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Nitric Oxide Signaling Pathway01:28

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Multimodality Diagnosis of Mesenteric Ischemia
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Direct peritoneal resuscitation improves mesenteric perfusion by nitric oxide dependent pathways.

Sina Khaneki1, Amanda R Jensen1, Natalie A Drucker1

  • 1Section of Pediatric Surgery, Department of Surgery, Indiana University School of Medicine, Riley Hospital for Children and Indiana University Health, Indianapolis, Indiana.

The Journal of Surgical Research
|June 12, 2017
PubMed
Summary

Direct peritoneal resuscitation (DPR) using minimum essential medium (MEM) enhances survival after intestinal ischemia and reperfusion (I/R) by improving mesenteric perfusion and reducing injury. These benefits depend on endothelial nitric oxide pathways.

Keywords:
Direct peritoneal resuscitationEndothelial nitric oxide synthaseIntestinal ischemiaIschemia and reperfusionPerfusionSuperior mesenteric artery

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Area of Science:

  • Surgical Research
  • Gastroenterology
  • Vascular Biology

Background:

  • Direct peritoneal resuscitation (DPR) improves survival in intestinal ischemia and reperfusion (I/R) injury.
  • Minimum essential medium (MEM) is a key component in DPR, showing therapeutic benefits.
  • The role of endothelial nitric oxide pathways in MEM-mediated DPR is not fully understood.

Purpose of the Study:

  • To investigate the effects of MEM-based DPR on mesenteric perfusion, intestinal injury, and inflammation following I/R.
  • To determine if the benefits of MEM-based DPR are dependent on endothelial nitric oxide synthase (eNOS) pathways.

Main Methods:

  • Wild-type (WT) and eNOS knockout (eNOS KO) mice underwent induced intestinal ischemia for 60 minutes.
  • Following ischemia, 1 mL of phosphate-buffered saline (vehicle) or MEM was administered intraperitoneally.
  • Mesenteric perfusion, intestinal mucosal injury, and hepatic/intestinal inflammation were assessed after 48 hours.

Main Results:

  • MEM-based DPR significantly improved mesenteric perfusion in WT mice compared to vehicle (91.58% vs. 44.27%, P < 0.05).
  • This perfusion benefit was lost in eNOS KO mice, indicating dependence on nitric oxide signaling.
  • MEM treatment preserved mucosal architecture in WT mice, an effect absent in eNOS KO mice. Hepatic inflammation was elevated in eNOS KOs.

Conclusions:

  • DPR with MEM demonstrates significant therapeutic potential for intestinal I/R injury.
  • The protective effects of MEM-based DPR are critically dependent on endothelial nitric oxide signaling.
  • Further research into eNOS-dependent mechanisms could optimize DPR strategies for I/R injury.