Diagrammatic representation of the nervous control of hormone secretion by enteroendocrine cells of the gastrointestinal tract.

<p>Extrinsic vagal parasympathetic nerves either directly or via activation of the enteric neurones trigger release of hormones (hypothesised circulating cardioprotective factors) by releasing acetylcholine (among other transmitters). ACh, acetylcholine; AChR, acetylcholine receptor; BOM, bombesin; CCK, cholecystokinin; CGPR, calcitonin gene-related peptide; GliC, glicentin; GLP-1/2, glucagon-like peptide-1 and 2; OXM, oxyntomodulin; PYY, peptide YY; VIP, vasoactive intestinal peptide.</p

Cardioprotection established by remote ischaemic preconditioning (RPc) requires intact parasympathetic innervation of visceral organs.

<p><b>(a)</b> Illustration of the experimental protocols. RPc was induced by 15 min occlusion of both femoral arteries, followed by 10 min reperfusion. Sham-RPc procedure involved dissection of both femoral arteries without occlusion. Arrows indicate time of total subdiaphragmatic vagotomy, selective sectioning of individual visceral branches or sham surgery. <b>(b)</b> Total subdiaphragmatic vagotomy, bilateral gastric vagotomy and selective sectioning of the posterior gastric branch abolished the cardioprotective effect of RPc, whereas sectioning of the anterior gastric, celiac or hepatic branches had no effect on RPc cardioprotection. The infarct size is presented as the percentage of the area at risk. Individual data and means ± SEM are shown. P-values correspond to the Dunn’s post-hoc tests.</p

Electrical stimulation of the posterior gastric vagal branch mimics RPc cardioprotection.

<p><b>(a)</b> Illustration of the experimental protocols. Electrical stimulation (stim.) of individual vagal branches commenced 25 min before the onset of myocardial ischaemia (MI) and continued 10 min into the period of reperfusion. Sham procedure involved surgical dissection of the nerve and placing it on the electrodes without stimulation. <b>(b)</b> Electrical stimulation of the posterior gastric vagal branch reduced the extent of myocardial ischaemia/reperfusion injury, whereas stimulation of the hepatic vagal branch or sham stimulation of the posterior gastric branch had no effect. The infarct size is presented as the percentage of area at risk. Individual data and means ± SEM are shown. P-values correspond to the Dunn’s post-hoc tests.</p

Experimental interventions.

<p>Previous studies—DVMN silencing, cervical vagotomy. Six types of subdiaphragmatic vagotomy performed in the current study: total, bilateral gastric, anterior gastric, posterior gastric, hepatic and celiac, are shown on a schematic representation of typical distribution of rat abdominal vagal branches. Agb, anterior gastric branch; Avt, anterior vagal trunk; Ccb, common celiac branch; Hb, hepatic branch; Lvn, left vagus nerve; Pgb, posterior gastric branch; Pvt, posterior vagal trunk; Rvn, right vagus nerve. Brain, lungs, heart, diaphragm, liver, stomach, pancreas, small intestine and colon are depicted schematically.</p