Mechanotransduction as a mechanistic explanation for edema-induced intestinal dysfunction

Shah, Shinil K.; Fogle, Lindsey N.; Aroom, Kevin R.; Gill, Brijesh S.; Uray, Karen; Laine, Glen A.; Stewart, Randolph H.; Cox, Charles S.

doi:10.1016/j.jamcollsurg.2009.06.098

Cited by 3 publications

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“…(7, 12) Based on our published data, we suspect that STAT-3 elevation in our model occurs via a non-canonical pathway and not via an inflammatory related mechanism. (31–33) Additionally, somewhat different from other models, iNOS mRNA is elevated much later than STAT-3, suggesting it is not a preceding step. (13) iNOS/NO does not seem to be a major modulator or initiator of signaling cascades that cause ileus, specifically STAT-3, in hydrostatic edema.…”

Section: Discussionmentioning

confidence: 89%

Evaluating the Potential Role of Nitric Oxide as a Mediator of Hydrostatic Edema Mediated Intestinal Contractile Dysfunction

Shah¹,

Xue²,

Jiménez³

et al. 2010

Journal of Surgical Research

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Background Administration of L-nil, a selective inhibitor of inducible nitric oxide synthase (iNOS), improves ileus in an animal model of resuscitation induced intestinal edema. The purpose of this study was to elucidate the iNOS/nitric oxide (NO) signal transduction pathway in intestinal edema. Materials and Methods Male Sprague Dawley rats were divided into two groups; CONTROL and RESUS + VH (edema, 80cc/kg normal saline (resuscitation) with mesenteric venous hypertension). iNOS mRNA and protein, iNOS activity, NO tissue levels, soluble guanylyl cyclase (sGC) expression, and cyclic guanosine monophosphate (cGMP) levels were measured. As a functional endpoint, we evaluated intestinal contractile strength and frequency in L-nil treated animals. Results Edema was associated with increased iNOS mRNA and protein expression without subsequent increases in iNOS activity or tissue NO levels. There was no significant change in sGC expression or increase in cGMP induced by edema. Administration of L-nil did not decrease edema development or preserve contractile strength, but increased contractile frequency. Conclusion Hydrostatic intestinal edema is not associated with increased iNOS activity or tissue NO levels. Administration of L-nil in edema increases intestinal contractile frequency. This may represent a potential mechanism for the amelioration of ileus seen with the administration of L-nil.

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Section: Discussionmentioning

confidence: 89%

Evaluating the Potential Role of Nitric Oxide as a Mediator of Hydrostatic Edema Mediated Intestinal Contractile Dysfunction

Shah¹,

Xue²,

Jiménez³

et al. 2010

Journal of Surgical Research

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“…(5–7, 19) The data presented currently builds on our previous work and further demonstrates the potential role of mechanical changes and mechanosensitive channels in edema induced contractile dysfunction. (8, 20)…”

Section: Discussionmentioning

confidence: 99%

Sodium hydrogen exchanger as a mediator of hydrostatic edema-induced intestinal contractile dysfunction

Uray¹,

Shah²,

Radhakrishnan³

et al. 2011

Surgery

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Resuscitation-Induced Intestinal Edema and Related Dysfunction: State of the Science

Shah¹,

Uray

Stewart

et al. 2011

Journal of Surgical Research

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High volume resuscitation and damage control surgical methods, while responsible for significantly decreasing morbidity and mortality from traumatic injuries, are associated with pathophysiological derangements that lead to subsequent end organ edema and dysfunction. Alterations in hydrostatic and oncotic pressures frequently result in intestinal edema and subsequent dysfunction. The purpose of this review is to examine the principles involved in the development of intestinal edema, current and historical models for the study of edema, effects of edema on intestinal function (particularly ileus), molecular mediators governing edema-induced dysfunction, potential role of mechanotransduction, and therapeutic effects of hypertonic saline. We review the current state of the science as it relates to resuscitation induced intestinal edema and resultant dysfunction.

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Mechanotransduction as a mechanistic explanation for edema-induced intestinal dysfunction

Cited by 3 publications

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Evaluating the Potential Role of Nitric Oxide as a Mediator of Hydrostatic Edema Mediated Intestinal Contractile Dysfunction

Evaluating the Potential Role of Nitric Oxide as a Mediator of Hydrostatic Edema Mediated Intestinal Contractile Dysfunction

Sodium hydrogen exchanger as a mediator of hydrostatic edema-induced intestinal contractile dysfunction

Resuscitation-Induced Intestinal Edema and Related Dysfunction: State of the Science

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