Abstract
This study was designed to determine neurochemical properties of the coeliac-superior mesenteric ganglion (CSMG) neurons supplying the prepyloric area of the porcine stomach in physiological state and following experimentally induced hyperacidity. To localize sympathetic neurons innervating the studied area of stomach, the neuronal retrograde tracer Fast Blue (FB) was applied to control animals and hydrochloric acid infusion (HCl) groups. After 23 days, animals of the HCl group were reintroduced into a state of general anesthesia and intragastrically given 5 mL/kg of body weight of 0.25 M aqueous solution of hydrochloric acid. On the 28th day, all animals were sacrificed. The CSMG complexes were then collected and processed for double-labeling immunofluorescence. In the control animals, FB-positive perikarya displayed immunoreactivity to tyrosine hydroxylase (TH), dopamine β-hydroxylase (DβH), neuropeptide Y (NPY), and galanin (GAL). Experimentally induced gastric hyperacidity changed the neurochemical phenotype of the studied neurons. An upregulated expression of GAL and NPY and the de novo synthesis of neuronal nitric oxide synthase (nNOS) and leu5-enkephalin (LENK) as well as downregulated expression of TH and DβH in the stomach-projecting neurons were observed. These findings enrich existing knowledge about the participation of these active substances in adaptive mechanism(s) of the sympathetic neurons during pathological processes within the gastrointestinal tract.
Highlights
Gastrointestinal disorders, especially acid-related diseases, including peptic and duodenal ulcers, gastroesophageal reflux disease, upper GI bleeding, or stress-related mucosal disease, are currently serious health issues encountered very frequently in patients worldwide [1]
The gastroscopic examination performed on the first day of the experiment excluded lesions in the gastric mucosa in animals of the hydrochloric acid infusion (HCl) group
The coeliac-superior mesenteric ganglion (CSMG) neurons innervating the prepyloric area of the porcine stomach were localized exclusively within the region of coeliac poles of the CSMG complex
Summary
Gastrointestinal disorders, especially acid-related diseases, including peptic and duodenal ulcers, gastroesophageal reflux disease, upper GI bleeding, or stress-related mucosal disease, are currently serious health issues encountered very frequently in patients worldwide [1]. Many gastrointestinal diseases, such as Zollinger-Ellison syndrome, retained antrum syndrome, antral G cell hyperplasia, and gastric outlet obstruction, are disorders whose etiology involves gastrin hypersecretion [2,3,4]. It has been shown that gastrin, histamine, and acetylcholine stimulate gastric acid secretion, while somatostatin, cholecystokinin, glucagon-like peptide-1, and atrial natriuretic peptide reduce secretory stomach activity [5]. The mechanisms of the above-mentioned pathological states are not quite clear, but disturbances in the gastric secretion of hydrochloric acid seem to be one of the main causes. The fundamental role of hyperacidity has been proven in the development of gastric ulcerative disease [3]. Many aspects connected with gastric acidrelated diseases remain obscure. One of them is the function of the nervous system supplying the gastrointestinal (GI) tract during pathological processes
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