Ammonia absorption from the intestine in adult cockerels

Two ml of w mM ammonium acetate solution was introduced into 10 cm chicken intestinal sack having Meckel's diverticulum in the middle part. After the introduction, blood ammonia concentration in the mesenteric vein draining the sack reached a maximal increase within 5 min and returned to the initial level in 30 min. The difference of ammonia concentration between cardiac and mesenteric venous blood also showed a similar tendency. About 91% of the ammonia introduced into the intestinal lumen disappeared in 30 min. Amino acid metabolism in intestinal tissue appears to be affected by the introduction of ammonia into the intestinal lumen.     

Incorporation of intraportal ammonia-N into blood and tissue nitrogenous compounds in chickens fed low and high protein diets

1. 15N-Percentage of the amide of glutamine in total blood non-protein-15N was 42 and 48% in chickens fed 5 and 20% protein diets, respectively, when 15N-ammonia was intraportally-infused for 6 hr. 2. The infused ammonia-15N also appeared in the amide of free glutamine in the liver and kidney in large amounts at both levels of protein intake. 3. The 15N incorporated into glutamine-amide in the blood, liver and kidney and non-protein-15N in plasma were greater in chickens fed the low protein diet than in those fed the high protein diet (P less than 0.05 except kidney of P less than 0.01). 4. About 60% of the amide-N of the glutamine which was increased during 6 hr infusion of ammonia was derived from infused ammonia-N and the remainder from endogenous nitrogen, irrespective of protein intake. 5. These results suggest that glutamine is the most important intermediate in detoxication of intraportal ammonia in chickens.     

Sites of action of adenosine in interorgan preconditioning of the heart

The mechanism underlying interorgan preconditioning of the heart remains elusive, although a role for adenosine and activation of a neurogenic pathway has been postulated. We tested in rats the hypothesis that adenosine released by the remote ischemic organ stimulates local afferent nerves, which leads to activation of myocardial adenosine receptors. Preconditioning with a 15-min mesenteric artery occlusion (MAO15) reduced infarct size produced by a 60-min coronary artery occlusion (60-min CAO) from 68 +/- 2% to 48 +/- 4% (P < 0.05). Pretreatment with the ganglion blocker hexamethonium or 8-(p-sulfophenyl)theophylline (8-SPT) abolished the protection by MAO15. Intramesenteric artery (but not intraportal vein) infusion of adenosine (10 microg/min) was as cardioprotective as MAO15, which was also abolished by hexamethonium. Whereas administration of hexamethonium at 5 min of reperfusion following MAO15 had no effect, 8-SPT at 5 min of reperfusion abolished the protection. Permanent reocclusion of the mesenteric artery before the 60-min CAO enhanced the cardioprotection by MAO15 (30 +/- 5%), but all protection was abolished when 8-SPT was administered after reocclusion of the mesenteric artery. Together, these findings demonstrate the involvement of myocardial adenosine receptors. We therefore conclude that locally released adenosine during small intestinal ischemia stimulates afferent nerves in the mesenteric bed during early reperfusion, initiating a neurogenic pathway that leads to activation of myocardial adenosine receptors.     

Transmucosal passage of polyalkylcyanoacrylate nanocapsules as a new drug carrier in the small intestine

The enteral absorption of particles has been investigated in the dog using a colloidal drug carrier, polyalkylcyanoacrylate nanocapsules loaded with an iodized oil (Lipiodol), as a tracer for X-ray microprobe analysis in a scanning electron microscope. Nanocapsules are spherical capsules, 100 to 200 nm in diameter, with a continuous polymeric wall surrounding a cavity which encapsulates the drug. Administered in the jejunal lumen, Lipiodol nanocapsules improved the absorption of the tracer as indicated by increased concentration of iodine in the plasma of mesenteric blood. In order to follow nanocapsules at the cellular level, all tissue compartments were preserved in a life-like state by cryofixation and freeze-drying of intestinal biopsies. Nanocapsules appeared in the intestinal lumen close to the mucus, then in intercellular spaces and defects of the mucosa and finally in the lamina propria and blood capillaries; in this latter compartment, the iodine content was four-fold higher than after intra-jejunal administration of Lipiodol emulsion. This complete phenomenon occurred only at the tip of the villi and happened within less than 60 min. We conclude that nanocapsules enhance the rate of absorption of Lipiodol and transport the drug from the intestinal lumen to the vascular compartment using a paracellular pathway. Thus they may be useful as drug carrier for oral administration of many chemicals.     

