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AIM: To study the inhibitive effects of valsartan and spironolactone on expression of insulin like growth factor 1 in cardiacmyocytes of spontaneously hypertensive rats. METHODS: 18 SHRs were randomly divided into 3 groups (n=6 in each): valsartan group treated with 30 mg?kg -1 ?d -1 valsartan, spironolactone group treated with 20 mg?kg -1 ?d -1 spironolactone, and control group treated with placebo. All were administrated by gastric perfusion. 6 WKY rats were served as control. After 13 weeks administration, the expressions of IGF 1 in cardiacmycytes were measured by immunohistochemistry and the IGF 1 concentrations in myocardium were measured by radiommunoassay. RESULTS: The expression of IGF 1 was higher in SHR group than that in the WKY group (P
RESUMO
AIM: To investigate the effects of fluvas-tatin on expression of intercellular adhesion molecule-1 after myocardial ischemia-reperfusion in rabbits with hyper-lipidemia. METHODS: 30 rabbits which were gastric perfusion administered intralipid were randomly divided into 3 groups ( n - 10 in each) : IR ( ischemia-reperfusion) group, S (sham-operation) group and F (fluvastatin 10 mg?kg-1 ) group. Electrocardiography and cardiac function were recorded during the experiment. At the end of reperfusion, ischemic area and infarct size were defined by Evans blue and triphenyltetrazolium chloride staining. The expression of ICAM-1 in myocardium was measuredby RT-PCR. RESULTS: After ischemia-reperfusion, the expression of ICAM-1 mRNA in myocardial and infarct size decreased and cardiac function significantly improved in F group compared with IR group. CONCLUSION: The increase of expression of ICAM-1 mRNA in myocardial may be one of the important factors in inducing myocardial ischemia-reperfusion injury. The myocardial protective mechanism of fluvastatin maybe attribute to its effect on decreasing the expression of ICAM-1 mRNA in myocardial .
RESUMO
AIM: To investigate the protective effect of fluvastatin and its influence on ICAM-1 mRNA expression in ischemia/reperfusion myocardium of normocholesterolemic rabbits. METHODS: 24 rabbits were divided into three groups randomly and myocardial ischemia/reperfusion model in the rabbit was made. Rabbits were subjected to 45 min of regional myocardial ischemia and 2 h of reperfusion. 10 mg?kg~ -1 ?d~ -1 fluvastatin were administered for one week. Dynamic index of blood flow was recorded and analyzed. Serum activity of CK, CKMB, LDH and LDH-1 were measured. The expression of ICAM-1 mRNA in ischemic myocardium was detected with semi-quantitative RT-PCR. RESULTS: In comparison with control group, pretreatment with fluvastatin decreased LVEDP at the whole observed duration, and spontaneously increased ?dp/dt_ max . Serum activities of CK, CKMB and LDH-1 in control group were significantly higher than those in sham group, but heavily reduced in fluvastatin group. Increased expression of ICAM-1 mRNA due to ischemia reperfusion was reduced significantly in fluvastatin group compare to control group. CONCLUSION: Pretreatment of fluvastatin may reduce inflammation reaction in reperfused myocardium, and this may contribute to its protective effect against experimental myocardial ischemia reperfusion injury.
