Neither Xenon nor Fentanyl Induces Neuroapoptosis in the Newborn Pig Brain

摘要: BACKGROUND Some inhalation anesthetics increase apoptotic cell death in the developing brain. Xenon, an anesthetic, increases neuroprotection when combined with therapeutic hypothermia after hypoxic-ischemic brain injury newborn animals. The authors, therefore, examined whether there was any neuroapoptotic effect of breathing 50% xenon continuous fentanyl sedation for 24 h at normothermia or on pigs. METHODS Twenty-six healthy pigs (<24-h old) were randomized into four groups: (1)  h inhaled (Trec = 33.5 °C), (2) 24 h 38.5 (3) normothermia, (4) nonventilated juvenile controls normothermia. Five additional nonrandomized 2% isoflurane to verify proapoptotic our model. Pathological cells morphologically assessed cortex, putamen, hippocampus, thalamus, and white matter. To quantify findings, immunostained (caspase-3 terminal deoxynucleotidyl transferase-mediated deoxyuridine-triphosphate nick-end labeling) counted same regions. RESULTS For groups (4), total number less than 5 per region, representing normal developmental neuroapoptosis. After immunostaining counting, regression analysis showed that neither nor alone increased Isoflurane caused average a 5- 10-fold cells. CONCLUSION At hypothermia, induces neuroapoptosis neonatal pig Breathing