BACKGROUND: The purpose of this work was to determine the effects of hypoxemia on systemic hemodynamic variables and regional conduit arterial blood flows in neonatal piglets. MATERIALS AND METHODS: Using transit time blood flow probes, cardiac output and cranial mesenteric artery blood flow were monitored in groups of prematurely delivered (90% of term gestational age) and 2-week-old piglets prior to, during, and after exposure to a 30-min hypoxic (FIO2 = 0.12) challenge. RESULTS: The documented alterations in systemic mean arterial pressure and cardiac output pressure during hypoxia and reoxygenation were consistent with the maturational age of the animals. In response to hypoxia, all animals demonstrated significant reductions in mesenteric blood flow, with returns to baseline levels during the 30-min reoxygenation phase. In still other prematurely delivered piglets, nutrient mesenteric arterial blood flows were measured using in vivo videomicroscopy. The marked hypoxemia-induced decline in mucosal blood flow was reversed by reoxygenation. CONCLUSIONS: The physiologic mechanisms responsible for neonatal mesenteric vasoactive responsiveness are present in conduit and in nutrient vessels well prior to birth and can be activated by a significant perturbation. These observations are germane insofar as they provide a stable, age-matched acute animal model to study neonatal intestinal ischemic diseases, including necrotizing enterocolitis. Copyright 1998 Academic Press.
BACKGROUND: The purpose of this work was to determine the effects of hypoxemia on systemic hemodynamic variables and regional conduit arterial blood flows in neonatal piglets. MATERIALS AND METHODS: Using transit time blood flow probes, cardiac output and cranial mesenteric artery blood flow were monitored in groups of prematurely delivered (90% of term gestational age) and 2-week-old piglets prior to, during, and after exposure to a 30-min hypoxic (FIO2 = 0.12) challenge. RESULTS: The documented alterations in systemic mean arterial pressure and cardiac output pressure during hypoxia and reoxygenation were consistent with the maturational age of the animals. In response to hypoxia, all animals demonstrated significant reductions in mesenteric blood flow, with returns to baseline levels during the 30-min reoxygenation phase. In still other prematurely delivered piglets, nutrient mesenteric arterial blood flows were measured using in vivo videomicroscopy. The marked hypoxemia-induced decline in mucosal blood flow was reversed by reoxygenation. CONCLUSIONS: The physiologic mechanisms responsible for neonatal mesenteric vasoactive responsiveness are present in conduit and in nutrient vessels well prior to birth and can be activated by a significant perturbation. These observations are germane insofar as they provide a stable, age-matched acute animal model to study neonatal intestinal ischemic diseases, including necrotizing enterocolitis. Copyright 1998 Academic Press.
Authors: Erika Haase; David L Bigam; Quentin B Nakonechny; Laurence D Jewell; Gregory Korbutt; Po-Yin Cheung Journal: Ann Surg Date: 2004-08 Impact factor: 12.969