Mechanical Intestinal Obstruction in a Porcine Model: Effects of Intra-Abdominal Hypertension. A Preliminary Study

Introduction

Mechanical intestinal obstruction is a disorder associated with intra-abdominal hypertension and abdominal compartment syndrome. As the large intestine intraluminal and intra-abdominal pressures are increased, so the patient’s risk for intestinal ischaemia. Previous studies have focused on hypoperfusion and bacterial translocation without considering the concomitant effect of intra-abdominal hypertension. The objective of this study was to design and evaluate a mechanical intestinal obstruction model in pigs similar to the human pathophysiology.

Materials and Methods

Fifteen pigs were divided into three groups: a control group (n = 5) and two groups of 5 pigs with intra-abdominal hypertension induced by mechanical intestinal obstruction. The intra-abdominal pressures of 20 mmHg were maintained for 2 and 5 hours respectively. Hemodynamic, respiratory and gastric intramucosal pH values, as well as blood tests were recorded every 30 min.

Results

Significant differences between the control and mechanical intestinal obstruction groups were noted. The mean arterial pressure, cardiac index, dynamic pulmonary compliance and abdominal perfusion pressure decreased. The systemic vascular resistance index, central venous pressure, pulse pressure variation, airway resistance and lactate increased within 2 hours from starting intra-abdominal hypertension (p<0.05). In addition, we observed increased values for the peak and plateau airway pressures, and low values of gastric intramucosal pH in the mechanical intestinal obstruction groups that were significant after 3 hours.

Conclusion

The mechanical intestinal obstruction model appears to adequately simulate the pathophysiology of intestinal obstruction that occurs in humans. Monitoring abdominal perfusion pressure, dynamic pulmonary compliance, gastric intramucosal pH and lactate values may provide insight in predicting the effects on endorgan function in patients with mechanical intestinal obstruction.     

PCT及CRP在急性肠梗阻大鼠血清中的表达水平及其临床意义

目的:探讨降钙素原(Procalcitonin,PCT)及C反应蛋白(C-reactive protein,CRP)在急性肠梗阻大鼠血清中的水平及其临床意义。方法:将83只Wistar大鼠分为对照组(n=13)、假手术组(n=35)和急性肠梗阻组(n=35)。对照组大鼠采集标本后处死,肠梗阻组行开腹手术结扎回肠末端,假手术组仅行开腹手术。检测8 h、24 h、48 h、72 h及96 h血清PCT及CRP水平,观察急性肠梗阻大鼠回肠组织的病理学改变情况。结果:假手术组PCT与CRP水平在术后24 h内显著升高,48 h至96 h逐渐下降;各时间点PCT水平明显高于对照组,而CRP水平在实验结束时已恢复至正常水平。肠梗阻组PCT和CRP水平在各时间点均明显高于对照组,并逐渐增加,到实验结束时达到高峰;肠梗阻组PCT和CRP水平在48 h-96 h均显著高于假手术组,差异具有统计学意义(P0.05)。组织病理学检查显示,对照组大鼠肠壁粘膜结构正常,假手术组可见轻度病理改变,肠梗阻组大鼠回肠组织可见粘膜结构明显破坏,绒毛坏死,严重水肿和炎症细胞浸润。结论:血浆PCT和CRP水平能够反映肠梗阻的状态和肠粘膜受损程度。     

Incomplete intestinal obstruction as the possible main complaint in Behcet’s disease after surgery for recurrent abdominal aortic pseudoaneurysms: a case report and literature review

Background

Behcet’s disease (BD) is a systemic vasculitis characterized by oral and genital aphthosis, and ocular and skin lesions. The disease is involved in vascular, gastrointestinal, and central nervous systems. Vasculitis may exacerbate fatal problems, such as anastomotic pseudoaneurysms. If the mesenteric vessels are involved, severe abdominal symptoms such as intestinal obstruction may occur.

Case presentation

This case report describes a young female patient who suffered from BD with recurrent abdominal aortic pseudoaneurysms, as well as deep venous thrombosis and subsequent complications of incomplete intestinal obstruction. This patient first underwent stent grafting, which was followed by rupture of two newly formed anastomotic pseudoaneurysms within six months. Emergency open surgical repair (OSR) was then performed on the ruptured pseudoaneurysms. Thrombosis and incomplete ileus occurred five months after surgery. This case was unique due to the presence of incomplete intestinal obstruction being the possible main complaint for a patient with Behcet’s disease, and it is the first ever case to be reported.

