| Objective This study was designed to investigate the effects of simple obesity on myocardial function of rats and protective action of Losartan(angiotensin IT receptor blocker) and to explore the possible mechanism .Method Established the obesity model induced by high fat feed , 32 rats were selected and randomized to two groups: normal control group and hyperlipidemia group, the hyperlipidemia group was divided into two groups .including Losartan group,non-medication group,these rats were given high fat feed and common roughage respectively in Mweeks. The hyperlLpidemia medication group (Losartan 10mg/kg -d)was administrated intragastrically by the gavage begin with 8th weeks. The non-medication group was given the saline. The rats' s weight, height, lee' s index, blood pressure, blood triglyceride, cholesterol, high and low density Lipoprotein, and angiotensin II, aldosterone were measured . The indices of myocardial function were also measured .The changes of histology and pathology were observed by pathological section. Result Compared with normalcontrol group, the obesity group had higher Bp, TG, Teh, LDL, Angll, ALD. Angll and ALD both had positive correlation with LVW. The hyperlipidemia group had the myocardium hypertrophy and the indexes of +dp/dtmax, -dp/dtmax were decreased significantly. (p<0. 05); Compared with non-medication group, Losartan group was declined in LVW, LVWI ,the indexes of heart function were all improved, such as+dp/dtmax . -dp/dtmax , LVSP , LVEDP. (p<0. 05). Conclusion Hypertension ,serum lipids disorder and myocardium hypertrophy , dysfunction of myocardial diastole and systole were all presented in the obesity rats. Renin-angiotensin-aldosterone system(RAAS) is activated in obesity groups. The activated RAAS is the possible mechanism of the myocardial malfunction . The protective mechanism of Losartan may be realized by inhibiting synthesis of ATI mRNA. |