Similar concentrations of enterokinase in portal blood were also detected in response to luminal ethanol and lysolecithin. The capacity of the normal liver rapidly to clear the enzyme from portal blood was demonstrated. Of the estimated total endogenous enterokinase displaced, 0.2-0.4% was recovered in catalytically active form from the pooled bile of luminally perfused but not control animals. The readiness with which enterokinase was displaced into the circulation in the absence of mucosal damage raises the unexpected possibility that the event may be physiological. Induced penetration of the mucosa and absorption of luminal components is clearly different from the release into portal venous blood of endogenous mucosal macromolecules.