Myoelectric bowel activity in ischemia/reperfusion damage. Role of sensory neurons.

The present knowledge indicates that afferent sensory neurons (C-fibres) play an important role in the relationship between intestinal myoelectric activity (IMA) and blood flow (LDBF). The aim of this study was to evaluate the role of C-fibers in myoelectric activity of small intestine during its ischemia and reperfusion. A neurotoxin-capsaicin (CAP) was used to induce functional ablation of afferent sensory neurons. Experiments were performed on 6 groups of anesthetized rats. In the I, II, III group of rats IMA and LDBF were recorded during 100% ischemia induced by AMA 15, 30 and 60 min total occlusion and during 60 min reperfusion period. In group V and VI, IMA and LDBF were registered after intrajejunal placement of 1% CAP. In group IV we measured effects of intraluminal instillation of CAP alone. Intraluminal placement of CAP induced an early increase in slow wave amplitude SWA and slow wave frequency SWF by 35+/-11% and 19+/-10% (p<0.05) with the subsequent decrease in both by 25+/-6 and 24+/-8% (p<0.05) respectively. Short 15 min lasting ischemia induced by 100% occlusion of AMA evoked only a slight increase of SWA. During reperfusion period SWA and SWF returned to the baseline values after 15 min. Total 30 min occlusion decreased SWA and SWF by 25+/-9 and 24+/-6% (p<0.05) respectively. During reperfusion period recovery of IMA parameters to preocclusion values were slower. Intestinal hyperemia was smaller than in previous group. After 60 min lasting intestinal ischemia SWA and SWF were decreased by 58+/-7 and 40+/-6% (p<0.01) respectively. There was no return of IMA parameters to control values. These data demonstrated that intestinal ischemia induces typical changes in the bowel myoelectric activity. These changes possess their own electrical characteristics which can be used in clinical practice for evaluation of the degree ischemically-induced intestinal injury. Capsaicin pretreatment significantly decreased SWA and SWF and LDBF in comparison with those observed in group II and III during 30 and 60 min occlusion and reperfusion period. We conclude that afferent neurons C activated during mesenteric ischemia/reperfusion play an important role in protecting ischemic bowel viability.     

Calcium-dependent translocation of calbindin-D28k from intestine to blood

Calbindin-D (vitamin D-induced calcium-binding protein; CaBP) is known to be present in blood at concentrations which vary directly with levels in the intestinal mucosa. Employing a sensitive radioimmunoassay and sampling mesentery venous blood, the present experiments demonstrated a direct relationship between intestinal calcium absorption and serum CaBP. Solutions containing 150 mM NaCl and 45Ca-labeled calcium chloride (5 or 20 mM) were placed in the lumen of ligated duodenal preparations in situ and mesentery venous blood sampled with time. The concentration of absorbed 45Ca in serum was maximal at 5 min, followed by a significant increase in mesentery CaBP maximizing at 15-20 min. Elevation of serum CaBP was not observed when calcium in the dosing solution was omitted or replaced by either glucose or glycine. The possible transfer of absorbed calcium from the enterocyte to the circulation as a CaBP complex was ruled out by calculations revealing that considerably more calcium was transferred than could be accounted for by the low and high affinity binding sites on the protein. It is proposed that vitamin D-dependent enhanced transcellular calcium transport constitutes a stimulus for the increased release of intestinal CaBP into the circulation.     

Modulation of caudal intestinal permeability in the rat during infection by the tapeworm Hymenolepis diminuta.

