Role of NO and other vascular mediators in the etiopathogenesis of necrotizing enterocolitis

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The etio-pathogenesis of necrotizing enterocolitis (NEC) is complex and multifactorial. Decades of research have not identified a definite etiology. Prematurity, enteral feeding, intestinal hypoxia/ischemia, inflammation and an abnormal microbiome are potential risk factors for developing this multisystem illness. Lack of specific diagnostic and prognostic markers adds to the challenges faced in managing NEC. Vascular mediators such as Nitric oxide (NO), catecholamines and endothelin (ET) regulate neonatal intestinal vascular resistance and may influence the pathophysiology of NEC. Neonatal morbidities, medications, transfusions, an altered microbiome and breast milk feeds may influence the vasculature in various ways. Better understanding of these mediators and their role in regulation of intestinal microcirculation and pathogenesis of NEC will assist in identifying strategies in prevention and management of this devastating illness.

Original languageEnglish (US)
Pages (from-to)9-28
Number of pages20
JournalFrontiers in Bioscience - Scholar
Volume11
Issue number1
DOIs
StatePublished - Mar 1 2019

Fingerprint

Microcirculation
Necrotizing Enterocolitis
Endothelins
Catecholamines
Blood Vessels
Nitric Oxide
Microbiota
Enteral Nutrition
Human Milk
Vascular Resistance
Ischemia
Inflammation
Morbidity
Research

Keywords

  • Endothelin
  • Mesenteric Circulation
  • Necrotizing Enterocolitis
  • Neonatal
  • Nitric Oxide
  • Review
  • Vasoconstriction

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

Cite this

Role of NO and other vascular mediators in the etiopathogenesis of necrotizing enterocolitis. / Nair, Jayasree; Lakshminrusimha, Satyanarayana.

In: Frontiers in Bioscience - Scholar, Vol. 11, No. 1, 01.03.2019, p. 9-28.

Research output: Contribution to journalArticle

@article{e0b66712efa34919b25ab1c7be4a7c4c,
title = "Role of NO and other vascular mediators in the etiopathogenesis of necrotizing enterocolitis",
abstract = "The etio-pathogenesis of necrotizing enterocolitis (NEC) is complex and multifactorial. Decades of research have not identified a definite etiology. Prematurity, enteral feeding, intestinal hypoxia/ischemia, inflammation and an abnormal microbiome are potential risk factors for developing this multisystem illness. Lack of specific diagnostic and prognostic markers adds to the challenges faced in managing NEC. Vascular mediators such as Nitric oxide (NO), catecholamines and endothelin (ET) regulate neonatal intestinal vascular resistance and may influence the pathophysiology of NEC. Neonatal morbidities, medications, transfusions, an altered microbiome and breast milk feeds may influence the vasculature in various ways. Better understanding of these mediators and their role in regulation of intestinal microcirculation and pathogenesis of NEC will assist in identifying strategies in prevention and management of this devastating illness.",
keywords = "Endothelin, Mesenteric Circulation, Necrotizing Enterocolitis, Neonatal, Nitric Oxide, Review, Vasoconstriction",
author = "Jayasree Nair and Satyanarayana Lakshminrusimha",
year = "2019",
month = "3",
day = "1",
doi = "10.2741/S524",
language = "English (US)",
volume = "11",
pages = "9--28",
journal = "Frontiers in Bioscience - Scholar",
issn = "1945-0516",
publisher = "Frontiers in Bioscience",
number = "1",

}

TY - JOUR

T1 - Role of NO and other vascular mediators in the etiopathogenesis of necrotizing enterocolitis

AU - Nair, Jayasree

AU - Lakshminrusimha, Satyanarayana

PY - 2019/3/1

Y1 - 2019/3/1

N2 - The etio-pathogenesis of necrotizing enterocolitis (NEC) is complex and multifactorial. Decades of research have not identified a definite etiology. Prematurity, enteral feeding, intestinal hypoxia/ischemia, inflammation and an abnormal microbiome are potential risk factors for developing this multisystem illness. Lack of specific diagnostic and prognostic markers adds to the challenges faced in managing NEC. Vascular mediators such as Nitric oxide (NO), catecholamines and endothelin (ET) regulate neonatal intestinal vascular resistance and may influence the pathophysiology of NEC. Neonatal morbidities, medications, transfusions, an altered microbiome and breast milk feeds may influence the vasculature in various ways. Better understanding of these mediators and their role in regulation of intestinal microcirculation and pathogenesis of NEC will assist in identifying strategies in prevention and management of this devastating illness.

AB - The etio-pathogenesis of necrotizing enterocolitis (NEC) is complex and multifactorial. Decades of research have not identified a definite etiology. Prematurity, enteral feeding, intestinal hypoxia/ischemia, inflammation and an abnormal microbiome are potential risk factors for developing this multisystem illness. Lack of specific diagnostic and prognostic markers adds to the challenges faced in managing NEC. Vascular mediators such as Nitric oxide (NO), catecholamines and endothelin (ET) regulate neonatal intestinal vascular resistance and may influence the pathophysiology of NEC. Neonatal morbidities, medications, transfusions, an altered microbiome and breast milk feeds may influence the vasculature in various ways. Better understanding of these mediators and their role in regulation of intestinal microcirculation and pathogenesis of NEC will assist in identifying strategies in prevention and management of this devastating illness.

KW - Endothelin

KW - Mesenteric Circulation

KW - Necrotizing Enterocolitis

KW - Neonatal

KW - Nitric Oxide

KW - Review

KW - Vasoconstriction

UR - http://www.scopus.com/inward/record.url?scp=85061983904&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85061983904&partnerID=8YFLogxK

U2 - 10.2741/S524

DO - 10.2741/S524

M3 - Article

VL - 11

SP - 9

EP - 28

JO - Frontiers in Bioscience - Scholar

JF - Frontiers in Bioscience - Scholar

SN - 1945-0516

IS - 1

ER -