Effects of autonomic nervous system on gastric damage by ethanol in the rat

Foschi, Diego; Castoldi, Laura; Soldato, Piero Del; Musazzi, M; Callioni, F.; Rovati, V.; Trabucchi, E; Montorsi, W

doi:10.1007/bf01540339

Cited by 20 publications

(10 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This could be explained by the fact that vagotomy, which would interfere with the signal transmission inside the capsaicin-sensitive afferent fibers of the vagus nerve, may adversely influence the defensive mechanism of the gas tric mucosa against ethanol-evoked damage [11,18]. It had been reported that the adaptive cytoprotection in duced by low concentration of ethanol was abolished by surgical vagotomy [ 19,20], In the present study, there was only a partial abolition of the cytoprotective action in duced by 20% ethanol after subdiaphragmatic vagotomy. Lidocaine completely abolished the protective action of 20% ethanol, it is therefore suggested that the enteric ner vous system seems to be important, in addition to possi ble involvement of the vagal reflex in such cytoprotective action.…”

Section: Discussionmentioning

confidence: 99%

Adaptive Gastric Mucosal Cytoprotection in Rats: Different Modes of Action by Three Mild Irritants

Ko¹,

Cho²

1996

Digestion

View full text Add to dashboard Cite

The mechanisms of adaptive mucosal cytoprotection by mild irritants were investigated in rats. In an ex vivo chamber preparation, application of 20% ethanol, 5% NaCl or 0.3 M ΗCl to the posterior side of the mucosa significantly protected that side of the stomach against mucosal damage caused by subsequent exposure to 100% ethanol, with contralateral transmission of protection to the anterior side by 20% ethanol and 0.3 M HCl. Atropine or lidocaine significantly reversed the cytoprotection of 20% ethanol. Bilateral vagotomy partially prevented the antilesion action of 20% ethanol, and completely prevented the action of 0.3 M HCl. However, the three mild irritants did not affect gastric mucosal blood flow, but restored the ion transport mechanism which was depressed by ethanol. It is therefore concluded that the three mild irritants have their own distinctive cytoprotective mechanisms against ethanol ulceration, which is predominantly not mediated by effects on the vascular system of the gastric mucosa.

show abstract

Section: Discussionmentioning

confidence: 99%

Adaptive Gastric Mucosal Cytoprotection in Rats: Different Modes of Action by Three Mild Irritants

Ko¹,

Cho²

1996

Digestion

View full text Add to dashboard Cite

show abstract

“…There is little information regarding the role of the sympathetic nervous system in gastric mucosal defense. Sympathectomy has been reported to worsen damage by ethanol and to abolish adaptive protection in rats (27). N/OFQ is reported to decrease peripheral resistance and to increase blood flow to peripheral organs, including stomach, in the rat (34,35).…”

Section: Fig 5 Effect Of Pretreatment With Cgrpmentioning

confidence: 99%

“…Although controversial, there are studies in which vagotomy is reported to cause a tendency to worsen ethanol-induced lesions (27,28). Protection by peripherally administered prostaglandin E 2 , prostacyclin, and mild irritants (28,29) and by centrally administered TRH (18) is reduced in vagotomized rats.…”

Section: Fig 5 Effect Of Pretreatment With Cgrpmentioning

confidence: 99%

Peripheral Mechanisms Involved in Gastric Mucosal Protection by Intracerebroventricular and Intraperitoneal Nociceptin in Rats