Conclusion

Intestinal obstruction may present as the possible main complaint in BD. Careful and attentive strategy should be carried out to prevent fatal outcomes.

     

Inhibition of the biosynthesis of uroporphyrinogen and heme in rat liver during obstructive jaundice produced by bile duct ligation

Altered hepatic microsomal drug metabolism has been reported to occur in afflicted with hyperbilirubinemia. Similarities of the chemical structures of hydroxymethylbilane, an intermediate in the biosynthesis of uroporphyrinogen, to bilirubin prompted investigations of the effect of bilirubin on the activity of uroporphyrinogen I synthase (porphobilinogen deaminase, EC 4.3.1.8) and the biosynthesis of heme. Bilirubin was found to be a reversible, noncompetitive inhibitor of uroporphyrinogen I synthase. The inhibition constant (Ki) for bilirubin was 1.5 microM. Bile acids had no effect on rat hepatic uroporphyrinogen I synthase activity. Hyperbilirubinemia was achieved in rats by biliary ligation in order to investigate whether elevated levels of bilirubin impair the biosynthesis of hepatic heme in vivo. The relative rate of heme biosynthesis, as measured by the rate of incorporation of delta-[4-14C]aminolevulinic acid into heme, was decreased 59% 24 h after biliary obstruction. The levels of hepatic microsomal heme and cytochrome P-450 were decreased by 43 and 40%, respectively, 72 h after biliary obstruction. The activities of hepatic delta-aminolevulinic acid synthase and uroporphyrinogen I synthase were increased by 39 and 46%, respectively, 72 h after biliary obstruction. During the 48- to 72-h period following biliary obstruction, the urinary excretion of porphobilinogen and uroporphyrin was increased 3.0- and 3.5-fold, respectively, whereas, the urinary excretion of delta-aminolevulinic acid was not altered. During this 48-to 72-h time interval following biliary obstruction, 100% of the uroporphyrin was excreted as isomer I. These results indicate that bilirubin is capable of depressing the biosynthesis of rat hepatic heme and thus cytochrome P-450-mediated drug metabolism by inhibition of the formation of uroporphyrinogen. These findings are a plausible mechanism for reports of impaired clearance of various drugs in patients afflicted with hyperbilirubinemic disease states.     

Host Responses to Intestinal Microbial Antigens in Gluten-Sensitive Mice

Background and Aims

Excessive uptake of commensal bacterial antigens through a permeable intestinal barrier may influence host responses to specific antigen in a genetically predisposed host. The aim of this study was to investigate whether intestinal barrier dysfunction induced by indomethacin treatment affects the host response to intestinal microbiota in gluten-sensitized HLA-DQ8/HCD4 mice.

Methodology/Principal Findings

HLA-DQ8/HCD4 mice were sensitized with gluten, and gavaged with indomethacin plus gluten. Intestinal permeability was assessed by Ussing chamber; epithelial cell (EC) ultra-structure by electron microscopy; RNA expression of genes coding for junctional proteins by Q-real-time PCR; immune response by in-vitro antigen-specific T-cell proliferation and cytokine analysis by cytometric bead array; intestinal microbiota by fluorescence in situ hybridization and analysis of systemic antibodies against intestinal microbiota by surface staining of live bacteria with serum followed by FACS analysis. Indomethacin led to a more pronounced increase in intestinal permeability in gluten-sensitized mice. These changes were accompanied by severe EC damage, decreased E-cadherin RNA level, elevated IFN-γ in splenocyte culture supernatant, and production of significant IgM antibody against intestinal microbiota.

Conclusion

Indomethacin potentiates barrier dysfunction and EC injury induced by gluten, affects systemic IFN-γ production and the host response to intestinal microbiota antigens in HLA-DQ8/HCD4 mice. The results suggest that environmental factors that alter the intestinal barrier may predispose individuals to an increased susceptibility to gluten through a bystander immune activation to intestinal microbiota.     

