ABSTRACT
Objective To investigate the effects of sevoflurane anesthesia in diabetic pregnant rats on the cognitive function of the offspring rats. Methods Forty female Sprague?Dawley rats and 5 male rats, weighing 200-250 g, were used in the study. Twenty pregnant rats at 7 weeks of gestation were randomly selected, and diabetes mellitus was induced by intraperitoneal streptozotocin 45 mg∕kg and confirmed by blood glucose level>10.4 mmol∕L. Twenty pregnant rats at 20 days of gestation, in which diabetes mellitus was not induced, were selected and divided into 2 groups ( n=10 each) using a random number table:sevoflurane group (group S) and control group (group C). Twenty pregnant rats at 20 days of gestation with diabetes mellitus were selected and divided into 2 groups ( n=10 each) using a random number table:sevoflurane group (group DS) and control group ( group DC). In DS and S groups, the pregnant rats were placed in a self?made anesthetic box and inhaled 2% sevoflurane for 2 h. At 6 weeks after birth, the offspring rats were selected, and Morris water maze test was performed. The rats were sacrificed, brains were removed, and the hippocampi and cortex were removed for determination of phosphorylated cyclic a?denosine monophosphate response element?binding protein ( p?CREB) expression using immuno?histochem?istry. Results Compared with group C, the escape latency was significantly prolonged, and the frequency of crossing the original platform was significantly decreased in S and DC groups ( P<0.05) . Compared with group DC, the escape latency was significantly prolonged, and the frequency of crossing the original plat?form was significantly decreased in group DS (P<0.01). Compared with group S, the escape latency was significantly prolonged, the frequency of crossing the original platform was significantly decreased ( P<0.05) , and lighter staining for p?CREB was found, and the number of p?CREB positive cells was decreased in the hippocampus and cortex in group DS. Conclusion Sevoflurane anesthesia?induced cognitive dys?function is aggravated in the offspring rats of diabetic pregnant rats, and the mechanism is related to inhibi?tion of CREB phosphorylation.
ABSTRACT
Objective To evaluate the effect of sleep deprivation on cognitive function in the rats undergoing propofol anesthesia.Methods Sixty healthy male Sprague Dawley rats,aged 14-18 weeks,weighing 200-250 g,were randomly assigned into 3 groups (n=20 each) using a random number table:control group (group C),propofol anesthesia group (group P),and sleep deprivation + propofol anesthesia group (group SDP).Propofol was given as a bolus of 15 mg/kg followed by an infusion of 40 mg · kg-1 · h-1 for 2 h in group P.After the rats were subjected to rapid eye movement sleep deprivation for 24 h,the rats received propofol anesthesia in group SDP.Before sleep deprivation,after sleep deprivation,and at 1,3 and 7 days after anesthesia,Morris water maze test was used to assess the learning and memory function,and the escape latency and frequency of crossing the original platform were recorded.Ten rats randomly selected from each group at 1 and 7 days after anesthesia were sacrificed,and brains were removed to observe the morphology of nerve cells in the hippocampal CA1 region (by Nissl's staining) and to detect the expression of phosphorylated Tau at Thr231 (Tau-pThr231) in the hippocampal CA1 region (by immunohistochemisty).Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform was decreased,the expression of Tau-pThr231 in the hippocampal CA1 region was up-regulated at 1 day after anesthesia in P and SDP groups (P＜0.05),especially in group SDP (P＜0.05),and there was no significant difference between the groups at the other time points (P＞0.05).The pathological changes were aggravated at 1 day after anesthesia in group SDP compared with group P,and there was no significant difference at 3 and 7 days after anesthesia between group SDP and group P.Conclusion Sleep deprivation can aggravate the transient cognitive dysfunction after propofol anesthesia,and the mechanism is related to promotion of Tau phosphorylation in the rats.