Effects Of Recombinant Human Brain Natriuretic Peptide On Lef Ventricular Remodeling After Myocardial Infarction In Rats

objective Application of long-term recombinant human brain natriureticpeptide(rhBNP)for left ventricular remodeling and mechanism after myocardialinfarction in rats.Method Ligation of male Wistar rats left anterior descending coronaryartery after 1 week,Surviving rats were randomly divided into two: the modelgroup (n =14rats), treatment group (n =14rats), a separate sham group (n=10rats).Rats-treatment group were received Intraperitoneal injection of rhBNP(15μg/kg,once daily),while rats -model group and sham operation group, only an equalvolume of saline intraperitoneally. the detection of left ventricular remodeling index,cardiac function parameters,Plasma and myocardial angiotensin II, aldosteroneconcentration,Heart specimens HE, Masson staining by Optical microscopeobservation or electron microscopy after 5 weeks.Results①Compared the index of left ventricular remodeling in rats , Modelgroup, treatment group compared with sham operation group, left ventrieularabsolute weight(LVAW)and left ventricular relative weight(LVRW)all increased,Spherical index(SI) decreased,they were all Significant difference (P <0.01 or P<0.05), Showed that left ventricular remodeling after myocardial infarction.Treatment group compare with model group, LVAW, LVRW reduced, SI increased,were Significant difference (P <0.01 or P <0.05). Showing that rhBNP can inhibitthe development of ventricular remodeling in rats.②compared cardiac function in groups, compared Model group, treatment group with sham operation group,Systolic blood pressure (SBP),Diastolic blood pressure (DBP),Left ventricularsystolic pressure (LVSP)and the largest rise and decline in left ventricular pressurerate (±dp / dt)were all decreased, Left ventricular end diastolic pressure (LVEDP)was increased,they were significant difference (P <0.01 or P <0.05), Showed thatleft ventricular remodeling after myocardial infarction reduced cardiac function inrats.Treatment group compare with model group, SBP,DBP,LVSP,±dp/dt weresignificantly higher, LVEDP was significantly decreased,The difference betweenthe two groups was significant (P <0.01), showing that rhBNP significantlyimproved Cardiac function after ventricular remodeling in rats.Heart rate( HR )wasnot significant in each group.③rats hematoxylin - eosin staining (HE) lightmicroscopy, myocardial cells of Sham group arranged in neat rows and dense, nopathological changes. Model group, a large number of myocardial necrosis,musclebundle fracture, myocardial hypertrophy, arranged in loose disorder. Treatmentgroup, muscle bundle fracture less, mild myocardial hypertrophy, arranged in order,more compact.④Masson stain light microscopy in rats, Sham group, nopathological changes. Model group, Myocardial tissue insteaded of by the amountof fibrous tissue. Treatment group, Fibrous tissue decreased significantly.Showingthat rhBNP treatment of left ventricular remodeling after myocardial infarction inrats can inhibit myocardial fibrosis.⑤ultrastructure of rats, Sham group,myocardial sarcomere light and shade with clear, muscle fibers were arrangedregularly, no broken filaments twisted, mitochondria are uniform in size, ovalnucleus,prominent nucleoli, intercalated disk structure was normal; Model group,Myocardial sarcomere structure is incomplete, myofilament array of free,disorderedand extremely loose, twisted filaments break, dissolution is serious, mitochondrialcondensation, condensation nuclei; Treatment group, cardiac muscle cells withclear light and dark sections, cardiac muscle cells with clear light and darksections,local muscle wire fracture, mitochondria were slightly swollen.⑥plasma and myocardial angiotensin II concentrations in each group,compared Model group,treatment group with sham operation group, Plasma and myocardial angiotensin IIlevels were significantly higher, Significant difference (P <0.01); Treatment groupcompare with model group, Plasma and myocardial angiotensin II levels weresignificantly lower, Plasma and myocardial angiotensin II levels were significantlylower.⑦Aldosterone concentration in plasma and myocardium in each groups,compared Model group, treatment group with sham operation group, Plasma andcardiac aldosterone levels were increased, the difference was significant (P <0.01);Treatment group compare with model group, Plasma and cardiac aldosterone levelswere significantly lower, the difference was significant (P <0.01).conclusioconclusion rhBNP continuous application inhibit ventricular remodeling,improve cardiac function after myocardial infarction in rats,the mechanism isinhibition of plasma and myocardial angiotensin II, aldosterone.