Pulmonary mechanical responses to intestinal ischaemia-reperfusion and endotoxin preconditioning

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Abstract

During intestinal ischaemia-reperfusion, endotoxin can be translocated. Pretreatment with sublethal doses of endotoxin develops tolerance to ischaemia-reperfusion in different organs; however, the tolerance to intestinal ischaemia-reperfusion in the lung has rarely been investigated. Our aim was to study the role of endotoxin pretreatment in the mechanical responses and inflammatory activation induced by intestinal ischaemia-reperfusion in the lung. Wistar rats were preconditioned with a sublethal dose of endotoxin on day -3 or -1. On day 0, anesthetized, paralyzed and mechanically ventilated rats were subjected to a 60-min occlusion of the superior mesenteric artery and a subsequent 240-min reperfusion. The low-frequency forced oscillation technique was employed to characterize the separate mechanical responses of the airways and respiratory tissues. Intestinal ischaemia-reperfusion caused a significant decrease in airway resistance and increases in tissue resistance and elastance, nitric oxide synthase and myeloperoxidase activities. Pretreatment with endotoxin modified both the pulmonary mechanical responses and the inflammatory markers in the lung during intestinal ischaemia-reperfusion. We conclude that endotoxin or the endotoxin-induced processes (and humoral mediators) have significant roles in the pathomechanism of the remote pulmonary effect of intestinal ischaemia-reperfusion.

Original languageEnglish
Pages (from-to)289-301
Number of pages13
JournalActa Physiologica Hungarica
Volume99
Issue number3
DOIs
Publication statusPublished - szept. 1 2012

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Endotoxins
Reperfusion
Ischemia
Lung
Airway Resistance
Superior Mesenteric Artery
Nitric Oxide Synthase
Peroxidase
Wistar Rats

ASJC Scopus subject areas

  • Physiology (medical)

Cite this

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abstract = "During intestinal ischaemia-reperfusion, endotoxin can be translocated. Pretreatment with sublethal doses of endotoxin develops tolerance to ischaemia-reperfusion in different organs; however, the tolerance to intestinal ischaemia-reperfusion in the lung has rarely been investigated. Our aim was to study the role of endotoxin pretreatment in the mechanical responses and inflammatory activation induced by intestinal ischaemia-reperfusion in the lung. Wistar rats were preconditioned with a sublethal dose of endotoxin on day -3 or -1. On day 0, anesthetized, paralyzed and mechanically ventilated rats were subjected to a 60-min occlusion of the superior mesenteric artery and a subsequent 240-min reperfusion. The low-frequency forced oscillation technique was employed to characterize the separate mechanical responses of the airways and respiratory tissues. Intestinal ischaemia-reperfusion caused a significant decrease in airway resistance and increases in tissue resistance and elastance, nitric oxide synthase and myeloperoxidase activities. Pretreatment with endotoxin modified both the pulmonary mechanical responses and the inflammatory markers in the lung during intestinal ischaemia-reperfusion. We conclude that endotoxin or the endotoxin-induced processes (and humoral mediators) have significant roles in the pathomechanism of the remote pulmonary effect of intestinal ischaemia-reperfusion.",
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