| Acute myocardial infarction (AMI) is an important type of coronary heart disease (CAD). AMI is associated with robust, neutrophil-rich inflammatory reaction, including the infiltration of neutrophils in infarct site, substitution of necrotic myocardium by fibrous tissue and scar formation. Profit can be gained from the inflammatory reaction intervention, togather with some side effects. Aspirin, Provastatin, Roxithromycin and Lefluomide have their own main pharmacology, and recent studies have shown that those drugs have other effects such as antiinflammation. In this study, the left circumflex arteries of rabbits were ligated to obtain the animal models of AMI. The animals in different groups were treated with different drugs or without drugs. After that, the related indexes of the experimental groups were determined to study the therapeutic effects and mechanisms of each drug on rabbits with experimental AMI. Objective:1. To obtain the animal models of AMI by ligating the left circumflex arteries of rabbits.2. To compare the specimens harvested at 6 hours, 4 days and 4 weeks after AMI from the untreated group with those from the treated groups and study the therapeutic effect and mechanisms of each drug on rabbits with experimental AMI.3. To evaluate the effects and mechanisms of aspirin at low and middle dose on AM.4. To evaluate the effect and mechanisms of provastatin on AMI.5. To evaluate the effect and mechanisms of lefluomide on AMI.6. To evaluate the effect and mechanisms of roxithromycin on AML-5-Meterials and methods:66 rabbits (10 were dead during the experiment and another 10 were added, so the total were 76) were divided into 6 groups randomly: an untreated group(12), a low-dose aspirin treated group(12), a middle-dose aspirin treated group(12), a provastatin treated group (6), a lefluomide treated group(12) and a roxithromycin treated group(12). The left circumflex arteries of rabbits were ligated to obtain the animal models of AMI. The animals of five drug-treated groups were treated with different drugs. After 6 hours, 4 days and 4 weeks after AMI, we measured the following indexes: (1). The indexes of all rabbits: leukocyte count of periphery blood of all three phases, NO, MDA at 4 days and 4 weeks after AMI. (2). The indexes of hemodynamic function of all animals: left ventricular end dilated pressure (LVEDP), PEP/LVET, atrial natriuretic peptide (ANP). (3). The indexes of infarction size at 4 days and scar size, scar thickness at 4 weeks after AMI. (4). Light microscopic examination of specimens harvested at 4 days after AMI. Results:1. The animal models of AMI were obtained by thorax operation and ligating the left circumflex arteries of rabbits. We dyed the myocardium with nitro blue tetrazolium (NET) to observe the blue or purple living myocardium, the white or yellow necrotic myocardium, the thin ventricular wall and scars at 4 days after AMI2. The results by comparing the untreated group with the treated groups: The periphery blood leukocyte count in treated group were significantly reduced compared with that in untreated group at the first 6 hours (except low-dose and middle-dose asprin treated group), 4 days and 4 weeks after AMI. In treated groups, NO was similar to untreated group, but ANP, PEP/LVET, LVEDP were significantly decreased compared with untreated group. MDA was significantly decreased compared with untreated group at 4 days except the roxithromycin group-6-but was similar to untreated group at 4 weeks after AMI (provastatin treated group wasn't measured). Myocardial infarct size in treated groups were significantly decreased at 4 days after AMI, while were similar to untreated group at 4 weeks except the lefluomide group (provastatin treated group wasn't measured). Scar thickness in treated groups(provastatin treated group wasn't measured) were thinner than that in untreated group at 4 weeks after AMI. Light microscopic examination of myocardial infarct site revealed similar leukocytic infiltration...
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