Abstract 458: The Baroreflex Modulates The Anti-inflammatory Response Caused By Intravenous Lipopolysaccharide (lps)

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2014-09, Vol.64 (suppl_1)
• Main Authors: Brognara, Fernanda, Becari, Christiane, Castania, Jaci A, Martins Dias, Daniel P, Tezini, Geisa, Lopes, Alexandre, Cunha, Thiago M, Fazan, Rubens, Salgado, Helio C
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.64.suppl_1.458

Abstract only Activation of the baroreflex elicits parasympathetic overactivity combined with sympathetic inhibition. The effect of electrical stimulation (ES) of the aortic depressor nerve (ADN) on the hemodynamic and inflammatory responses elicited by LPS (1.5 mg/kg iv) was examined in conscious rats. Rats were divided into 4 groups: 1) SALINE (n=6); 2) ES+SALINE (n=5); 3) LPS (n=7); 4) ES+LPS (n=5). Under ketamine/xylazine anesthesia the subjects were implanted with a pair of electrodes around the ADN and catheters into the femoral artery and jugular vein. On the next day, mean arterial pressure (MAP) and heart rate (HR) were recorded. ES (0.5mA; 0.25ms; 15Hz) was performed during 60 min after saline or LPS administration. Plasma was collected 1, 2 and 3h after saline or LPS administration, while the spleen and hypothalamus were collected after 3h to quantify interleukin (IL10) and tumor necrosis factor (TNFα). ES in the SALINE group promoted a prompt (5s) fall in MAP (-16± 5 mmHg) and HR (-39±12 bpm) followed by complete recovery of the MAP (7± 3 mmHg) and partial recovery of the HR (-8 ± 10 bpm) after 1h. In the LPS group ES promoted a prompt (5s) fall in MAP (-19± 6 mmHg) and HR (-40± 15 bpm) followed by complete recovery of the MAP (1 ± 3 mmHg) combined with significant tachycardia (30± 14bpm). Plasma TNFα increased 1h after LPS (400±78 vs 11±4 pg/μL from SALINE) followed by a decrease 2h (80±14 pg/μL) and 3h (34,4±5 pg/μL). After LPS the ES augmented IL-10 in the spleen (344±37 vs. 518± 79 pg/μL from ES+LPS) and decreased in the hypothalamus (73±8 vs 57±5 pg/μL from ES+LPS); while after saline ES increased IL-10 in the spleen (63±18 vs 314±99 pg/μL from ES+SALINE) but did not change in the hypothalamus (84±10 vs 97±17 pg/μL from ES+SALINE). After LPS administration ES did not change TNFα in the spleen (428±50 vs 450±98 pg/μL from ES+LPS) and hypothalamus (48±4 vs 38±5 pg/μL from ES+LPS); likewise in the spleen (285±38 vs 286±83 pg/μL from ES+SALINE) and hypothalamus (51,7±6 vs 54±8 pg/μL from ES+SALINE) after saline administration. These findings indicate that electrical activation of the baroreflex in conscious rats was capable to modulate the inflammatory response, promoting an increase of anti-inflammatory mediators in the LPS model of inflammation.