Bidirectional movement of solutes between the intestinal lumen and systemic circulation is restricted by tissue barriers that may be altered under conditions such as intestinal infection. In a study using an in vitro everted sac preparation to assess small intestinal permeability in a lumen-to-serosa direction, 51Cr-EDTA movement was compared regionally in the jejunum and ileum of rats infected and uninfected by tapeworms. Whereas jejunal segments showed no significant differences in permeability to 51Cr-EDTA at 6, 15, or 32 days postinfection (dpi), ileal segments displayed an increased permeability on 15 and 32 dpi, but not 6 dpi. The alterations in permeability were not reversed 1 wk after removal of the tapeworm from the intestine. In conclusion, the strictly lumen-dwelling tapeworm infection allows increased movement of molecules from the lumen into ileal, but not jejunal, tissues by 15 dpi.     

Proteolytic digestion of reovirus in the intestinal lumens of neonatal mice.

Two approaches were used to demonstrate proteolysis of reovirus in the intestine of the neonatal mouse. The first approach utilized peroral inoculation of radiolabeled virus into neonatal mice; the intestinal washings were harvested at 0 to 30 min postinoculation. The virus recovered from the intestinal washings was electrophoresed in polyacrylamide to determine whether proteolytic digestion of viral proteins had occurred. Complete loss of sigma 3 and generation of the mu 1c cleavage product delta demonstrated that digestion occurred within 10 to 30 min after the inoculation, resulting in the rapid generation of intermediate subviral particles (ISVPs). The products formed resembled those seen when the virus is digested in vitro with chymotrypsin. The second approach took advantage of the fact that ISVPs grow in cells treated with NH4Cl, whereas intact virus does not grow under these conditions (L. J. Sturzenbecker, M. Nibert, D. Furlong, and B. N. Fields, J. Virol. 61:2351-2361, 1987). Thus, assaying virus for its ability to grow in NH4Cl-treated cells represents a means of ascertaining whether the samples contain ISVPs. Using this approach, we demonstrated that up to 8 h postinoculation ISVPs predominate in the intestinal tissue and in the intestinal lumen. Between 8 and 15 h postinoculation, there is a loss in the proportion of ISVPs in the tissue so that by 15 h postinoculation ISVPs are no longer detectable in intestinal tissue washed of lumen contents and virus. In contrast, the lumen of the intestine contains some ISVPs at all times postinoculation. Thus, after peroral inoculation, the mammalian reoviruses are converted to proteolytically cleaved virus, suggesting that proteolysis plays an important role in initiation of infection in the gastrointestinal tract.     

Perfusion pressure manipulation in porcine sepsis: effects on intestinal hemodynamics

Limited information is available about selection of the threshold for arterial blood pressure in critically ill patients, particularly in sepsis when normal organ blood flow autoregulation may be altered. The present experimental study investigated whether increasing perfusion pressure using norepinephrine in normotensive hyperdynamic porcine bacteremia affects intestinal macro- and microcirculation. Nine pigs received continuous i.v. administration of Pseudomonas aeruginosa (PSAE) to develop hyperdynamic, normotensive (mean arterial pressure [MAP] 65 mm Hg) sepsis. Norepinephrine was used to achieve 10-15 % increase in MAP. Mesenteric arterial blood flow (Q(gut)), ileal mucosal microvascular perfusion (LDF(gut)) and ileal-end-tidal PCO(2) gap (PCO(2) gap) were measured before norepinephrine, after 60 min of norepinephrine infusion and 60 min after norepinephrine infusion had been discontinued. During a 12 h period of PSAE infusion all pigs developed hyperdynamic circulation with significantly decreased MAP. Although the mesenteric blood flow remained unchanged, infusion of PSAE resulted in a gradual fall of ileal microvascular perfusion, which was associated with progressively rising PCO(2) gap. Norepinephrine which induced a 10-15 % increase in perfusion pressure (i.e. titrated to attain near baseline values of MAP) affected neither Q(gut) nor the intestinal blood flow distribution (Q(gut)/CO). Similarly, norepinephrine did not change either LDF(gut) or PCO(2) gap. In this hyperdynamic, normotensive porcine bacteremia, norepinephrine-induced increase in perfusion pressure exhibited neither beneficial nor deleterious effects on intestinal macrocirculatory blood flow and ileal mucosal microcirculation. The lack of changes suggests that the gut perfusion was within its autoregulatory range.     