et al. 2005

View full text Add to dashboard Cite

Nociceptin (N/OFQ) exerts multiple effects in the gastrointestinal tract after central or peripheral administration. In the present study, we examined the possible peripheral mechanisms mediating gastric protection by N/OFQ in rats. Gastric mucosal lesions were induced by 50% ethanol (1 ml/rat intragastrically). N/OFQ, administered either intracerebroventricularly (3 g/rat) or ip (10 g/kg), significantly reduced macroscopic and histological damage. capeptide, isolated from brain extract, which shows a structural homology to the opioid peptide dynorphin A and binds to the orphan opioid receptor-like 1 receptor, now termed NOP receptor (1, 2). Since the early studies, it became evident that N/OFQ was involved in modulation of pain, anxiety, feeding, and memory processes (3-6). Central and peripheral administration of the peptide has also been reported to exert multiple effects in the gastrointestinal tract, affecting gastric and intestinal motility (7-9) and secretion (10, 11).We have recently shown that N/OFQ protects against gastric mucosal damage induced by intragastric (ig) ethanol exposure in the rat and that its effect that is reversed by the selective antagonist UFP-101, suggesting the peptide exerts gastric protection through the NOP receptor (12). The evidence that N/OFQ protects the gastric mucosa after both central and peripheral administration suggests that the peptide interacts with distinct central and peripheral pathways. Accordingly, the NOP receptor has been identified in the central and peripheral nervous systems and along the entire gastrointestinal tract of the rat (13,14). Nerve fibers immunoreactive to N/OFQ were found in the myenteric plexus and circular muscle layer of the rat colon (7).Resistance of the gastric mucosa against damage by endogenous and exogenous aggressors is ensured by a complex system of mediators. A crucial role has been attributed to the neuropeptide calcitonin gene-related peptide (CGRP), released by capsaicin-sensitive extrinsic nerve fibers and to nitric oxide (NO), synthesized by the neuronal and endothelial enzymes. The sensory neuropeptide and NO appear to act in concert in the modulation of mucosal integrity (15,16). There is also evidence for an interaction between autonomic nervous system and peripheral CGRP/NO pathways (17). Indeed, neuropeptides like TRH, peptide YY (PYY), and adrenomedullin, acting at the central level, reduce gastric lesions caused by ethanol in rats through vagal cholinergic pathways associated with peripheral release of CGRP and activation of .The present study was aimed to further characterize the protective activity of N/OFQ, injected centrally or peripherally, against ethanol damage in rats, by evaluating the possible peripheral neural mechanisms mediating the effect of the peptide. In particular, we have examined the role of NO and of afferent nerve fibers as well as of parasympathetic and sympathetic systems. Materials and Methods AnimalsMale Wistar rats, weighing 180 -200 g (Harlan, S. Pietro al Natisone, Italy) were individually hou...

show abstract

“…Hence, the possibility of having other potential mediators of adaptive cytoprotection had been evolved after the discovery of certain protective substances in the gastric luminal fluid of rats receiving a low concentration of HCl, which was unaffected by indomethacin. It was found that adaptive cytoprotection could be weakened or completely abolished after surgical sialoadenectomy, vagotomy or sympathectomy [5]. Since there is no unifying hypothesis regarding the mediation of adaptive cytoprotection, it is reasonable to assume that more than one mediator is involved in its mode of action, with the participation of multiple biological systems.…”

Section: Cytoprotection and Adaptive Cytoprotectionmentioning

confidence: 99%

Adaptive Cytoprotection and the Brain-Gut Axis

Cho

2011

Digestion

View full text Add to dashboard Cite

Adaptive cytoprotection is a concept to counteract against the gastric mucosal injury caused by stress, strong irritants and drugs such as non-steroidal anti-inflammatory drugs. The process is mediated through diverse mediators and mechanisms. Studies on adaptive cytoprotection began from the discovery of prostaglandin (PG)-dependent and PG-independent pathways, followed by the investigation on the types and concentrations of mild irritants to be used. Upon the confirmation on the importance of the vagus nerve and the vago-vagal pathway in regulating the mucosal protective actions of the mild irritants, individual participating mediators for the neuronal modulatory processes were explored, including peptide neurotransmitters such as calcitonin gene-related peptide and substance P. Further correlation with the sympathetic nervous system, the sensory afferent neurons and the enteric nervous system of the gastric mucosa had been made. A close working relationship between the hypothalamic-pituitary-adrenal axis, the autonomic nervous system and the enteric nervous system was then proposed, with concurrent regulation of PG, nitric oxide and sensory neuropeptides by different mild irritants. Apart from these conventional concepts, there are now contemporary ideas on newer forms of adaptive cytoprotection such as ischemic preconditioning and heat-shock proteins, which will cast new light to novel approaches in facilitating gastric mucosal protection.

show abstract

Effects of autonomic nervous system on gastric damage by ethanol in the rat

Cited by 20 publications

References 15 publications

Adaptive Gastric Mucosal Cytoprotection in Rats: Different Modes of Action by Three Mild Irritants

Adaptive Gastric Mucosal Cytoprotection in Rats: Different Modes of Action by Three Mild Irritants

Peripheral Mechanisms Involved in Gastric Mucosal Protection by Intracerebroventricular and Intraperitoneal Nociceptin in Rats

Adaptive Cytoprotection and the Brain-Gut Axis

Contact Info

Product

Resources

About