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Objective To observe the effects of combined penebyclidine hydrochloride-ketamine-propofoi intravenous anesthesia with local anesthesia in transcatheter occlusion of congenital heart diseases (CHD).Methods Eighty-six patients suffered in CHD scheduled for transcatheter Amplatzer occlusio were divided randomly and averagely into two groups with 43 cases each.Group A received combined ketamine--propofol ina'avenous anesthesia with local anesthesia. Group B received combined hydrochloride-ketamine-propofol intavenous anesthesia with local anesthesia.Results The rate of upper airway obstruction of child patient that was caused by increased oral secretion in group B (4.7%) was significantly lower than that in group A(14.0%) (P ＜ 0.05 ).The upper airway obsa-uction was removed by aspirating sputum and oxygen therapy in group A,while removed "by decreasing anesthetic depth in group B.The rate of arrhythmia in operation,the time of operation and wake-up time were not significantly different between two groups [37.2%,(2.65±1.85)h,(45.4±15.2)min in group A,but 34.9%,(2.58±1.74)h,(50.2±17.3)rain in group B (P＞0.05)].Conclusion The combined penehyclidine hydrochloride-ketamine-propofol intravenous anesthesia with local anesthesia is feasible and safe in transcatheter occlusion of congenital heart diseases.
RESUMO
Objective To develop a forebrain ischemic preconditioning model in C57BL/6 mice and determine the protective effects of ischemic preconditioning on brain ischemia-reperfusion injury. Methods Forty-eight 8-10 week old C57BL/6 mice weighing 19-23 g were randomly divided into four groups of 12 animals, A: sham-operation group; B: ischemic preconditioning group; C: ischemia-reperfusion group (I/ R); D: ischemic preconditioning + I/R group. The animals were anesthetized with halothane. Bilateral common carotid artery (BCCA) was exposed and occluded for 6min (ischemic preconditioning) or 18min followed by 3h reperfusion (I/R). In group D BCCA was firstly occluded for 6 min, then released and 48h later occluded again for 18min followed by 3h reperfusion. 6 animals in each group were sacrificed 72h after reperfusion and brain was immediately removed for detection of DNA fragmentation of neurons in hippocampus by TUNEL. Another 6 animals were sacrificed on the 7th day after I/R and neuronal damage was identified by microtubule-associated protein-2 immunochemistry and quantified by cresyl violet staining. Results I/R resulted in severe damage to hippocampus in C57BL/6 mice. The ischemic preconditioning caused neither noticeable hippocampal neuronal damage nor DNA fragmentation but significantly reduced hippocampal neuronal damage and DNA fragmentation caused by I/R. Conclusion Our results indicate that hippocampal neuronal injury induced by I/R can be greatly reduced by ischemic preconditioning in C57BL/6 mice. Many kinds of gene-altered C57BL/6 mice are available, this preconditioning model may provide an useful method for investigating the molecular mechanisms of ischemic preconditioning.