Intestinal cholesterol esterase: intracellular enzyme or contamination of cytosol by pancreatic enzymes?

The location of cholesterol esterase in rabbit intestine was re-evaluated. In three different experiments that were designed to eliminate contaminating mucus and pancreatic enzymes from the lumen of the small intestine, it was observed that the activities of cholesterol esterase and amylase in intestinal cytosol and whole homogenate decreased in parallel fashion. After the mucus was carefully wiped from the intestinal mucosa prior to the preparation of cytosol, amylase and cholesterol esterase activities decreased sevenfold. The recovery of the total activity of both enzymes in the cytosol was approximately 15%. When the lumen of the small intestine was filled with phosphate buffer and incubated at 37 degrees C for 20 min, cholesterol esterase and amylase activities in the cytosol prepared from this segment were further decreased. Moreover, the activities of amylase and cholesterol esterase were completely recovered from the lumen. Amylase and cholesterol esterase activities in the cytosol were eliminated if dithiothreitol was used as a mucolytic agent to prepare intestinal mucosa for the isolation of intestinal cells. In whole homogenates prepared from these intestinal segments, approximately 10-15% of the total cholesterol esterase activity remained. This activity, which could not be accounted for by pancreatic contamination, was associated with intestinal nuclei and cellular debris. Progesterone, ethinyl estradiol, and 25-hydroxycholesterol regulated microsomal acyl CoA:cholesterol acyltransferase activity and caused similar directional changes in the rate of cholesteryl ester synthesis in isolated intestinal cells. These same sterols, however, failed to affect cytosolic cholesterol esterase activity in vitro.     

Intestinal handling of a glucose gavage by the rat

An oral gavage of either 3, 1 or 0.1 mmoles of ¹⁴C-labelled glucose was given to rats under standard feeding conditions or food deprived for 24 hr. The fate of the glucose label was determined at 10, 15, 30 and 60 min after gavage; at 60 min 40% of the glucose was absorbed in fed rats (60% in food deprived). The portal vein blood flows were determined and the levels of glucose, lactate, alanine and pyruvate, and their radioactivity, as well as that of CO, were measured in both portal and arterial blood.The net computed glucose and 3-carbon carriers (lactate, alanine and pyruvate) actually released into the portal system by the intestine was lower than the amount of glucose taken up from the intestinal lumen in one hour. Oxidation to ¹⁴CO₂ accounted for a 12–15% of the absorbed glucose. The size of the gavage deeply affected the proportion of glucose released into the portal blood (c. 50% with a 3 mmoles gavage and practically nil with a 0.1 mmoles gavage), but it affected much less the generation of lactate and other 3 C carriers. In fed rats, the net intestinal balance of non-radioactive glucose was negative, and that of lactate positive; when radioactive glucose was considered, the pattern was inverted. In starved rats, both glucose and lactate were released in large proportions by the intestine, but alanine efflux was lower.It can be concluded that the intestine consumes a considerable proportion of glucose in the fed state. Glucose handling by the intestine is compartmentalized in two functional circuits: glucose is taken up from the arterial blood and used for intestinal metabolism and lactate production, luminal glucose is absorbed mainly unaltered and transferred to the portal blood. Thus, the generation of lactate is mainly related to the availability of arterial glucose. In addition to the release of the ingested glucose as 3 C carriers or glucose, an extraportal pathway for glucose transfer into the bloodstream is postulated.     

