Abstract P184: Effects of Vagus Nerve Stimulation on Hemodynamics and Inflammation in a Rheumatoid Arthritis Model in Rats

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2015-09, Vol.66 (suppl_1)
• Main Authors: Salgado, Helio C, Dias, Daniel P, Bassi, Gabriel S, Kanashiro, Alexandre, Cunha, Thiago M
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.66.suppl_1.p184

Abstract only The electrical stimulation of neural pathways has been considered a reliable alternative for treating some pathophysiological conditions, for instance, rheumatoid arthritis. Recently, the concept of electroceuticals has emerged and suggests that proper anatomic mapping associated with identification of electrical stimulation patterns for each neural pathway would tailor this tool. The effects of electrical stimulation of the vagus nerve (VNS) on hemodynamics and inflammatory responses were assessed in a rheumatoid arthritis experimental model. Male Wistar rats (280 g body mass) were anesthetized (ketamine: 57 mg/kg; xylazine: 10 mg/kg) and instrumented with a polyethylene catheter into the femoral artery combined with a stainless steel bipolar electrode around the left vagus nerve. Animals were kept anesthetized and had the pulsatile arterial pressure recorded at baseline during 10 minutes, followed by a single session (2-minutes long) of VNS under three different conditions: A) 5 Hz, 0.1 ms, 1 V; B) 10 Hz, 0.1 ms, 1 V; and, C) 20 Hz; 0.1 ms; 3 V. Immediately after VNS ceased, rats were injected with zymosan (100 μg/50 μL) into the femorotibial joint to elicit rheumatoid arthritis. Rats were allowed to rest over the next six hours and afterwards were killed and had the synovial fluid collected for neutrophil count. Control rats were subjected to similar procedures but without VNS. The VNS condition A and B elicited a transitory bradycardia (A: 23±3, B: 23±2 Δbpm; as compared to baseline). No changes in blood pressure were seen following VNS at conditions A and B. VNS under C condition elicited pronounced transient bradycardia (101±13 Δbpm; as compared to baseline) and produced a transient hypotensive response (26±6 ΔmmHg, as compared to baseline). VNS at conditions A and B had anti-inflammatory effect showed by neutrophil count (A: -44±8, B: -38±7; percentage change as compared to control rats). However, VNS at C condition had no anti-inflammatory effect. Therefore, VNS was an effective anti-inflammatory tool that did not elicit remarkable hemodynamic alterations.