Forty-five rats were used to establish the AMI rat models by using the coronary artery ligation. A total of 39 rats were successfully modeled and were randomly divided into model group， AT1R blocker group， and carvedilol group， and there were 13 rats in each group. Another 13 rats were selected as sham operation group. The rats in AT1R blocker group were given 10 mg·kg^－1 losartan by gavage， and the rats in carvedilol group were given 10 mg·kg^－1 carvedilol by gavage. The left ventricular end systolic diamension（LVESD）， left ventricular end diastolic diamension （LVEDD） and left ventricular ejection fraction （LVEF） of the rats in various groups were detected by the small animal ultrasonic diagnostic system. The serum levels of creatine kinase isozyme-MB （CK-MB）， cardiac troponin I（cTnI）， lactate dehydrogenase （LDH） and brain natriuretic peptide precursors （Pro-BNP） of the rats in various groups were detected by ELISA method. 2，3，5-triphenyltetrazolium chloride （TTC） method was used to detect the percentages of myocardium infarction areas of the rats in various groups. HE staining was used to observe the morphology of myocardium tissue of the rats in various groups.TUNEL staining was used to detect the percentages of TUNEL positive cells of the rats in various groups. Immunohistochemical staining was used to detect the expressions of thioredoxin 1 （Trx1） and thioredoxin reductase 1 （TrxR1） in myocardium tissue of the rats in various groups.The protein expression levels of Trx1， TrxR1， nicotinyl adenine dinucleotide phosphate （NADPH）， cleaved Caspase 3， B-cell lymphoma-2 （Bcl-2） and Bcl-2 associated X protein （Bax） in myocardium tissue of the rats in various groups were detected by Western blotting method.

Compared with sham operation group， the LVESD and LVEDD of the rats in model group were increased（P<0.05）， while the LVEF was decreased （P<0.05）； the serum levels of CK-MB， cTnI， LDH， and Pro-BNP were increased （P<0.05）； the percentage of myocardium infarction area was increased （P<0.05）； the pathological phenomena appeared in the myocardium tissue， and the percentage of TUNEL positive cells was increased （P<0.05）； the expression level of Trx1 protein in the myocardium tissue was decreased （P<0.05）， while the expression levels of TrxR1， cleaved Caspase 3， and Bax proteins in the myocardium tissue were increased （P<0.05）， and the expression level of Bcl-2 protein in the myocardium tissue was decreased （P<0.05）. Compared with model group， the LVESD， LVEDD， and LVEF of the rats in AT1R blocker group and carvedilol group were decreased （P<0.05），and the LVEF of the rats was increased （P<0.05）； the serum levels of CK-MB， cTnI， LDH and Pro-BN were decreased （P<0.05）， the percentages of myocardium infarction areas were decreased （P<0.05），the pathomorphology of myocardium tissue was significantly improved， and the percentages of TUNEL positive cells were decreased （P<0.05）， the expression levels of Trx1 and Bcl-2 proteins in the myocardium tissue were increased（P<0.05）， and the expression levels of TrxR1，cleaved Caspase 3， and Bax proteins in the myocardium tissue were decreased （P<0.05）.

The ATIR blocker losartan can protect the rats with AMI， and its mechanism may be related to the regulation of Trx system.