兔急性肠道缺血再灌注损伤模型的建立

目的:建立小肠急性缺血再灌注损伤模型,确定合适的肠系膜上动脉阻断时间.方法:将70只新西兰兔随机按不同的肠系膜缺血时间(0、15、30、45、60min)分为A、B、C、D、E5组,每组14只,取8只用于恢复血供2h后留取各组兔下腔静脉血标本及肠组织,检测血清中MDA含量的变化,光镜下观察小肠组织形态学变化并对小肠黏膜损伤程度进行评分.另6只用于术后24h、 48h及72h生存率的观察.结果:A、B、C组的术后生存率均>83.3%.C、D、E组的MDA含量及肠黏膜损伤评分与A组比较,差异均有显著性(F=12.13～280.24,p<0.01).结论:肠系膜缺血30min,再灌注2h是建立兔小肠急性再灌注损伤的合适时间.     

Absorption, transportation and digestion of egg white in quail embryos

The present study was done to reveal how egg white is taken up by embryonic tissues, the pathway through which egg white is transported, and the location where it is digested during the development of the quail Coturnix japonica. Antiserum against quail ovalbumin was raised in rabbit and used as a probe. By immunoelectron microscopy, the uptake of ovalbumin on a small scale by receptor-mediated endocytosis was observed in the ectodermal cells of the yolk sac on days four to seven of incubation. The uptake of egg white on a large scale by fluid-phase endocytosis took place in the cells generally referred to collectively as the 'albumen sac'. The ovalbumin was transported through the albumen sac into the extraembryonic cavity during days eight to 10, and then into the amniotic cavity through the amnion approximately on day 10. Ovalbumin was present in the intestinal lumen on days 11 and 14, but it was not digested in the intestinal epithelial cells. The ovalbumin was detected in the yolk of embryos after day 10. Immunoblot testing, as well as a fluoroimmunoassay, revealed that the location where the amount of ovalbumin was highest changed chronologically from the extraembryonic cavity on day 10 to the amniotic cavity on day 11, the intestinal lumen on day 12 and then to the yolk on day 13. Several low molecular proteins which cross-reacted with the antiserum were observed in the extracts of the yolk. The reaction producing these proteins depended on low pH (approximately 3.0) and was inhibited by pepstatin A. The ovotransferrin was similarly digested. These results indicate that egg white is, for the most part, transported through the albumen sac to the yolk via the extraembryonic cavity, the amniotic cavity, and the intestinal lumen, and is digested in the yolk by aspartic proteinases.     

Appearance of intraportally infused [15N]urea in blood and urine of domestic fowl

The time course of the occurrence of intraportally infused [15N]urea in blood and urine was investigated in chickens. The infused urea appeared in ureteral urine, mostly in the form of urea, as early as 30 min after the start of infusion and the excretion further increased up to the end of 2 hr infusion. Blood urea concentration rapidly increased and reached about three times the initial level at the end of the experiment (P < 0.05 after 20 min), but no significant effects were observed on uric acid, ammonia and glutamine concentrations. Fifty-seven percent of blood urea N and 3% of blood glutamine-amide N and 1% of blood ammonia N, which were determined at the end of experiment, were derived from the infused urea N. It is concluded that urea, which is rapidly increased in blood and urine after feeding urea to chickens, is mostly derived from dietary urea.     

The effect of intestinal ischemia duration on changes in plasma antioxidant defense status in rats

The purpose of this study was to follow up the changes in antioxidative adaptive mechanisms induced by various periods of small intestinal ischemia in Wistar rats. The superior mesenteric artery was occluded for 15, 30, 45, 60 and 90 min. After the respective ischemic intervals, a reperfusion was set for 120 min. Samples of the serum and intestinal mucosa were taken at the end of ischemia or at the end of reperfusion. Total radical-trapping antioxidant parameter (TRAP) of the serum and the oxidative burst of neutrophils were evaluated using luminol-enhanced chemiluminescence. Individual antioxidants in the serum and the concentration of thiobarbituric acid reactive substances (TBARs) in both serum and intestinal mucosa were measured spectrophotometrically. Increased activation of circulating neutrophils was found after the reperfusion irrespective of the duration of ischemia. TRAP of the serum was increased at the end of the ischemia lasting from 30 to 90 min. This effect was further enhanced by the subsequent reperfusion period. Ascorbate and urate contributed considerably to the TRAP value especially after reperfusion following 60 and 90 min of ischemia. On the other hand, no significant changes in albumin and bilirubin serum concentrations were observed. Contrary to the mobilized antioxidative mechanisms, increased lipid peroxidation was observed in both serum and mucosa samples.     

