2005
DOI: 10.1097/01.ta.0000188935.66504.00
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Hypertonic Saline Resuscitation After Mesenteric Ischemia/Reperfusion Induces Ileal Apoptosis

Abstract: HS resuscitation after mesenteric I/R significantly increased ileal mucosal apoptosis while decreasing mucosal injury and may represent a novel mechanism by which HS resuscitation after mesenteric I/R reduces inflammation and imparts protection to the gut.

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Cited by 11 publications
(8 citation statements)
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“…The only common pathway exhibited by hibernation and IPC is that there are variations in intestinal blood flow patterns which lead to intestinal mucosal preservation. Intestinal injury is triggered by the ischemia/reperfusion sequence that produces a local and systemic inflammatory response, promotes apoptosis, and generates reactive oxygen species [25][26][27]. We conducted global gene expression profiling using microarrays to characterize the gene changes occurring in ileum of rats subjected to early and late ischemic preconditioning to begin to dissect the molecular basis for the phenomenon of IPC described above.…”
Section: Discussionmentioning
confidence: 99%
“…The only common pathway exhibited by hibernation and IPC is that there are variations in intestinal blood flow patterns which lead to intestinal mucosal preservation. Intestinal injury is triggered by the ischemia/reperfusion sequence that produces a local and systemic inflammatory response, promotes apoptosis, and generates reactive oxygen species [25][26][27]. We conducted global gene expression profiling using microarrays to characterize the gene changes occurring in ileum of rats subjected to early and late ischemic preconditioning to begin to dissect the molecular basis for the phenomenon of IPC described above.…”
Section: Discussionmentioning
confidence: 99%
“…29 The concept of a beneficial effect of hyperosmolality is corroborated by in vivo studies showing that hypertonic solutions improve cardiac function in children after open-heart surgery 30 and improve the outcome after hemorrhagic shock. 31-34 …”
Section: Discussionmentioning
confidence: 99%
“…This endothelial dysfunction is characterized by endothelial cell tight junction breakdown, inflammation, and leukocyte diapedesis (36,37). The leaky endothelium induced by traumatic shock is susceptible to excessive crystalloid resuscitation and unbalanced blood product administration, which leads to tissue injury, interstitial edema, acute respiratory distress syndrome and multiple organ failure (38). Plasma is thought to reverse the "endotheliopathy" induced by HS by restoring tight junctions and the glycocalyx, and inhibiting inflammation thus minimizing leakage of fluid across the leaky endothelium (39).…”
Section: A C C E P T E D Accepted Manuscriptmentioning
confidence: 99%