Cellular mechanisms of the development of gastric mucosal damage and of gastrocytoprotection induced by prostacyclin in rats. A pharmacological study

Mózsik, Gy.; Pavón-Morón, Francisco Javier; Jávor, T

doi:10.1016/0262-1746(82)90074-9

Cited by 94 publications

(26 citation statements)

References 11 publications

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“…117 -118 Clinicians began to discuss an ill-defined metabolic protection by prostacyclin against ischemic injury of affected limbs. Later, they borrowed the term cytoprotection from Andr6 Robert, 119 who coined it to describe the ability of several prostaglandins (including prostacyclin 120 ) to protect the gastric mucosa from damage by noxious agents. Recently, the term cellular protection has been proposed for the protective effects of prostacyclin in vitro 121 and histoprotection for the protection of tissues in vivo.…”

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confidence: 99%

Mediators produced by the endothelial cell.

1988

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SUMMARY This review discusses the role of three mediators, synthesized by vascular endotheiial cells, that help to keep the surface of the normal endotheliuin nonthrombogenic. The first is prostacydin, a product of arachldonic add metabolism discovered hi 1976. This labile prostanoid, with a half-life of approximately 3 minutes, relaxes vascular smooth musde and inhibits the aggregation of blood platelets. Prostacydin and its analogues are currently being tested clinically for use hi cardiovascular diseases such as primary pulmonary hypertension. The second mediator discussed is endothelium-derived relaxing factor (EDRF), discovered in 1980, which also relaxes smooth muscle and inhibits the aggregation and adhesion of platelets. Substances that stimulate the release of EDRF include acetykhoUne, bradykinin, and adenosine 5'-diphosphate. EDRF is even more labile than prostacydin, with a half-life of about 6 seconds, and it has recently been identified as nitric oxide. Prostacydin and EDRF are released together following stimulation of endothelial receptors and synergize to inhibit platelet aggregation. 13-Hydroxy-9,11-octadecadienoic add, a third suggested mediator, is not released but acts from inside the cell to make the endothelial surface nonadhesive for circulating blood ceils. It is proposed that these three mediators form the endothelial defense mechanism against blood-borne cells and chemicals and that breakdown of this barrier results in diseases such as hypertension and atherosclerosis. (Hypertension 12: 530-548,1988) KEY WORDS • prostacyclin • endothelium-derived relaxing factor • thromboresistance • 13-hydroxy-9,ll-octadecadienoic add • endothelin • 6-keto-prostaglandin E,

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confidence: 99%

Mediators produced by the endothelial cell.

1988

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“…Prostacyclin has other important properties. Apart from being a powerful vasodilator and preventing platelets from sticking to each other, it also has a cytoprotective action [21], This is best seen in rats where the cells of the stomach mucosa are damaged with alcohol, acid, aspirin or with heat. Several prostaglandins, includ ing prostacyclin, will prevent the damage occurring in some way as yet not properly understood [22], This action is the so called 'cytoprotective effect' of some pros taglandins.…”

Section: Prostacyclinmentioning

confidence: 99%

Control of the Circulation by Endothelial Mediators

Vane

1993

Int Arch Allergy Immunol

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“…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. Fibers contained in the vagus nerve are both efferent and afferent, with 90% of vagal fibers in the subdiaphragm being afferent fibers (30).…”

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

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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...

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Cellular mechanisms of the development of gastric mucosal damage and of gastrocytoprotection induced by prostacyclin in rats. A pharmacological study

Cited by 94 publications

References 11 publications

Mediators produced by the endothelial cell.

Mediators produced by the endothelial cell.

Control of the Circulation by Endothelial Mediators

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

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