Salicylate as an in vivo free radical trap: studies on ischemic insult to the rat intestine.

Ischemia of rat intestine was induced in vivo by occlusion of the superior mesenteric artery (SMA) for 15 min. Sodium salicylate, 100 mg/kg, given IP, 30 min prior to the ischemic event served as a specific trap for hydroxyl radicals. Portions of the bowel were sequentially isolated and removed--2 min prior to ischemia, 2 min prior to declamping of the SMA, and 10 min following reperfusion. The bowel segments were homogenized in 3% TCA. The homogenate was centrifuged and filtrated through a 0.22 mu filter. The hydroxylation products of salicylate, dihydroxybenzoic acid (DHBA) derivatives, were isolated, identified, and quantified by HPLC coupled with electrochemical detection (ECD). The level of 2,5-DHBA (M +/- SE, ng/g tissue) in the preischemic bowel (N = 21) was 241.8 +/- 10.0. In the ischemic specimen the level of 2,5-DHBA increased significantly to 313.3 +/- 15.5 (p = 0.0129), and remained unchanged in the reperfusion period (322.8 +/- 15.5). The histological examination correlated well with these levels: mild villi damage in the ischemic period with no further exacerbation during the reperfusion period. This study in an in vivo animal model of intestinal ischemia-reperfusion provides direct evidence for the involvement of free radicals during the ischemic insult.     

Differential arterial blood flow response of splanchnic and renal organs during low-intensity cycling exercise in women

To investigate the regional hemodynamic responses of abdominal arteries at the onset of exercise and to focus on their transient responses, eight female subjects (21-30 yr) performed ergometer cycling exercise at 40 W for 4 min in a semi-supine position. Mean blood velocities (MBVs) in the right renal (RA), superior mesenteric (SMA), and splenic (SA) arteries were measured by pulsed echo-Doppler ultrasonography, with beat-by-beat measurements of heart rate (HR) and mean arterial pressure (MAP). The vascular resistance index (RI) of each artery was calculated from MBV/MAP. MAP (76 +/- 9 to 83 +/- 8 mmHg at 4 min) and HR (60 +/- 7 to 101 +/- 9 beats/min at 4 min) increased during exercise (P < 0.05). The MBV of RA and SA rapidly decreased after the onset of exercise (30 s; -19 +/- 5% and -19 +/- 12%, respectively), reaching -27 +/- 7% and -27 +/- 15% at the end of exercise (P < 0.05). RI did not change during the initial 30 s of exercise, reflecting a reduction in MAP, and increased toward the end of the exercise (+55 +/- 21% and +59 +/- 39%, respectively). In contrast, both the MBV and RI in the SMA remained constant throughout the exercise. The results indicate that, whereas the responses of renal and splenic vessels changed similarly throughout the protocol, the vascular response of SMA that mainly supplies blood to the intestinal tract was unchanged during exercise. We, therefore, conclude that low-intensity cycling exercise resulted in differential blood flow responses in arteries supplying the abdominal organs.     

Analytical method for monitoring concentrations of cyclosporin and lovastatin in vitro in an everted rat intestinal sac absorption model

