Trituration The Rat Model Of Chronic Kidney Disease Microinflammation State With Heart Failure And Research On The Pathogenesis Of Their Heart Failure

Objective:To trituration the rat model of Chronic kidney disease microinflammation state with heart failure and research on the pathogenesis of their heart failure.Methodology:In this study,we divided 70 Sprague-Dawley rats into three groups at random:10 in control group,30 in Chronic kidney disease(CKD)group,and 30 in modeling group.The rats in control group were fed with edible oil(10ml/kg/d)by means of intragastric administration.The rats in CKD group were fed with 3% adenine edible oil solution(10ml/kg/d)by means of intragastric administration.The rats in modeling group were fed with 3% adenine edible oil solution by means of intragastric administration with the same frequency and dosage as the rats in CKD group at the incipient stage,the frequency of which was decreased to once 3 days when the Serum creatinine(Scr)is 1.5 times what it was,and meanwhile,the rats were given adriamycin(2.5mg/kg)by means of intraperitoneal injection once 7 days,and their drinking water was substituted with Kalium brOmicum(KbrO)solution(10 mg/L).The renal function,C-Reaction Protein(CRP),and echocardiography were monitored routinely.The three groups were compared with each other in terms of the echocardiography,heart mass index(Heart Mass/Body Mass,HM/BM),left ventricle mass index(Left Ventricle Mass/Body Mass,LVM/BM),and the HE staining results of the left ventricular tissues.The Matrix MetalloProteinase(MMP)-2,MMP-9,Tissue Inhibitor of Matrix metalloProteinases(TIMP)-1,pathology of VG staining and area percentage of collagen,ultra-structure by electron microscope,and apoptosis of cardiac muscle cell were compared with each other.Results(1)From the evaluation of CKD,heart failure,and microinflammation,the model is up to the standards.(2)Compared with control group and CKD group,the Left Ventricular End-Diastolic dimension(LVEDd),Left Ventricular End-Systolic dimension(LVESd),Left Ventricular End-Diastolic Volume(LVEDV)and Left Ventricular End-Systolic Volume(LVESV)were significantly increased in modeling group;while the InterVentricular Septal thickness at end-systole(IVSs),Left Ventricular Posterior Wall thickness at end-systole(LVPWs),Fractional Shortening(FS)and Left Ventricular Ejection Fraction(LVEF)were decreased(P<0.05).Compared with control group,LVESd and LVESV were increased in CKD group,while FS and LVEF were decreased(P<0.05).(3)Compared with control group,the HM/BM and LVM/BM in CKD group and modeling group were strikingly increased(P<0.05),while there was no difference between the two groups.(4)Both cells and fibers of cardiac muscle were damaged in modeling group,with infiltration of monocyte.The damages of cardiac muscle cells and fibers in CKD group were relatively slighter than those in modeling group,without infiltration of monocyte.The pathologic damages of cardiac muscle in VG staining and electron microscope aggravate in the order of uremia group,and congestive heart failure group which simulated modeling group.The arearatios of collagen and visual field are 0.132,0.151,and 0.053.(5)MMP2 decreases in the order of control group,uremia group,and congestive heart failure group which simulated modeling group.Regarding MMP-9 and TIMP-1,there are no differences among each groups,but their ratio steps up as the aggravation of heart failure.(6)There is no apoptosis of cardiac muscle cell in each group.Conclusions:(1)Simulated rat model of CKD microinflammation state with heart failure can be established by adenine,adriamycin and KbrO.(2)CKD microinflammation state with heart failure can enlarge heart through the increase of dimensions both at end-diastole and end-systole of left ventricle,and can thin heart down by decreasing the thickness at end-systole,with descent of heart function,relative weight gain of heart,and pathological damage of cardiac muscle.Except for relative weight gain of heart,the other aspects in CKD were apparently slighter than those in CKD microinflammation state with heart failure.(3)Which did not evoke apoptosis of cardiac muscle cell yet,meanwhile,the extracellular matrix of cardiac muscle cell reduces which lead to cardiac remodeling.