简介：Enteralnutritionhasbeenstronglyrecommendedbymajorscientificsocietiesforthenutritionalmanagementofpatientswithacutepancreatitis.Providingsevereacutepancreatitispatientswithenteralnutritionwithinthefirst24-48hofhospitaladmissioncanhelpimproveoutcomescomparedtoparenteralnutritionandnofeeding.Newresearchisfocusinginonwhenandwhattofeedtobestimproveoutcomesforacutepancreatitispatients.Earlyenteralnutritionhavethepotentialtomodulatetheimmuneresponses.Despitethisconsistentevidenceofearlyenteralnutritioninpatientswithacutepancreatitis,clinicalpracticecontinuestovaryduetoindividualclinicianpreference.Achievingtheimmunemodulatingeffectsofenteralnutritionheavilydependonproperplacementofthefeedingtubeandmanaginganytubefeedingassociatedcomplications.Thecurrentarticlereviewstheimmunemodulatingeffectsofenteralnutritionandpro-andprebioticsandsuggestssomepracticaltoolsthathelpimprovethepatientadherenceandtolerancetothetubefeeding.Properselectionofthetypeofthetube,closemonitoringofthetubeforitsplacement,patencyandsecuringitsproperplacementandroutinecheckingthegastricresidualvolumecouldallhelpimprovetheoutcome.Usingpeptide-basedandhighmediumchaintriglyceridesfeedingformulashelpimprovingfeedingtolerance.

简介：Splanchniccirculationistheprimarymechanismthatregulatesvolumesofcirculatingbloodandsystemicbloodpressureinpatientswithcirrhosisaccompaniedbyportalhypertension.Recently,interesthasbeenexpressedinmodulatingsplanchniccirculationinpatientswithlivercirrhosis,becausethiscapabilitymightproducebeneficialeffectsincirrhoticpatientsundergoingalivertransplant.Pharmacologicmodulationofsplanchniccirculationbyuseofvasoconstrictorsmightminimizevenouscongestion,replenishcentralbloodflow,andthusoptimizemanagementofbloodvolumeduringalivertransplantoperation.Moreover,splanchnicmodulationminimizesanyhighportalbloodflowthatmayoccurfollowingliverresectionandthesubsequentlivertransplant.Thiseffectissignificant,becausehighportalflowimpairsliverregeneration,andthusadverselyaffectsthepostoperativerecoveryofatransplantpatient.Anincreaseinportalbloodflowcanbeminimizedbyeithersurgicalmethods（e.g.,splenicarteryligation,splenectomyorportocavalshunting）oradministrationofsplanchnicvasoconstrictordrugssuchasVasopressinorterlipressin.Finally,modulationofsplanchniccirculationcanhelpmaintainperioperativerenalfunction.Splanchnicvasoconstrictorssuchasterlipressinmayhelpprotectagainstacutekidneyinjuryinpatientsundergoinglivertransplantationbyreducingportalpressureandtheseverityofahyperdynamicstate.Theseeffectsareespeciallyimportantinpatientswhoreceiveatoosmallforsizegraft.TerlipressinselectivelystimulatesV1receptors,andthuscausesarteriolarvasoconstrictioninthesplanchnicregion,withaconsequentshiftofbloodfromsplanchnictosystemiccirculation.Asaresult,terlipressinenhancesrenalperfusionbyincreasingbotheffectivebloodvolumeandmeanarterialpressure.

简介：AIM:Toassessthemechanismsofprotectiveactionbydifferentmildirritantsthroughmaintenanceofgastricmucosalintegrityandmodulationofmucosalnitricoxide(NO)inexperimentalgastritisrats.METHODS:Etcher200mL/Lethanol,50g/LNaGor0.3mol/LHClwaspretreatedtonormalor800mL/Lethanol-inducedacutegastritisSprague-Dawleyratsbeforeasubsequentchallengewith500mL/Lethanol.Bothmacroscopiclesionareasandhistologicaldamagescoresweredeterminedinthegastricmucosaofeachgroupofanimals.Besides,gastricmucosalactivitiesofNOsynthaseisoformsandofsuperoxidedismutase,alongwithmucosallevelofleukotriene(LT)C4weremeasured.RESULTS:Macroscopicmucosaldamageswereprotectedby200mL/Lethanoland50g/LNaCIingastritisrats.However,although200mL/Lethanolcouldprotectthesurfacelayersofmucosalcellsinnormalanimals(protectionattenuatedbyNG-nitro-L-argininemethylester),nocytoprotectionagainstdeeperhistologicaldamageswasfoundingastritisrats.Besides,inducibleNOsynthaseactivitywasincreasedinthemucosaofgastritisanimalsandunalteredbymildirritants.Nevertheless,theelevationinmucosalLTC4levelfollowing500mL/Lethanoladministrationandundergastritisconditionwassignificantlyreducedbypretreatmentofallthreemildirritantsinbothnormalandgastritisanimals.CONCLUSION:Thesefindingssuggestthattheaggravated500mL/Lethanol-evokedmucosaldamagesundergastritisconditioncouldbeduetoincreasedinducibleNOandLTC4productioninthegastricmucosa.Only200mL/Lethanolistruly'cytoprotective'atthesurfaceglandularlevelofnongastritismucosa.Furthermore,themacroscopicprotectionofthethreemildirritantsinvolvesreductionofLTC4levelinbothnormalandgastritismucosa,implicatingpreservationofthevasculature.

简介：AIM:Toinvestigatetheabilityofproteaseinhibitorstomodulatehistaminereleasefromhumancolonmastcells.METHODS:Enzymaticallydispersedcellsfromhumancolonwerechallengedwithanti-IgEorcalciumionophoreA23187intheabsenceorpresenceoftryptaseandchymaseinhibitors,andhistaminereleasewasdetermined.RESULTS:IgEdependenthistaminereleasefromcolonmastceilswasinhibitedbyuptoapproximately37%,26%and36.8%bychymaseinhibitorsZ-Ile-Glu-Pro-Phe-CO2Me(ZIGPFM),N-TosyI-L-phenylalanyl-chloromethylketone(TPCK),andC~l-antitrypsin,respectively.Similarly,inhibitorsoftryptaseleupeptin,N-tosyI-L-lysinechloromethylketone(TLCK),lactoferrinandprotaminewerealsoabletoinhibitanti-IgEinducedhistaminereleasebyamaximumofsome48%,37%,40%and34%,respectively.Preincubationoftheseinhibitorswithcellsfor20rainbeforechallengedwithanti-IgEhadsmalleffectontheinhibitoryactionsoftheseinhibitorsoncolonmastcells.Aspecificinhibitorofaminopeptidaseamastatinhadnoeffectonanti-IgEinducedhistaminerelease.Thesignificantinhibitionofcalciumionophoreinducedhistaminereleasewasalsoobservedwiththeinhibitorsoftryptaseandchymaseexamined.Apartfromleupeptinandprotamine,theinhibitorstestedbythemselvesdidnotstimulatecolonmastcells.CONCLUSION:ItwasdemonstratedthatbothtryptaseandchymaseinhibitorscouldinhibitIgEdependentandcalciumionophoreinducedhistaminereleasefromdispersedcolonmastcellsinaconcentrationdependentofmanner,whichsuggestthattheyarelikelytobedevelopedasanovelclassofanti-inflammatorydrugstotreatchronicofcolitisinman.