Literature DB >> 22266357

Induction of chronic non-inflammatory widespread pain increases cardiac sympathetic modulation in rats.

Larissa Resende Oliveira1, Vitor Ulisses de Melo, Fabricio Nunes Macedo, Andre Sales Barreto, Daniel Badaue-Passos, Marcio Roberto Viana dos Santos, Daniel Penteado Martins Dias, Kathleen A Sluka, Josimari M DeSantana, Valter J Santana-Filho.   

Abstract

Fibromyalgia (FM) is characterized by chronic non-inflammatory widespread pain (CWP) and changes in sympathetic function. In attempt to elucidate the pathophysiological mechanisms of FM we used a well-established CWP animal model. We aimed to evaluate changes in cardiac autonomic balance and baroreflex function in response to CWP induction in rats. CWP was induced by two injections of acidic saline (pH 4.0, n=8) five days apart into the left gastrocnemius muscle. Control animals were injected twice with normal saline (pH 7.2, n=6). One day after the second injection of acidic saline or normal saline, the animals had pulse interval (PI) and systolic arterial pressure (SAP) variability, and spontaneous baroreflex sensitivity (BRS) evaluated. After induction of CWP, there was an increase of power in the low frequency (LF) band of PI spectrum (12.75 ± 1.04 nu), a decrease in the high frequency (HF) band (87.25 ± 1.04 nu) and an increase of LF/HF ratio (0.16 ± 0.01), when compared to control animals (7.83 ± 1.13 nu LF; 92.16 ± 1.13 nu HF; 0.08 ± 0.01 LF/HF). In addition, there was an increase of power in the LF band of SAP spectrum (7.93 ± 1.39 mmHg(2)) when compared to control animals (2.97 ± 0.61 mmHg(2)). BRS was lower in acidic saline injected rats (0.59 ± 0.06 ms/mmHg) when compared to control animals (0.71 ± 0.03 ms/mmHg). Our results showed that induction of CWP in rats shifts cardiac sympathovagal balance towards sympathetic predominance and decreases BRS. These data corroborate findings in humans with FM. Copyright Â
© 2011 Elsevier B.V. All rights reserved.

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Year:  2012        PMID: 22266357      PMCID: PMC4667978          DOI: 10.1016/j.autneu.2011.12.004

Source DB:  PubMed          Journal:  Auton Neurosci        ISSN: 1566-0702            Impact factor:   3.145


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