| ObjectivesMyocardial infarction(MI)is very harmful to human health and life of cardiovasculardisease, and has a high mortality rate. Left ventricular function and structure have certainchanges after MI, including myocardial cells breaking down, infarction area disproportionatethinner and expansion, ventricular enlargement with decreased cardiac function, which willresult in the deadly arrhythmia and heart failure, even cardiac death. By many researches thedevelopment of atrial fibrillation(AF)has yet to be confirmed, whether the atrial structureremodeling after MI. Recently, a study showed that the patients of MI, especially with leftventricular systolic dysfunction, have the highest risk of new atrial fibrillation in two months,which had a higher risk of death, and the incidence was about four times previously reported.So we should pay attention to the atrial fibrillation and make clear the mechanism to heightenpreventing of atrial fibrillation. The present studies have showed that the occurrence and mainmechanism of AF include atrial structure remodeling, electrical remodeling and neuralremodeling. So the key of our research is to confirm whether atrial fibrillation after MIexactly has structure, electrical and nerve remodeling, and to learn to how to prevent theremodeling to reduce the occurrence of AF after MI. In recent years, the prevention andtreatment effect of cardiovascular disease of statins have aroused more and more people’sattention, especially the effect of ventricular arrhythmia, compared to the atrial fibrillation after myocardial infarction. Therefor what we should do is to try to explain the changes ofremodeling of AF after MI and the effect of statins. The main research aim is to investigatethe effect of rosuvastatin on neural and electrical remodeling of atrium in rabbit withmyocardial infarction.MethodsThe MI model was established by ligation of the anterior descending coronary artery inrabbits, twenty-four hours later after the procedure, the surviving rabbits were randomlydivided into MI group(MI, n=7), medicine intervention group(Rt, n=8), sham group wasalso established(S, n=9). After administration of rosuvastatin for eight weeks, all animalswere killed; The nerve sprouting in atrium were observed, the contents of TH and CHAT andexpression levels of TH mRNA and KCND3potassium voltage-gated channel mRNA weremeasured.ResultsAfter8weeks, compared with the sham operating group, the density of TH and CHATpositive staining nerve fibers and the expression of TH and TH mRNA were significantlyhigher in MI group, the expression level of KCND3potassium voltage-gated channel mRNAwas lower in MI group(P<0.05for all). Compared with the MI group, the density of TH andCHAT positive staining nerve fibers and the expression of TH and TH mRNA weresignificantly lower in medicine intervention group, the expression level of KCND3potassiumvoltage-gated channel mRNA was higher in medicine intervention group(P<0.05for all).And there are no significant differences in these parameters between sham group andmedicine intervention group (P>0.05for all).Conclusions1.There were significantly neural and electrical remodeling of atrium with myocardialinfarction.2.The results suggested that rosuvastatin has improving effect on the neural remodelingof atrium after myocardial infraction. |