Resveratrol protects vascular endothelial cell from ox-LDL-induced reduction in antithrombogenic activity

Dietary antioxidants are thought to be beneficial in reducing the incidence of coronary heart disease. In this study, the antithrombogenic endothelial cells (EC) defense was investigated in an experiment model in which cultured endothelial cells were incubated with aggregating platelets in the aggregometer. We examined the possible protective effect of trans-resveratrol (RSV) on oxidized low density lipoprotein (ox-LDL)-induced insults on the antithrombogenic activity of the vascular EC. EC were treated with ox-LDL (25-100 microg/ml) for 1 h with or without a 30 min-preexposure to RSV. The antiplatelet property of the endothelial cells was then shown by measuring platelet aggregation, [Ca2+]i and cGMP contents in the platelets and EC. Exposure of EC to ox-LDL reduced the antiplatelet aggregating property of EC, and this effect was attenuated by pretreatment with RSV. Further studies revealed that exposure of EC to ox-LDL reduced the protein contents of endothelial nitric oxide synthase (NOS). The effect of ox-LDL on the NOS protein content was abrogated by pretreating EC with RSV. The results suggest that ox-LDL acts via reducing the endothelial NOS activity to suppress the antithrombogenic activity of the EC.     

Epinephrine infusion induces hyporesponsiveness of vascular smooth muscle

Exposure to vasoactive drugs may lead to desensitization of vascular smooth muscle responsiveness. We have explored this phenomenon by infusing epinephrine into awake rabbits for 2h and then assessing smooth muscle contraction, both in vivo and ex vivo. Epinephrine was infused at a rate of 1 microgram X min-1 which resulted in a 15-fold increase in the plasma epinephrine concentration. The dose of phenylephrine required to cause a 25 mmHg increase in mean arterial pressure significantly increased from 109 +/- 56 micrograms prior to the infusion to 261 +/- 143 at the end of the 2h infusion (p less than 0.01). The sensitivity to phenylephrine remained decreased when reassessed 2h later. Untreated rabbits displayed no change in alpha-adrenergic responsiveness when assessed at 2 hourly intervals over the time-course of the experiment. Contraction of aortic rings removed from both epinephrine-treated and control rabbits was determined in vitro in tissue baths. The EC50 of norepinephrine-induced contraction increased from 31 +/- 6 to 210 +/- 20 nM while there was also a 30% decrease in the maximal force of contraction (EMax) in treated vessels. The EC50 only partially recovered after 4h of incubation ex vivo, while the EMax was restored to the control value. The EC50 for histamine in the aortic rings from epinephrine-treated rabbits was not different from controls although there was a 25% reduction in the EMax at 2h. We conclude that desensitization of alpha-adrenergic mediated vascular contractility develops rapidly in vivo and is only slowly reversible after removal of the agonist.     

奥曲肽治疗急性粘连性肠梗阻疗效观察

目的:探讨生长抑素对腹部手术后急性粘连性肠梗阻的治疗作用。方法:70例急性粘连性肠梗阻患者随机分为观察组与对照组各35例。对照组予胃肠减压、灌肠、补液及抗感染治疗等常规治疗;观察组在此基础上加用奥曲肽(生长抑素类似物)0.1 mg皮下注射,每8h一次,治疗72 h。观察两组患者腹痛评分、腹痛缓解时间、胃肠减压量、肛门恢复排气时间、立卧位腹部平片、临床缓解情况。结果:观察组34例(97.1%)临床缓解,明显高于对照组的28例(80.0%)(P<0.05)。与对照组相比,观察组在治疗第1、2天后腹痛评分明显下降(均为P<0.01),腹痛缓解时间显著缩短(P<0.01),治疗第1、2、3天的胃肠减压量均显著减少(均为P<0.01),恢复排气时间也明显缩短(P<0.01)。结论:急性粘连性肠梗阻在常规治疗基础上加用生长抑素,可明显改善临床症状,提高疗效。     

(−)-Epicatechin mitigates radiation-induced intestinal injury and promotes intestinal regeneration via suppressing oxidative stress

Abstract

The high radiosensitivity of the intestinal epithelium limits the survival of victims by nuclear accidents or terrorism and limits effective radiotherapy against abdominal malignancies. Recently, we reported that (?)-epicatechin (EC) modulates oxidative stress and exerts neuroprotection. Here, we investigate the protective effects of EC against intestinal damage induced by radiation. The established model is acute moderate but reversible intestinal injury damage. We also set up the injured model of “minigut” ex vivo, which mimic the process of intestinal regeneration in vivo. We found that EC can repress oxidative stress by regulating SOD and MDA levels in serum and intestine tissue. Correspondingly, EC can decrease apoptosis of crypt cells in Lgr5-EGFP-IRES-creERT2 mice after radiation. Further studies demonstrated that EC can promote Nrf2 translocation from cytoplasm to nuclear and then activate the expression of HO1 and NQO1. Interestingly, EC can enhance the activity of intestine stem cells labelled by Lgr5 and promote intestinal epithelium regeneration determined by HE and immunofluorescence staining in vivo and in vitro. We also found that EC can activate the Wnt/β-catenin signal pathway confirmed by TCF/LEF luciferase reporter assay. Together, EC can provide the protective effect on intestine and promote intestinal regeneration after radiation through Nrf2 and Wnt/β-catenin signal pathway.     

