Background Atrial fibrillation (AF) lead to calcium overload and Myocardial cell death, which could have inflammatory response in body. The autonomic nervous system (ANS) plays an important role in AF and inflammation.
Objective The aim of the study was to explore effect of vagosympathetic trunks stimulationon IL-1 and IL-6 in dogs with rapid atrial pacing (RAP).
Methods Fifteen mongrel dogs were randomly divided into three groups: cervical vagosympathetic nerve stimulation (VNS) group, RAP group, VNS+RAP group. Bbilateral cervical vagosympathetic trunks was isolated in every dog, and the cranial ends of the vagosympathetic nerves were ligated. A pair of Teflon-coated silver wires was inserted into the cervical vagosympathetic trunks for stimulation. A bipolar pacing catheter was placed in the high right atrium by way of the left jugular vein. In VNS group, vagus stimulator connected with silver wires to give electric stimulation in order to decrease the baseline heart rate by 50%. In RAP group, a acute atrial electrical remodelling (AAER) was performed through rapid atrial pacing at 600 beats/min with square waves of 2× threshold and 2 ms duration. In VNS+RAP group, dogs underwent both VNS and RAP. Blood samples were collected at 0h, 1h, 2h, 3h, 4h after RAP or VNS. Radioimmunoassay was preformed to measure the serum IL-1, IL-6 levels.
Results In VNS group, Baseline IL-1 level was 97.05 ± 9.50pg/ml, the IL-1 level at 1h, 2h, 3h and 4h during stimulation were 102.05 ± 13.70 pg/ml, 106.39 ± 13.67 pg/ml, 99.61 ± 17.43 pg/ml, 106.30 ± 6.51 pg/ml. Baseline IL-6 level was 220.78 ± 6.22 pg/ml, the IL-1 level at 1h, 2h, 3h and 4h during stimulation were 216.46 ± 8.38 pg/ml, 207.26 ± 27.96 pg/ml, 213.71 ± 24.35 pg/ml, 229.05 ± 9.91 pg/ml. With VNS, there were no significant differences in the serum levels of IL-1, IL-6 throughout the 4-hour stimulation period. At RAP group, Baseline IL-1 level was 97.58 ± 3.2 pg/ml, the IL-1 level at 1h, 2h, 3h and 4h during stimulation were 100.23 ± 2.95 pg/ml, 103.18 ± 1.48 pg/ml, 109.97 ± 2.24 pg/ml, 118.81 ± 3.98 pg/ml. Baseline IL-6 level was 223.07 ± 1.72, the IL-6 level at 1h, 2h, 3h and 4h during stimulation were 225.78 ± 3.26 pg/ml, 230.60 ± 2.28 pg/ml, 235.41 ± 2.28 pg/ml, 245.65 ± 4.07 pg/ml. The IL-1, IL-6 levels elevated markedly after 2h of RAP, and were progressively elevated throughout the 4-hour pacing period. In VNS+RAP group, Baseline IL-1 level was 103.18 ± 1.48 pg/ml, the IL-1 level at 1h, 2h, 3h and 4h during stimulation were 111.44 ± 1.98 pg/ml, 141.82 ± 4.09 pg/ml, 176.62 ± 3.36 pg/ml, 214.07 ± 6.87 pg/ml. Baseline IL-6 level was 226.98 ± 2.23 pg/ml, the IL-6 level at 1h, 2h, 3h and 4h during stimulation were 237.22 ± 1.96 pg/ml, 273.05 ± 3.12 pg/ml, 314.00 ± 6.60 pg/ml, 353.14 ± 6.60 pg/ml. The IL-1, IL-6 levels elevated markedly after 1h of RAP, and wereprogressively elevated throughout the 4-hour pacing period. Compare with RAP Group, IL-1 levels significantly elevated after 2h in VNS+RAP group, IL-2 levels significantly elevated after 1h in VNS+RAP group, and both of them were progressively elevated throughout the 4-hour pacing period.
Conclusions RAP could result in information. This further proof that the atrial fibrillation can cause inflammation; VNS without RAP can’t cause inflammation, but VNS can aggravate the inflammation caused by RAP. These findings suggest that ANS not only aggravate atrial electrical remodelling, but also lead to be structural remodelling via inflammation.
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