If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
Background: The inflammatory response plays a pivotal role in the pathogenesis of
chronic heart failure (CHF). Although vagal nerve stimulation (VNS) improves CHF independent
of heart rate reduction, the mechanism that benefits CHF remains unclear. Since VNS
exerts the powerful anti-inflammatory effect, we investigated how VNS impacts on the
inflammation in the development of CHF after large myocardial infarction (MI) in rats.
Methods: In 8 weeks Sprague–Dawley rats, we created large myocardial infarction (MI) and started
VNS 2 weeks after MI (CHF: n = 8, VNS: n = 13). We adjusted the intensity of VNS (20Hz) below the level to induce bradycardia.
To elucidate the pure impact of VNS on inflammation, we evaluated systemic (blood)
and local (heart) inflammatory markers at 3 days after the initiation of VNS. Results: At 3 days, VNS change neither hemodynamic parameters nor plasma BNP as an index of CHF.
VNS significantly reduced the invasion of CD 68 positive cells (CHF: 295.1 ± 142.1, VNS: 110.7 ± 59.6 counts/mm2, p < 0.01) and decreased MCP-1 in the left ventricle (LV). In addition, VNS markedly reduced
interleukin-1β (IL-1β) in plasma (CHF: 75.7 ± 27.6, VNS: 32.9 ± 6.8 pg/mL, p < 0.01) and heart (CHF: 13.2 ± 4.6, VNS: 9.3 ± 2.4 pg/mg, p < 0.05). TNF-α and IL-6 remained unchanged between two groups. Conclusion: VNS significant
attenuates IL-1β production and the invasion of inflammatory cells prior to the improvement
of hemodynamics. Early suppression of the excessive inflammatory response may attribute
to the beneficial effect of VNS on CHF in the long-term.
To read this article in full you will need to make a payment