![m_aex219f1.png?Expires=1501939504&Signat](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_sZY8KqfM6Wca5FlRK2CtxH9QOzOD8-k-JiKkHeIA3PfhBojQvg49k00BsIhgTz93SNpHhwAZX58g=s0-d "Schematic of method for quantification of apoptotic neurones in representative brain regions.21 (A) Similar sections were coronally cut from each animal to analyse tissue samples from prefrontal cortex (PFC), hippocampal cornu ammonis CA1 and CA2/3, thalamic laterodorsal nucleus (LDN), thalamic ventroposterior nucleus (VPN), somatosensory cortex (SSC), subiculum (S), and retrosplenial cortex (RSC), as outlined in red. (B) Quantification of degenerating neurones that were colabelled with the apoptotic executioner caspase 3, the neuronal marker NeuN, and the nuclear marker DAPI performed by unbiased stereology using the optical disector method after confocal microscopy imaging of z-stacks throughout entire tissue sections. Cells were excluded from counts if they transected the three exclusion planes (top, back, and right side, represented by "x" in schematic) and were included if located within the counting frame or transecting the other three sides of the frame (labelled with check marks in schematic). Density counts were calculated using tissue volume determined in Neurolucida using the counting dimensions and width of the tissue, and were averaged for each experimental group by brain region.")
Abstract
Background. Brain injury in newborn animals from prolonged anaesthetic exposure has raised concerns for millions of children undergoing anaesthesia every yr. Alternative anaesthetic techniques or mitigating strategies are urgently needed to ameliorate potentially harmful effects. We tested dexmedetomidine, both as a single agent alternative technique and as a mitigating adjuvant for sevoflurane anaesthesia.Methods. Neonatal rats were randomized to three injections of dexmedetomidine (5, 25, 50, or 100 µg kg−1 every 2 h), or 6 h of 2.5% sevoflurane as a single agent without or with dexmedetomidine (1, 5, 10, or 20 µg kg−1 every 2 h). Heart rate, oxygen saturation, level of consciousness, and response to pain were assessed. Cell death was quantified in several brain regions.Results. Dexmedetomidine provided lower levels of sedation and pain control than sevoflurane. Exposure to either sevoflurane or dexmedetomidine alone did not cause mortality, but the combination of 2.5% sevoflurane and dexmedetomidine in doses exceeding 1 µg kg−1 did. Sevoflurane increased apoptosis in all brain regions; supplementation with dexmedetomidine exacerbated neuronal injury, potentially as a result of ventilatory or haemodynamic compromise. Dexmedetomidine by itself increased apoptosis only in CA2/3 and the ventral posterior nucleus, but not in prefrontal cortex, retrosplenial cortex, somatosensory cortex, subiculum, lateral dorsal thalamic nucleaus, or hippocampal CA1.Conclusions. We confirm previous findings of sevoflurane-induced neuronal injury. Dexmedetomidine, even in the highest dose, did not cause similar injury, but provided lesser degrees of anaesthesia and pain control. No mitigation of sevoflurane-induced injury was observed with dexmedetomidine supplementation, suggesting that future studies should focus on anaesthetic-sparing effects of dexmedetomidine, rather than injury-preventing effects.http://ift.tt/2htSuzF
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