The Clinic Significance Of IL-8,IL-18,ET,NO And Endotoxin Determination In The Serum Of Hepatic Cirrhosis Patients Infected HP

The defence capability of the chronic liver disease patient degrade,so it cancause the changes of bacterioflora in the bowels and the changes of all kinds ofcytokine includes endotoxemia easily. The human leukocyte chemotaxis ofpatients also degrades, the lysatin produced by lercocyte neutrophil also decreases,the defence ability to the infection degrades,so it can easily cause all kinds ofinfections,and because the haemodynamics changes caused by hyperdynamiccirculation of petrol veins,all kinds of gastric mucosa diseases hanppened. Nowpeople have allround comprehended to the epidemiology of the infection of HP.But the reports of the dependablity between HP infection and hyperdynamiccirculation of petrol veins and gastric mucosa diseases are so differents. So thisexperiment choose 60 chronic liver disease patients which liver function iscompensation ,and then use 14C-carbamide breath test and HP antibodyimmunoblot to detect HP infected informations in the chronic liver diseasepatients,and at the same time we detect the level of all kinds of cytokine in theperipheral serum and some haemodynamics index of petrol circulation the chronicliver patients ,then compare the differents between the negative group andmasculine group of HP infection. So it can not only quantizate the dependabilitybetween the HP infection and the hyperdynamic circulation of petrol veins andgastric mucosa diseases ,but also approach how can HP infection induce thehyperdynamic circulation of petrol veins and gastric mucosa diseases from theangle of cytokine.This experiment discover that the level of IL-8,IL-18,NO,ET,endotoxinin the masculine group obviously higher than the negative group,so it indicate thatthe generation and development of the hepatic cirrhosis portal hypertensiongastric mucosal lesion not only related with the degree and time of the portalhypertension and the gastric acid contaminate and the pepsin digestion ,but alsorelated with the HP infection. Because when HP infects gastric mucosa,it canrelease heat shock protein\CagA,VacA,HP lipoidase\lipoidase A\urease. Theurase can depose the carbamide into NH3 and co2,then they can leak out from thegastric mucosa cellula epithelialis,so it can make the concentration of ammon inthe stomach increase notably,so that the normal H+ diliver to the cavus gastralisdifficultly,then cuase the H+counter diffusion,then it can induce lysosomalenzyme release of membrane cells,and the lysomal enzyme disrupt,gastric mucouscellula epithelialis damage,cause the gastric mucosa hyperemia\cutaneousdropsy\anabrosis\bleed and cellular necrosis. At the same time ,the acid poisoningcause the vasoactive substance such as histamine and 5-HT release,the patientsof HP infection also have immune reaction mediated by IgE,and it cause theveinlet and the blood capillary in the gastric wall broaden and congeste,so itaggravate the microcirculation disturbance of the gastric mucosa. At the sametime the lipopolysaccharide of HP have the character of endotoxin ,so it candamage the mucosal barrier straightly,it can also cause cellula epithelialis\monocyte produce and release cytokine such as IL-1\ TNF-α,and under thefunction of IL-1\ TNF-α the monocyte and the vascular endothelial cell releasemore IL-8,it can induce the level of IL-1\IL-8\ TNF-αin the peripheral bloodadvance,and in the process of cleaning HP the activated neutropilic leukocyterelease mediators of inflammation such as lysomal enzyme,so it can intensify theinflammatory reaction and tissue damage. So HP infection is one of the agents ofhepatic cirrhosis portal hypertension gastric mucosa diseases. This experimentdiscloses that the level of the endotoxin \ET\NO\in the hepatic cirrhosis HPinfection masculine group's peripheral blood is obviously higher than negativegroup,the level of the endotoxin \ET\NO\in the hepatic cirrhosis HP infectionmasculine group's peripheral blood is direct correlated with the SVF \SVMF,andinverse correlated with PVF,so it indicate HP infection correlated with portalhypertension of chronic liver disease patients.The initiating agent which caused this result is some reconstituents such asCagA\VacA\HPlipidase\lipidaseA and endotoxin released by HP ,they can inducecellula epithelialis \histoleucocyte release cytokine IL-1, TNF-α,and under thefunction of IL-1, TNF-α,histoleucocyte and vascular endothelial cell releasemore IL-8,so it cause the level of IL-1, TNF-α,IL-8 in the patient's peripheralblood ,these factors affect the liver cells especially the Kupffer's cells ,activateiNOS and induce more composition of NO. On the another hand ,above factorsalso can affect vascular endothelial cell,change the cellular structure\metabolismand osmolarity,excite it compose more ET.NO is one of the blood vessel relaxingfactors,it can relax blood vessel,degrade blood pressure.ET is a peptide chaincomposed by 21amino acid,it affect to the endothelin receptor of target cell. TheET receptor of liver live at the fat storing cell,the fat storing cell live at the Dissdiastematic. The construction of fat storing cell can accommodate thepylic-pressure,when ET combines with the ET receptor on the fat storing cells,thecells contract,then the resisting force of sinus hepaticus increased and portalvenous pressure increased,so it can induce portal venous flow reduce,in the end itcan cause the changes of haemodynamics of the portal system.