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Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat.

Abstract

The central nervous system modulates inflammation in the gastrointestinal tract via efferent vagal pathways. We hypothesized that these vagal efferents receive synaptic input from vagal afferents, representing an autonomic feedback mechanism. The consequence of this vagovagal reflex for afferent signal generation in response to LPS was examined in the present study. Different modifications of the vagal innervation or sham procedures were performed in anesthetized rats. Extracellular mesenteric afferent nerve discharge and systemic blood pressure were recorded in vivo before and after systemic administration of LPS (6 mg/kg iv). Mesenteric afferent nerve discharge increased dramatically following LPS, which was unchanged when vagal efferent traffic was eliminated by acute vagotomy. In chronically vagotomized animals, to eliminate both vagal afferent and efferent traffic, the increase in afferent firing 3.5 min after LPS was reduced to 3.2 +/- 2.5 impulses/s above baseline compared with 42.2 +/- 2.0 impulses/s in controls (P < 0.001). A similar effect was observed following perivagal capsaicin, which was used to eliminate vagal afferent traffic only. LPS also caused a transient hypotension (<10 min), a partial recovery, and then persistent hypertension that was exacerbated by all three procedures. Mechanosensitivity was increased 15 min following LPS but had recovered at 30 min in all subgroups except for the chronic vagotomy group. In conclusion, discharge in capsaicin-sensitive mesenteric vagal afferents is augmented following systemic LPS. This activity, through a vagovagal pathway, helps to attenuate the effects of septic shock. The persistent hypersensitivity to mechanical stimulation after chronic vagal denervation suggests that the vagus exerts a regulatory influence on spinal afferent sensitization following LPS.

Authors+Show Affiliations

Institute of Physiology, School of Medicine, Shandong University, Shandong, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17204546

Citation

Liu, C Y., et al. "Vagal Modulation of Intestinal Afferent Sensitivity to Systemic LPS in the Rat." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 292, no. 5, 2007, pp. G1213-20.
Liu CY, Mueller MH, Grundy D, et al. Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat. Am J Physiol Gastrointest Liver Physiol. 2007;292(5):G1213-20.
Liu, C. Y., Mueller, M. H., Grundy, D., & Kreis, M. E. (2007). Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat. American Journal of Physiology. Gastrointestinal and Liver Physiology, 292(5), pp. G1213-20.
Liu CY, et al. Vagal Modulation of Intestinal Afferent Sensitivity to Systemic LPS in the Rat. Am J Physiol Gastrointest Liver Physiol. 2007;292(5):G1213-20. PubMed PMID: 17204546.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat. AU - Liu,C Y, AU - Mueller,M H, AU - Grundy,D, AU - Kreis,M E, Y1 - 2007/01/04/ PY - 2007/1/6/pubmed PY - 2007/7/7/medline PY - 2007/1/6/entrez SP - G1213 EP - 20 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am. J. Physiol. Gastrointest. Liver Physiol. VL - 292 IS - 5 N2 - The central nervous system modulates inflammation in the gastrointestinal tract via efferent vagal pathways. We hypothesized that these vagal efferents receive synaptic input from vagal afferents, representing an autonomic feedback mechanism. The consequence of this vagovagal reflex for afferent signal generation in response to LPS was examined in the present study. Different modifications of the vagal innervation or sham procedures were performed in anesthetized rats. Extracellular mesenteric afferent nerve discharge and systemic blood pressure were recorded in vivo before and after systemic administration of LPS (6 mg/kg iv). Mesenteric afferent nerve discharge increased dramatically following LPS, which was unchanged when vagal efferent traffic was eliminated by acute vagotomy. In chronically vagotomized animals, to eliminate both vagal afferent and efferent traffic, the increase in afferent firing 3.5 min after LPS was reduced to 3.2 +/- 2.5 impulses/s above baseline compared with 42.2 +/- 2.0 impulses/s in controls (P < 0.001). A similar effect was observed following perivagal capsaicin, which was used to eliminate vagal afferent traffic only. LPS also caused a transient hypotension (<10 min), a partial recovery, and then persistent hypertension that was exacerbated by all three procedures. Mechanosensitivity was increased 15 min following LPS but had recovered at 30 min in all subgroups except for the chronic vagotomy group. In conclusion, discharge in capsaicin-sensitive mesenteric vagal afferents is augmented following systemic LPS. This activity, through a vagovagal pathway, helps to attenuate the effects of septic shock. The persistent hypersensitivity to mechanical stimulation after chronic vagal denervation suggests that the vagus exerts a regulatory influence on spinal afferent sensitization following LPS. SN - 0193-1857 UR - https://www.unboundmedicine.com/medline/citation/17204546/Vagal_modulation_of_intestinal_afferent_sensitivity_to_systemic_LPS_in_the_rat_ L2 - http://www.physiology.org/doi/full/10.1152/ajpgi.00267.2006?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -