作者: Shan-Shan Kong , Jin-Jun Liu , Tyzh-Chang Hwang , Xiao-Jiang Yu , Yi Lu
DOI: 10.1111/J.1440-1681.2011.05505.X
关键词:
摘要: 1. Acute myocardial infarction (AMI) often activates the sympathetic system and inhibits vagal system. Long-term nerve stimulation (VNS) exerts several beneficial effects on ischaemic heart, including an anti-inflammatory effect. The aim of present study was to investigate whether short-term VNS during AMI could inhibit tumour necrosis factor (TNF)-α expression effect TNF receptor (TNFR), key components in inflammatory responses AMI, a rodent model. 2. Adult male Sprague-Dawley rats were divided into four groups, namely control (C), (S), (M) group subjected prior (MS). In S MS right vagus stimulated electrically for 4 h; M induced by occlusion left anterior descending coronary artery. Haemodynamic data monitored continuously using multichannel physiological recorder. Lactate dehydrogenase (LDH) leakage, creatine kinase (CK) leakage infarct size determined. TNF-α its receptors analysed reverse transcription-polymerase chain reaction, western blotting ELISA. 3. Compared with group, had low blood pressure, high ventricular (LV) end-diastolic depressed maximum dP/dt LV higher LDH CK larger size, increased levels TNFR1/TNFR2 ratio. However, these presumably harmful all significantly ameliorated (MS group). 4. conclusion, can rectify ischaemia-induced cardiac dysfunction partly via inhibition TNF-α-mediated signalling pathway.