MGJ Nederhoff*, SAMW Verlinde, T van Zuuren, G Pasterkamp and RLAW Bleys
Introduction
Autonomic regulation of immune functions has increasingly been studied in recent decades. The attenuating effect of the parasympathetic nervous system on inflammatory processes is demonstrated in studies on inflammatory disease like rheumatoid arthritis, chronic bowel disease and heart failure. Similar inflammatory processes play a role in the development of tissue damage following myocardial infarction (MI). In this study, effects of vagus nerve stimulation (VS) on tissue damage and function loss after MI in the mouse heart were measured.
Methods
Anaesthetized male C57Bl6 mice were treated with or without 30 seconds of VS prior to experimental MI. Baseline and terminal heart function were studied. After 48 hours animals were sacrificed and infarct size and presence of inflammatory cells in different locations in the infarcted heart were determined. Inflammatory responsiveness and inflammatory cells in the blood were measured as well.
Results
The differences in ejection fraction and infarct size were found to be not significant. Counts of T-lymphocytes and macrophages were equal on baseline and at termination. Neutrophil counts were higher in the area remote from the infarction in the MI group compared to that in the VS+MI group. VEGF amounts were not different in the infarcted hearts of MI as compared to the hearts of VS+MI treated mice.
Conclusion
Ejection fraction decreased at 48 hours, less in the VS+MI group than in MI alone. However, this decrease, compared between groups was not significantly different. Although values of infarct size and cardiac function come close to significant reduction this study does not show clear proof for an inhibiting effect of VS on MI injury or function loss. Since the limited time period after MI could be of influence on the variation in the data future research is necessary to provide more information on the development of tissue damage and functional reduction.
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