Intestinal response to 1 alpha, 25-dihydroxycholecalciferol. I. RNA polymerase, alkaline phosphatase, calcium and phosphorus uptake in vitro, and in vivo calcium transport and accumulation

The dynamics of intestinal response in rachitic chicks to 1alpha,25-dihydroxycholecalciferol were evaluated by various biochemical parameters. The following observations were made: 1. The earliest detected intestinal response to 1alpha,25-dihydroxycholecalciferol was increased in vitro calcium uptake and in vivo calcium transport, occurring by 2 h and 2.5 h respectively. 2. Increased RNA polymerase activity was observed by 4 h after 1alpha,25-dihydroxycholecalciferol treatment. 3. Calcium binding protein was detected by 5 h, but could not be detected 2.5 h after 1alpha,25-dihydroxycholecalciferol treatment. 4. Increased alkaline phosphatase activity and in vitro accumulation of inorganic phosphate were first demonstrable 6 h after 1alpha,25-dihydroxycholecalciferol treatment. 5. In vivo duodenal calcium accumulation in the mucosa was elevated after 5 h, peaked at 6.5 h, and then began to decrease at 9 h. In vitro duodenal calcium accumulation was elevated at 2 h, peaked at 12 h, and decreased to control level by 18 h. Our data emphasize the lack of correlation between the appearance of calcium binding protein or increased alkaline phosphatase activity and the transport rate of calcium across the duodenum after treatment with 1alpha,25-dihydroxycholecalciferol. The data suggest a correlation between duodenal calcium accumulation and the appearance of calcium binding protein or increased alkaline phosphatase activity.     

Response of microbial activity and biomass in rhizosphere and bulk soils to increasing salinity

Background and aims

The impact of salinity on microbes has been studied extensively but little is known about the response of soil microbial activity and biomass to increasing salinity in rhizosphere compared to bulk (non-rhizosphere) soil.

Methods

Barley was grown for 5 weeks in non-saline loamy sand to which salt (NaCl) was added. The electrical conductivity in the saturated extract (ECe) was 1, 13 and 19 dS m^?1 for non-saline and two saline soils. Pots without plants were prepared in the same manner and placed next to those with plants. The water content in all pots was maintained at 75 % of water-holding capacity by weight. After 5 weeks the planted and unplanted pots were harvested to collect rhizosphere and bulk soil, respectively. The collected soil was then used for an incubation experiment. The EC levels in the pot experiment (EC1, EC13 and EC19, referred to as original) were either maintained or increased by adding NaCl to adjust the EC to 13, 19, 31 and 44 dS m^?1. CO₂ release was measured continuously for 20 days, microbial biomass C (MBC) was measured at the start and the end of the incubation experiment.

Results

In general, cumulative respiration and microbial biomass C concentration in rhizosphere and bulk soil decreased to a similar extent with increasing adjusted EC. However, compared to the treatments where the EC was maintained, the percentage decrease in cumulative respiration when the EC was increased to EC44 was smaller in rhizosphere than in bulk soil.

Conclusion

Overall, the reduction of cumulative respiration with increasing salinity did not differ between rhizophere and bulk soil. But microbes in rhizosphere soil were more tolerant to high EC than those in bulk soil which could be due to the greater substrate availability in the rhizosphere even after the soil was removed from the roots.     

