bq-123 and Enterocolitis--Necrotizing

Endothelin-1, prostaglandins (PGs), and nitric oxide (NO) have been implicated in the intestinal microvascular dysfunction of necrotizing enterocolitis (NEC). We hypothesized that direct peritoneal resuscitation (DPR) dilates the intestinal microvasculature and improves blood flow independent of these mechanisms.. Rat pups were assigned by litter to experimental NEC or CONTROL groups. Laser Doppler flowmetry evaluation of intestinal microvascular blood flow was studied at baseline, with mediator blockade (endothelin-A receptor, endothelin-B receptor, PG synthesis, or NO synthase) and with DPR. Repeated-measures analysis of variance test was applied with Tukey-Kramer honestly significant difference test (P < .05).. At baseline, NEC animals demonstrated significantly decreased ileal blood flow as compared with CONTROLs (P < .05). Endothelin-A receptor and PG inhibition increased flow in the intestinal microvasculature, but this was significantly augmented by the addition of DPR (P < .05). Blockade of NO synthase decreased intestinal blood flow, which was overcome with addition of DPR (P < .05).. Ileal blood flow was significantly reduced in NEC animals as compared with CONTROLs. The addition of DPR to the peritoneum increased ileal blood flow significantly in all groups in spite of blockade of these known vasoactive mechanisms. Direct peritoneal resuscitation may be a novel strategy to improve intestinal blood flow in NEC.

Topics: Animals; Animals, Newborn; Cyclooxygenase Inhibitors; Dialysis Solutions; Endothelin A Receptor Antagonists; Endothelin B Receptor Antagonists; Enterocolitis, Necrotizing; Ileum; Infusions, Parenteral; Mefenamic Acid; Microcirculation; Models, Animal; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase; Oligopeptides; Osmolar Concentration; Peptides, Cyclic; Piperidines; Random Allocation; Rats; Rats, Sprague-Dawley; Resuscitation; Solutions; Urinary Bladder