title: The effects of celiac ganglionectomy on sympathetic innervation to the splanchnic organs in the rat.
abstract: The sympathetic nervous system is important in blood pressure regulation, and regionally-specific increases in sympathetic nerve activity occur during the development of hypertension. Sympathetic neurons innervating the splanchnic organs may be especially critical, because sympathetic activity to the splanchnic region is increased early in hypertension development. The celiac ganglionic plexus contains the majority of the sympathetic neurons innervating the splanchnic organs and tissues. Celiac ganglionectomy (CGX) involves surgical removal of the celiac ganglionic plexus, and has been used to study the roles of the splanchnic sympathetic innervation in cardiovascular regulation. In the current study we characterized the short-term (two-week) and long-term (five-week and ten-week) effects of CGX in rats on splanchnic sympathetic nerve structure and function. In the short-term, norepinephrine concentrations in whole splanchnic organs and mesenteric arteries and veins were significantly decreased by CGX. Immunohistochemistry and glyoxylic acid staining showed an almost complete loss of the typical sympathetic innervation of mesenteric arteries and veins. Additionally, CGRP-containing sensory nerves largely disappeared. Constrictor responses of mesenteric arteries and veins to sympathetic nerve stimulation were abolished by CGX. However, the effects of CGX were time-dependent, since significant regeneration of sympathetic nerves in some organs was observed 5weeks after surgery. The inferior mesenteric ganglion had minimal impact on this reinnervation process. In vivo studies showed that CGX significantly lowers resting blood pressure in normal Sprague-Dawley rats. Therefore, CGX is an effective means to impair sympathetic input to the splanchnic organs, but the effect of the procedure is not permanent.
authors.affiliation: Department of Pharmacology and Toxicology, B440 Life Sciences, Michigan State University, East Lansing, MI 48824, USA.
authors.forename: Melissa
authors.initials: M
authors.lastname: Li
authors.forename: James
authors.initials: J
authors.lastname: Galligan
authors.forename: Donna
authors.initials: D
authors.lastname: Wang
authors.forename: Gregory
authors.initials: G
authors.lastname: Fink
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001703:Biophysics; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D004558:Electric Stimulation / Q000379:methods; D005728:Ganglia, Sympathetic / Q000502:physiology* / Q000601:surgery; D015171:Ganglionectomy / Q000379:methods; D006038:Glyoxylates / Q000378:metabolism; D007422:Intestines / Q000502:physiology; D007668:Kidney / Q000502:physiology; D008099:Liver / Q000502:physiology; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism*; D008642:Mesenteric Veins / Q000378:metabolism*; D009197:Myenteric Plexus / Q000502:physiology*; D009416:Nerve Regeneration / Q000502:physiology; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013153:Splanchnic Nerves / Q000502:physiology*; D013154:Spleen / Q000502:physiology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D006038:Glyoxylates; D014446:Tyrosine 3-Monooxygenase; D015740:Calcitonin Gene-Related Peptide; C031150:glyoxylic acid; D009638:Norepinephrine