Temporal and spatial dynamics underlying capacitative calcium entry in human colonic smooth muscle

Angiotensin converting enzyme (ACE) has been shown to be involved in regulation of apoptosis in nonintestinal tissues. This study examined the role of ACE in the modulation of intestinal adaptation utilizing ACE knockout mice (ACE-/-). A 60% small bowel resection (SBR) was used, since this model results in a significant increase in intestinal epithelial cell (EC) apoptosis as well as proliferation. Baseline villus height, crypt depth, and intestinal EC proliferation were higher, and EC apoptosis rates were lower in ACE-/- compared with ACE+/+ mice. After SBR, EC apoptosis rates remained significantly lower in ACE-/- compared with ACE+/+ mice. Furthermore, villus height and crypt depth after SBR continued to be higher in ACE-/- mice. The finding of a lower bax-to-bcl-2 protein ratio in ACE-/- mice may account for reduced EC apoptotic rates after SBR in ACE-/- compared with ACE+/+ mice. The baseline higher rate of EC proliferation in ACE-/- compared with ACE+/+ mice may be due to an increase in the expression of several EC growth factor receptors. In conclusion, ACE appears to have an important role in the modulation of intestinal EC apoptosis and proliferation and suggests that the presence of ACE in the intestinal epithelium has a critical role in guiding epithelial cell adaptive response.     

Intestinal absorption of hawthorn flavonoids--in vitro, in situ and in vivo correlations

Our previous studies identified hyperoside (HP), isoquercitrin (IQ) and epicatechin (EC) to be the major active flavonoid components of the hawthorn phenolic extract from hawthorn fruits demonstrating inhibitory effect on in vitro Cu(+2)-mediated low density lipoproteins oxidation. Among these three hawthorn flavonoids, EC was the only one detectable in plasma after the oral administration of hawthorn phenolic extract to rats. The present study aims to investigate the intestinal absorption mechanisms of these three hawthorn flavonoids by in vitro Caco-2 monolayer model, rat in situ intestinal perfusion model and in vivo pharmacokinetics studies in rats. In addition, in order to investigate the effect of the co-occurring components in hawthorn phenolic extract on the intestinal absorption of these three major hawthorn flavonoids, intestinal absorption transport profiles of HP, IQ and EC in forms of individual pure compound, mixture of pure compounds and hawthorn phenolic extract were studied and compared. The observations from in vitro Caco-2 monolayer model and in situ intestinal perfusion model indicated that all three studied hawthorn flavonoids have quite limited permeabilities. EC and IQ demonstrated more extensive metabolism in the rat in situ intestinal perfusion model and in vivo study than in Caco-2 monolayer model. Moreover, results from the Caco-2 monolayer model, rat in situ intestinal perfusion model as well as the in vivo pharmacokinetics studies in rats consistently showed that the co-occurring components in hawthorn phenolic extract might not have significant effect on the intestinal absorption of the three major hawthorn flavonoids studied.     

左半结直肠癌并急性肠梗阻经内镜介入治疗后再限期手术 的临床应用探讨

目的:探讨左半结直肠癌并急性肠梗阻经内镜介入治疗后再限期行肿瘤根治切除及一期肠吻合术的临床应用价值.方法:回顾性分析2006年-2011年我院收治的87例左半结直肠癌并急性肠梗阻的临床资料.结果:本组87例中,71例经内镜置入支架或肠梗阻导管介入减压治疗成功并完成了肿瘤根治性切除及一期肠吻合术.16例介入治疗失败行了急诊手术治疗,其中支架或导管置入失败7例,堵塞5例,减压效果差4例,无穿孔、出血并发症,介入治疗有效率81.6％.限期手术后切口感染5例(7.0％);急诊手术后切口感染4例(25.0％);吻合口漏2例(2.8％);无死亡病例发生.结论:左半结直肠癌并急性肠梗阻经内镜介入治疗后,限期行肿瘤根治性切除及一期肠吻合术,可以最大限度降低术后切口感染、吻合口漏机率,值得临床推广应用.     

Acute distal intestinal obstruction in gnotobiotic rats. Intestinal morphology and cell renewal.

1. Complete mechanical obstruction of the distal small intestine was produced in gnotobiotic rats. 72 h after the operation small intestinal morphology and epithelial cell renewal were investigated proximal and distal to the site of obstruction. 2. Proximal to the site of obstruction there were minor changes in villus height, base length and in villus cell number, a large increase in depth and diameter of the crypts and an approximately threefold increase in cell renewal. 3. Distal to the site of obstruction there were no differences between the intestines of rats with obstruction and controls. 4. The apparent lack of secretion by the goblet cells and the reduced number of intraepithelial leucocytes suggest that the barrier function of the small intestine is impaired in obstruction.     

Reduced chilling tolerance in elongating cucumber seedling radicles is related to their reduced antioxidant enzyme and DPPH-radical scavenging activity

Cucumber seedling radicles become more chilling sensitive as they elongate. Chilling seedlings with radicles 20 mm long for 48 h at 2.5°C inhibited subsequent growth by 36%, while it reduced the growth of 70 mm-long radicles by 63%. Although the growth rate of non-chilled cucumber radicles at 25°C is constant from 20 to 80 mm, tissue viability [i.e. reduction of TTC (2,3,5-triphenyltetrazolium chloride) to formazan] and DPPH ( α,α -diphenyl- β -picrylhydrazyl) radical scavenging activity of apical tissue declines as radicles elongate from 20 to 80 mm in length. TTC reduction, DPPH-radical scavenging activity and protein content of apical tissue were higher in 20 than in 70 mm radicles immediately after chilling and after an additional 48 h of growth at 25°C. Catalase (CAT; EC 1.11.1.6) and ascorbate peroxidase (APX; EC 1.11.1.11) activity was higher in the apical tissue of 20 than in 70 mm radicles before chilling. Immediately after chilling and after an additional 48 h at 25°C, superoxide dismutase (SOD; EC 1.15.1.1), glutathione reductase (GR; EC 1.6.4.2), and guaiacol peroxidase (GPX; EC 1.11.1.7) activity increased more rapidly in 70 mm radicles than in 20 mm radicles (SOD, GR, and GPX activity in 70 mm radicles was 1.5-, 1.9- and 8.6-fold higher, respectively, than in 20 mm radicles). However, APX and CAT activity in 20 mm radicles were always higher than in 70 mm radicles. Growth after chilling enhanced the activity of all antioxidant enzymes compared to that found in non-chilled tissue; however, CAT activity in 70 mm radicles did not recover to levels found in non-chilled tissue. Higher levels of CAT, APX and DPPH-radical scavenging activity are correlated with higher chilling tolerance of 20 mm-long cucumber radicles compared to 70 mm-long radicles.     

Hormonal regulation of 3-hydroxy-3-methylglutaryl coenzyme a reductase and alkaline phosphatase in cultured intestinal mucosa

The endocrine regulation of the key enzyme of cholesterol synthesis, 3-hydroxy-methylglutaryl-CoA reductase (EC 1.1.1.34) and of the brush border enzyme alkaline phosphatase (EC 3.1.3.1) was studied in short (2 h) and long tern (24 h) organ culture of rabbit ileum mucosa. In contrast to the hepatic enzyme, intestinal reductase is not subject to regulation by insulin or glucagon even at a pharmacological level. This applies to both ‘total’ and ‘active’ reductase, prepared in the absence or presence of sodium fluoride, respectively. During culture, there is a gradual, time-dependent increase in the active, dephosphorylated enzyme form. This endogenous activation was found to be unaffected by all hormones tested. Similarly, alkaline phosphatase was not influenced by both pancreatic hormones. In contrast, triamcinolone significantly (P < 0.05) suppressed reductase in a dose-dependent fashion to 38% of controls after 24 h, but not after 2 h culture. Alkaline phosphatase was induced after both periods, but the effect was more marked after 24 h. A parallel minor stimulation of both enzyme activities was noted in the presence of 10^?9 M triidothyronine (P < 0.05), lower and very high (10^?5 M) concentrations were ineffective. In view of the role of glucocorticoids as intestinal growth inhibitors and of thyroid hormones as growth stimulators, it is suggested that changes in reductase reflect alterations of crypt membrane cholesterol synthesis, whereas the induction of alkaline phosphatase is mediated through an enhanced enterocyte regeneration and/or maturation.     

Serotonin stimulates endotoxin translocation via 5-HT3 receptors in the rat ileum

