Diabetes insipidus remains a common complication of transsphenoidal surgery; however, it is most frequently transient in nature. Patients with an intraoperative CSF leak, a microadenoma, a craniopharyngioma, or an RCC appear to have an increased risk of transient DI. Risk factors for persistent DI include an intraoperative CSF leak, a craniopharyngioma, or an RCC.
The results suggest that isoflurane administrated after OGD or brain ischemia provides neuroprotection. Mitochondrial adenosine 5'-triphosphate-sensitive potassium channels may be involved in this protection.
BackgroundElderly patients are more likely to suffer from postoperative cognitive dysfunction (POCD) after surgery and anesthesia. Except for declined organ function, the particular pathogenesis of POCD in elderly patients remains unknown. This study is carried out to determine the critical role of the NOD-like receptor protein 3 (NLRP3)-caspase-1 pathway in isoflurane-induced cognitive impairment.MethodsYoung (6–8 months old) and aged (14 months old) healthy male C57BL/6 mice were exposed to 1.5% isoflurane for 2 h. Some mice received intraperitoneal injection of Ac-YVAD-cmk (8 mg/kg), a specific inhibitor of caspase-1, 30 min before the isoflurane exposure. Morris water maze test was carried out 1 week after the isoflurane anesthesia. Brain tissues were harvested 24 h after the isoflurane anesthesia. Western blotting was carried out to detect the expression of NLRP3, interleukin (IL)-1β, and IL-18 in the hippocampus. Mouse microglial cell line BV-2 and primary microglial cultures were primed by lipopolysaccharide for 30 min before being exposed to isoflurane. NLRP3 was downregulated by RNA interference.ResultsCompared to young mice, aged mice had an increased expression of NLRP3 in the hippocampus. Isoflurane induced cognitive impairment and hippocampal inflammation in aged mice but not in young mice. These effects were attenuated by Ac-YVAD-cmk pretreatment (P < 0.05). Isoflurane activated NLRP3-caspase-1 pathway and increased the secretion of IL-18 and IL-1β in cells pretreated with lipopolysaccharide but not in cells without pretreatment. Downregulation of NLRP3 attenuated the activation of NLRP3 inflammasome by isoflurane.ConclusionsNLRP3 priming status in aged mouse brain may be involved in isoflurane-induced hippocampal inflammation and cognitive impairment.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1137-1) contains supplementary material, which is available to authorized users.
A brief exposure to the volatile anesthetic isoflurane (preconditioning) induces ischemic tolerance in rat brain. However, whether isoflurane preconditioning improves long-term neurological outcome after brain ischemia and the mechanisms for this neuroprotection are not known. Here, we report that isoflurane preconditioning (2% isoflurane for 30 min at 24 h before brain ischemia) reduced brain infarct sizes and improved neurological deficit scores assessed 6, 24, and 72 h after permanent right middle cerebral arterial occlusion (MCAO) in adult male rats. More morphologically intact neurons and fewer dying cells existed in the ipsilateral frontal cortex area 1 and rostral subventricular zone of caudate putamen of isoflurane-preconditioned rats than rats undergoing MCAO alone at 14 days after the MCAO. This neuroprotection was abolished by an inhibitor of p38 mitogen-activated protein kinases (MAPK), 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580) (the percentages of infarct volumes in the ipsilateral hemisphere volumes were 34 Ϯ 7% for MCAO, 24 Ϯ 6% for isoflurane preconditioning plus MCAO, and 30 Ϯ 6% for SB203580 plus isoflurane preconditioning plus MCAO, n ϭ 8, P Ͻ 0.05 for isoflurane preconditioning plus MCAO to compare with MCAO alone or with SB203580 plus isoflurane preconditioning plus MCAO) and mimicked by an activator of these kinases, anisomycin. Isoflurane induced a rapid and prolonged increase of the phosphorylated p38 MAPK in cerebral neocortex. These active kinases distributed mainly in perikaryal regions of neurons. These results suggest that isoflurane preconditioning may improve long-term neurological outcome after focal brain ischemia and that the effects may be mediated by activating p38 MAPK.
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