The Protective Effect Of Rapamycin Intervening Inflammatory Cytokines After Myocardial Infarction In Mice

Objective To investigate the method of establishing myocardial infarction modelin mice.Methods After being anaesthetized with3.3%chloral hydrate, the mice wasintubated through oral and breathed with the assistance of ventilator. Then a leftanterior thoraeotomy was performed to ligate the left anterior descending branch ofthe coronary artery (LAD). During the surgery, changes in the ECG were monitored.The mice was examined by transthoracic echocardiography before operation and at the day5,17after the surgery. At the end of the8th week, the heart was detected bypathological examination.Results ECG showed ST segment elevated instantly when LAD was ligated andthe myocardium became pale around the ligation point. Heart ultrasonic cardiogramshowed there was progressive decline in the thickness of left ventricle and increase inthe diameter of left ventricle, and the wall motion became lower. The end dilationdimension and end systolic dimension of left ventricle were increased significantly(3.42±0.36) mm and (2.15±0.32) mm vs (5.92±0.66) mm and (5.46±0.77) mm P<0.05.At the day17postoperation pathologic examination revealed the size of theleft ventricular cavity increased obviously and the myocardial thickness wasdecreased; The myocardial fibers became frizzy, fracture and necrosis.Conclusion Intubating quickly and correctly; surgical field exposing clearly;LAD identifying and ligating correctly; pneumothorax preventing, identifying andtreating early were the keys in establishing a successful myocardial infarction modelin mice. Objective To observe the protective effect of rapamycin on cardiac function aftermyocardial infarction in mice and discuss the possible mechanism.Methods60Kunming mices were randomly divided into three groups shamoperation group (S group), myocardial infarction group (M group) and drugintervention group (R group). The mices in M group and R group were establishedmyocardial infarction model by ligating the left anterior descending branch of thecoronary artery, before and after operation the mices in R group were injectrapamycin by intraperitoneal. At the day12after surgery the mices in three groupswere examined by transthoracic echocardiography. At the day14, the quantitativeenzyme linked sandwich immunoassay(ELISA) was used to measure the levels ofInterleukin-1β IL-1β Interleukin-6IL-6Tumor necrosis factor-α TNF-αMacrophage inflammatory protein1MIP-1in the heart tissue.Results The levels of inflammatory cytokines in rapamycin intervention groupwere lower than those in myocardial infarction group P<0.05. Heart ultrasoundexamination showed the ejection fraction and fractional shortening in rapamycinintervention group were higher than those in myocardial infarction group P<0.01(20.734±5.525%vs11.005±1.981%10.774±4.468%vs5.486±0.899%). HEpathological examination shows that the degree of inflammatory cells infiltration andcollagen fibres proliferation in R group were lower than that in M group. Conclusion Rapamycin can protect the heart function after myocardial infarctionin mice, the mechanism may be related to improving the left ventricular remodelingby reducing the levels of inflammatory cytokines.