An experimental model of neonatal normocapnic hypoxia and resuscitation in Landrace/Large White piglets

Abstract

Haemodynamic fluctuations at baseline, during normocapnic hypoxia and reoxygenation in Landrace/Large White piglets are comparable to that in human neonates, making the breed a favorable model of human neonatal hypoxia investigation.

Histopathology of renal asphyxia in newborn piglets: Individual susceptibility to tubular changes

“…In the subcapsular regions, active glomerulogenesis was detected, represented by the tubuleglomerular nodules recently reported by our group as the typical developing unit in piglets [21] . Moreover, in the deep cortex, some senescent glomeruli with different degrees of sclerosis were detected and were occasionally associated with cellular or fibrotic crescents.…”

“…Experimental procedures were previously approved by the General Directorate of Veterinary Services (Permit no. 404/21-04-09) [21] . Briefly, following sedation with 10 mg/kg ketamine and 0.5 mg/kg midazolam, anesthesia was induced with 1 mg/kg propofol and 10 mg/kg fentanyl, administered through a peripheral vein.…”

“…In the present study we investigated the renal injury caused at the histological level by hypoxia-reoxygenation in an experimental neonatal swine model previously described by our group [21] .…”

Hypoxia-Induced Endothelial Damage and Microthrombosis in Myocardial Vessels of Newborn Landrace/Large White Piglets

“…As previously reported by our group the histological study of the myocardial cells in this experimental piglet model of normocapnic hypoxia/reoxygenation showed significant cardiac changes after hypoxia and reperfusion [12, 13]. This study aimed at identifying endothelial changes in the myocardium of newborn piglets following hypoxia, in order to examine if the endothelial cells represent a target of hypoxic injury in the cardiac vascular structures.…”

“…Microvascular dysfunction and endothelial cell damage have been identified as factors playing a key role not only in single organ dysfunction after asphyxia but also in the development of multiple organ failure in newborns affected by hypoxia [12]. In an in vitro system of coronary endothelial cells, energy depletion was shown to be responsible for endothelial hyperpermeability [14].…”