Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12249
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dc.contributor.authorSomjen, Gen
dc.contributor.authorFletcher, D Ren
dc.contributor.authorShulkes, Arthuren
dc.contributor.authorHardy, Kenneth Johnen
dc.date.accessioned2015-05-16T01:54:30Z
dc.date.available2015-05-16T01:54:30Z
dc.date.issued1989-05-06en
dc.identifier.citationJournal of Gastroenterology and Hepatology; 4(3): 251-8en
dc.identifier.govdoc2491151en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12249en
dc.description.abstractMesenteric ischaemia remains a frequently lethal condition. An improvement in survival is only likely with earlier diagnosis. Even with action upon early diagnosis and re-establishment of circulation, fatal shock often follows. This study was designed to determine the possible role of gastrointestinal regulatory peptides in the haemodynamic pathophysiology of acute mesenteric arterial ischaemia and whether measurement of these peptides would have diagnostic potential. Fourteen anaesthetized sheep were studied, seven with acute superior mesenteric artery (SMA) occlusion and seven with acute superior mesenteric and coeliac artery (SMA + CA) occlusion. Changes in peptide levels and haemodynamic changes were similar in the two experimental groups, but were more pronounced in the more severe ischaemia of SMA + CA occlusion. No major changes in systemic plasma gastrin, pancreatic polypeptide, neurotensin and vasoactive intestinal polypeptide (VIP) occurred during ischaemia. There was, however, a five-fold increase in VIP in portal venous plasma during SMA + CA occlusion. In the reperfusion period there were increases in VIP concentrations in both systemic and portal circulations in both groups. During ischaemia there was a rise in mean arterial pressure and peripheral resistance and a fall in cardiac output. Reperfusion was characterized by systemic and splanchnic vasodilation coincident with the rise in systemic plasma VIP. It is concluded that VIP which is released from the ischaemic intestine is likely to mediate a component of vasodilation seen during reperfusion.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherCeliac Arteryen
dc.subject.otherGastrins.metabolismen
dc.subject.otherHemodynamics.physiologyen
dc.subject.otherMesenteric Arteriesen
dc.subject.otherMesenteric Vascular Occlusion.physiopathologyen
dc.subject.otherNeurotensin.metabolismen
dc.subject.otherPancreatic Polypeptide.metabolismen
dc.subject.otherPortal System.physiopathologyen
dc.subject.otherReperfusionen
dc.subject.otherSheepen
dc.subject.otherVasoactive Intestinal Peptide.metabolismen
dc.titleExperimental mesenteric ischaemia in sheep: gut peptide release and haemodynamic changes.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Gastroenterology and Hepatologyen
dc.identifier.affiliationDepartment of Surgery, University of Melbourne, Austin Hospital, Victoria, Australiaen
dc.description.pages251-8en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/2491151en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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