Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Ischemia and necrotizing enterocolitis: where, when, and how.

Philip T Nowicki1

  • 1Center for Cell and Vascular Biology, Columbus Children's Research Institute, Columbus, OH 43205, USA. NowickiP@pediatrics.ohio-state.edu

Seminars in Pediatric Surgery
|August 9, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Oral tetrahydrobiopterin improves the beneficial effect of adenoviral-mediated eNOS gene transfer after induction of hindlimb ischemia.

Molecular therapy : the journal of the American Society of Gene Therapy·2010
Same author

Oxidized low-density lipoprotein induces apoptosis in endothelial progenitor cells by inactivating the phosphoinositide 3-kinase/Akt pathway.

Journal of vascular research·2010
Same author

Endothelial nitric oxide synthase affects both early and late collateral arterial adaptation and blood flow recovery after induction of hind limb ischemia in mice.

Journal of vascular surgery·2009
Same author

Recovery from hind limb ischemia is less effective in type 2 than in type 1 diabetic mice: roles of endothelial nitric oxide synthase and endothelial progenitor cells.

Journal of vascular surgery·2009
Same author

Regenerative medicine in the treatment of peripheral arterial disease.

Journal of cellular biochemistry·2009
Same author

Endothelial nitric oxide synthase in human intestine resected for necrotizing enterocolitis.

The Journal of pediatrics·2006

Ischemia plays a critical role in necrotizing enterocolitis (NEC) pathogenesis, likely originating in the intestinal microcirculation and triggered by inflammation. This process involves an imbalance between endothelin-1 and nitric oxide, leading to vasoconstriction and disease progression.

Area of Science:

  • Neonatal physiology
  • Gastrointestinal pathology
  • Vascular biology

Background:

  • Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease in neonates.
  • Ischemia is a known contributor to NEC pathogenesis, but its precise role remains unclear.
  • Understanding the vascular mechanisms of ischemia in NEC is crucial for developing targeted therapies.

Purpose of the Study:

  • To elucidate the location, timing, and mechanism of ischemia in necrotizing enterocolitis (NEC).
  • To investigate the role of the intramural microcirculation and the endothelin-1 (ET-1) and nitric oxide (NO) balance in NEC pathogenesis.

Main Methods:

  • Conceptual analysis of existing literature on intestinal circulation and NEC pathogenesis.
  • Examination of the regulation of vascular resistance in the newborn intestine.

Related Experiment Videos

  • Hypothesizing the sequence of events leading to ischemic injury in NEC.

    • Main Results:

    • Ischemia in NEC likely initiates in the intramural microcirculation, specifically small arteries and submucosal arterioles.
    • Ischemia is probably a secondary event triggered by inflammation, playing a critical role in disease extension.
    • The pathogenesis involves an altered balance between vasoconstrictor endothelin-1 (ET-1) and vasodilator nitric oxide (NO), favoring constriction and ischemic cascade.

    Conclusions:

    • Ischemia is a key factor in NEC, originating in the microvasculature and exacerbated by an ET-1/NO imbalance.
    • Inflammation likely triggers ischemic events, which then rapidly propagate within the intestinal circulation.
    • Further research into these vascular mechanisms could identify novel therapeutic targets for NEC.