Cyclosporin A (CSA) and lovastatin (LV) are lipophilic drugs, which show poor and erratic absorption when administered perorally. The permeability of these compounds can be increased transiently by altering the membrane characteristics of the absorptive epithelium by the use of sorption promoters (SPs). In the present work a simple validated HPLC method utilizing an isocratic mobile phase with short retention times for CSA and LV was developed in order to monitor their concentrations in Kreb's Ringer bicarbonate (KRB) solution in vitro in intestinal sac absorption model. The same method was utilized to determine the apparent permeability coefficients and absorption profiles of CSA and LV by a modified Wilson-Wiseman method. Drugs were analysed by a reversed-phase HPLC method using a Shim-pack C18 column. An isocratic mobile phase containing acetonitrile and water in the proportions 70:30 and 80:20 was used for the HPLC analysis of CSA and LV, respectively. The flow-rate was 2 ml/min and quantitative determinations were carried out at 215 nm at 70 degrees C for CSA. In the case of LV the flow-rate was 1 ml/min and detection was done at 238 nm at 25 degrees C. The method was found to be specific as none of the proposed SPs, components of KRB or intestinal sac artefacts interfered with the drug peaks. Recovery studies and intra- and inter-day variations were within statistical limits. The limits of detection were 250 and 10 ng/ml and the limits of quantitation were 400 and 30 ng/ml for CSA and LV, respectively. The calibration curve was found to be linear in concentration range of 0.5-6 microg/ml for CSA and 0.05-0.4 microg/ml for LV. The proposed method was found to be rapid and selective and hence can be applied for continuous monitoring of CSA and LV in vitro in intestinal sac absorption studies.     

Validation of ⁹⁹mTechnetium-labeled mebrofenin hepatic extraction method to quantify meal-induced splanchnic blood flow responses using a porcine model

The aim of this study was to evaluate the measurement of the total splanchnic blood flow (SBF) using a clinical diagnostic method based on Fick's principle and hepatic extraction of 99mTc-mebrofenin (99mTc-MBF) compared with a paraaminohippuric acid (pAH) dilution method in a porcine model. Another aim was to investigate whether enterohepatic cycling of 99mTc-MBF affected the SBF measurement. Five indwelling catheters were placed in each pig (n = 15) in the portal, mesenteric, and hepatic veins, as well as in the aorta and the vena cava. The SBF was measured using both methods. The portal blood flow; the intestinal and hepatic oxygen uptake; the net fluxes of oxygen, lactate, and glucose; and the extraction fraction (EF) of 99mTc-MBF were measured before and for 70 min after feeding. The mean baseline SBF was 2,961 ml/min vs. 2,762 ml/min measured by pAH and 99mTc-MBF, respectively, and increased significantly to 3,977 ml/min and 3,981 ml/min postprandially. The hepatic EF of 99mTc-MBF decreased from 40% at the start of the investigation to 16% 70 min after feeding. The arterial-portal difference in 99mTc-MBF concentration was 0.21% (P = 0.48), indicating no intestinal extraction or metabolism. The clinical method for measuring the SBF based on hepatic 99mTc-MBF extraction is robust compared with the indicator dilution method, despite the decrease seen in hepatic extraction of 99mTc-MBF. Because there was no difference in the content of 99mTc-MBF between the arterial and portal vein plasma, the SBF can be calculated from an arterial and a hepatic vein sample.     

Alterations of intestinal motor responsiveness in a model of mild mesenteric ischemia/reperfusion in rats

In this study we investigate the changes in intestinal motor responsiveness after mild mesenteric ischemia/reperfusion in anaesthetized rats. Motor responsiveness to pharmacological/electrical stimulation was studied in isolated ileum excised from sham-operated rats or animals which underwent occlusion of superior mesenteric artery (1 h) plus interruption of collateral blood flow and reperfusion for 0, 24, 72 h. Only 24 h reperfusion resulted in a significant suppression in acetylcholine induced contractile response and in indomethacin induced relaxation. In the presence of adrenergic and cholinergic blockade a greater relaxant response to field stimulation (trains 10 s every min, 120 mA, 1 ms and 10 Hz) was unmasked in all groups except 24 h reperfused rats. Such effect was sensitive to N(G)-Nitro-L-arginine methyl ester (NOS unselective inhibitor) and the proteolytic enzyme alpha-chymotrypsin but resistant to aminoguanidine (iNOS selective inhibitor). In conclusion, in this rat model, intestinal mild ischemia/24 h reperfusion induces reversible changes in enteric motility attributable to a decrease in eicosanoids, nitric oxide and neuropeptides availability.