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Roles of TNF-alpha and its receptors in the beneficial effects of vagal stimulation after myocardial infarction in rats.

Authors: Kong, SS  Liu, JJ  Hwang, TC  Yu, XJ  Lu, Y  Zang, WJ 
Citation: Kong SS, etal., Clin Exp Pharmacol Physiol. 2011 Mar 1. doi: 10.1111/j.1440-1681.2011.05505.x.
Pubmed: (View Article at PubMed) PMID:21362018
DOI: Full-text: DOI:10.1111/j.1440-1681.2011.05505.x

Acute myocardial infarction (AMI) often activates the sympathetic system and inhibits the vagal system. Long-term vagal nerve stimulation (VNS) exerts several beneficial effects on the ischemia heart including an anti-inflammatory effect. The goal of the current study is to investigate, in a rodent model, whether short term VNS during AMI could inhibit the expression of tumor necrosis factor-alpha (TNF-alpha) and the effect of TNF receptor (TNFR), key components in inflammatory responses to AMI. Adult male Sprague-Dawley rats were divided into four groups: control (C), vagal nerve stimulation (S), acute myocardial infarction (M), pre-VNS(+) AMI (MS). The right vagus nerve was electrically stimulated for 4 hours. The hemodynamic data were continuously monitored by a multichannel physiologic recorder. Lactate dehydrogenase (LDH) leakage and creatine kinase (CK) as well as infarct size were measured. The expression of TNF-alpha and its receptor were analyzed by reverse transcription polymerase chain reaction (RT-PCR), Western blotting and enzyme-linked immunosorbent assay (ELISA). In M group, AMI rats presented low blood pressure, high left ventricular end-diastolic pressure, a depressed maximum dP/dt of left ventricular pressure, higher LDH and CK leakage and larger infarct size as well as an increased TNF-alpha level and increased TNFR1/TNFR2 ratio. However, these presumably harmful effects of AMI were all significantly ameliorated by VNS during AMI. In conclusion, VNS can rectify ischemia-induced cardiac dysfunction partly through an inhibitory effect of VNS on the TNF-alpha-mediated signaling pathway.


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RGD Object Information
RGD ID: 5130892
Created: 2011-04-13
Species: All species
Last Modified: 2011-04-13
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.