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Inflammation Influence And Antinflammation Therapeutic Effect Of Sodium Diclofenac On Experimental Acute Myocardial Ischemia Of Rabbits

Posted on:2005-08-04Degree:MasterType:Thesis
Country:ChinaCandidate:B LiFull Text:PDF
GTID:2144360122490232Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
The coronary artery disease (CAD) is a kind of common disease endangering the human health seriously. The main dangerous factors such as age, sex, smoking, high blood pressure, high fat of blood, diabetes, etc. are widely known. In recent years research has shown that infecting can bring out the organism immune response and play a part in the coronary heart disease, but the pathogenesis has not been expounded yet. Study showed that the emergence, development of coronary heart disease and inflammation are closely related. From the formation of atheromatous stain to the emergence of acute coronary artery syndrome and the myocardial ischemia, inflammatory factor participate in all of them. This inflammation response plays an important role in the emergence of CAD. By obtaining the model of whole body inflammation response of rabbit, ligating the leftcircumflex arteries of rabbits, observe the influence of rise of inflammation medium to acute myocardial ischemia. And use noncyclooxygenase inhibitor to intervene AMI model with medicines, compare the relevant index among the groups, probe into the effect of cyclooxygenase inhibitor intervening to the heart of acute myocardial ischemia and the possible mechanism. Purpose:1. Bring out whole body inflammation response, by injecting right amount of LPS in vein, and than set up inflammation models.2. Set up acute myocardial ischemia model by the means of opening chest and ligating the left circumflex arteries of rabbits.3. Compare and study the change of leukocyte count, serum, bloodflow mechanics, pathology, immunity of the animals after operation among groups.4. Probe into the influence to heart of emergence at the time oforganism inflammation state and the mechanism.5. Probe into treatment effect of chlorine phenol sour sodium to AMI and mechanism.Material and Method:32 rabbits are divided into 5 groups randomly; Contrast group (6), myocardial ischemia group (6), lippolysaccharide (LPS) group (6), LPS and myocardial ischemia group (6), Dick and myocardial ischemia (8), All rabbits are intervened in various ways of according to requirements of experiment, then ligating the left circumflex arteries to build AMI model, and measure the following index 6h after ligature: (1) Study the index with blood of the animal: The periphery bloodleucocyte counts, serum MDA, SOD, iNOS, NO, MPO, ANP. (2) Mechanics index that the blood flows: LVEDP, LVPSP. (3) Keep the myocardium sample; organize chemistry to measure in immunity of carrying on pathology and COX-2.Results1. The model setting up: set up inflammation model by injecting right amount LPS in veins to bring out inflammation, opening chest and ligating the left circumflex arteries of rabbits and successfully copy AMI model. ECG record shows arch upward of ST; the color of tip of heart became dark, pathology check show myocardial ischemia cell swell. The express of COX-2 was increased in ischemia myocardium.2. Compare and study intervening groups and contrast groups: Experiment one: the expression of COX-2 was increased in ischemia myocardium. After 6 hours. The difference of the increased MDA, NO, MPO was significant between group D and groups B> C (P<0.05) ; The difference of ANP and LVEDP LVPSP were significantly increased between groups B,D(P<0.05) . Myocardial infarct sizes was similar to group B,D(P>0.05) . Experiment two: Plasma MDA,NO,MPO increasedsignificantly 6 h after AMI in groups B,C,D, those in group D weresignificantly increased compared with those in groups B C(P<0.05); ANP and LVEDP LVPSP were significantly increasedin group D compared with those of group B (P<0.05) . In group Dmyocardial COX-2 expression was significantly higher than that ingroup B, C.group B C. Conclusion:1. Set up rabbit's inflammation model by injecting LPS in vein to bring out the inflammation, and then ligating the left coronary artery to cause the acute myocardial ischemia, and offer the dise...
Keywords/Search Tags:Inflammation, acute myocardial ischemia, coronary artery disease, leucocytes, monoxide nitric, atrial natriuretic peptide, lipopolysaccharide, malondialdehyde, myeloperoxidase, super oxide dismutase, left ventricular end dilated pressure
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