Because few previous studies have investigated the mechanisms of endotoxin translocation induced by intestinal obstruction, we aimed to clarify whether or not serotonin [5-hydroxytryptamine (5-HT)], which is released from enterochromaffin (EC) cells, is responsible for alterations of the mucosal permeability to endotoxin and to identify the 5-HT receptor subtypes that mediate this action. FITC-labeled LPS (FITC-LPS) was injected into the ileum of rats, and the FITC-LPS level in the superior mesenteric vein was subsequently measured by using a fluorescence spectrophotometer. To measure the 5-HT release induced by high intraluminal pressure, ex vivo preparation of vascularly and luminally perfused rat ileum was used. Results demonstrated that elevated intraluminal pressure stimulates the translocation of FITC-LPS and the release of 5-HT from the EC cells into the intestinal lumen but not into the portal circulation. This FITC-LPS translocation, which was stimulated by exogenously applied 5-HT in the lumen and the jugular vein, was inhibited by 5-HT(3) receptor antagonist administration both intaluminally and intravenously. The stimulatory effect of elevated intraluminal pressure on the translocation of FITC-LPS was inhibited by the intraluminal and intravenous administration of 5-HT(3) receptor antagonist. These results suggest that 5-HT released from EC cells may be involved in the translocation of FITC-LPS induced by elevated intraluminal pressure and that this effect is mediated by 5-HT(3) receptors that may be located in the intestinal epithelium.     

Microbial activity and community composition in saline and non-saline soils exposed to multiple drying and rewetting events

Background and aims

The effects of drying and rewetting (DRW) have been studied extensively in non-saline soils, but little is known about the impact of DRW in saline soils. An incubation experiment was conducted to determine the impact of 1?C3 drying and re-wetting events on soil microbial activity and community composition at different levels of electrical conductivity in the saturated soil extract (ECe) (ECe 0.7, 9.3, 17.6 dS m^?1).

Methods

A non-saline sandy loam was amended with NaCl to achieve the three EC levels 21 days prior to the first DRW; wheat straw was added 7 days prior to the first DRW. Each DRW event consisted of 1 week drying and 1 week moist (50% of water holding capacity, WHC). After the last DRW, the soils were maintained moist until the end of the incubation period (63 days after addition of the wheat straw). A control was kept moist (50% of WHC) throughout the incubation period.

Results

Respiration rates on the day after rewetting were similar after the first and the second DRW, but significantly lower after the third DRW. After the first and second DRW, respiration rates were lower at EC17.6 compared to the lower EC levels, whereas salinity had little effect on respiration rates after the third DRW or at the end of the experiment when respiration rates were low. Compared to the continuously moist treatment, respiration rates were about 50% higher on day 15 (d15) and d29. On d44, respiration rates were about 50% higher at EC9.7 than at the other two EC levels. Cumulative respiration was increased by DRW only in the treatment with one DRW and only at the two lower EC levels. Salinity affected microbial biomass and community composition in the moist soils but not in the DRW treatments. At all EC levels and all sampling dates, the community composition in the continuously moist treatment differed from that in the DRW treatments, but there were no differences among the DRW treatments.

Conclusions

Microbes in moderately saline soils may be able to utilise substrates released after multiple DRW events better than microbes in non-saline soil. However, at high EC (EC17.6), the low osmotic potential reduced microbial activity to such an extent that the microbes were not able to utilise substrate released after rewetting of dry soil.     

Induction of oxidative stress and antioxidative mechanisms in Phaseolus vulgaris after Cd application.

Oxidative stress has been shown to be of great importance in the toxicity of several metals (copper, zinc, ...). In this study, the relationship of cadmium phytotoxicity and antioxidative reactions in bean (Phaseolus vulgaris L.) plants was investigated. Eleven-day-old seedlings were exposed to an environmentally realistic concentration of cadmium (2 microM CdSO(4)). Several biochemical and physiological parameters were influenced even by these low concentrations. At the biochemical level, the antioxidative defence mechanism was significantly activated after 24 h of cadmium exposure. Some enzymes able of quenching reactive oxygen species (syringaldazine peroxidase, EC 1.11.1.7; guaiacol peroxidase, EC 1.11.1.7) as well as enzymes important in the reduction of NAD(P)(+) (isocitrate dehydrogenase, EC 1.1.1.42; malic enzyme, EC 1.1.1.40) were significantly elevated by cadmium exposure. Furthermore, the ascorbate-glutathione cycle appeared to be a very important mechanism against cadmium-induced oxidative stress. In leaves, significant increases of ascorbate peroxidase (EC 1.11.1.11) and glutathione reductase (EC 1.6.4.2) and significant changes in the ascorbate and glutathione pool were observed. Morphological and other biochemical parameters (lipid peroxidation) were significantly enhanced 48 h after the start of the cadmium exposure. At the end of the experiment (72 h after the start of the metal treatment), even visual effects, such as chlorosis, were observed. The present data indicate that cadmium, like other metals, induces cellular redox disequilibrium suggesting that an environmentally realistic concentration of cadmium can cause oxidative stress.