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Objective@#To establish a rat model of polycystic ovary syndrome(PCOS) complicated with atherosclerosis(AS).@*Methods@#Sixteen female SD rats were selected and randomly divided into control group and model group, with 8 rats in each group.The rats in the control group were given routine rearing.The rats in the model group were subcutaneously given dihydrotestosterone(DHT) in neck and fed with high fat diet for a long term.The changes of food intake (FI), body weight(BW), testosterone (T), estrogen (E2), luteinizing hormone (LH), total cholesterol (TC), blood glucose (BG) and insulin (INS) were observed in the two groups.@*Results@#The levels of FI, T, E2, LH between the control group and model group had no obvious change[(86.13±7.83)g/r vs.(96.25±10.66)g/r, t=2.113, P=0.563, (10.79±1.74)mg/L vs.(11.47±1.89)mg/L, t=1.785, P=0.087; (36.58±2.57)ng/L vs.(38.64±1.78)ng/L, t=2.697, P=0.068; (15.47±1.96)IU/L vs.(16.01±0.80)IU/L, t=1.570, P=0.614]. The levels of BW, TC, DHT, INS in the model group were significantly higher than those in the control group[(234.54±17.14)g vs.(192.67±16.47)g, t=7.930, P<0.000; (2.47±0.13)mmol/L vs.(2.02±0.15)mmol/L, t=6.475, P<0.000; (139.75±12.12)ng/L vs.(55.63±7.80)ng/L, t=8.697, P<0.000; (283.25±33.47)pg/mg vs.(162.12±15.51)pg/mg, t=9.289, P<0.000]. Tube wall was markedly thickened in the model group after being given high fat feed for 12 weeks, and intimal wall was significantly thickened after 16 weeks, and endotheliocyte injury, deep collagen fiber, monocyte adhesion, visible atherosclerotic plaques were observed in the model grouop.@*Conclusion@#DHT-induced PCOS rat model by high fat feed reproduces the human typical clinical symptoms and pathological characteristics, it can provide a relatively simple and feasible rat model for further study of the mechanism of PCOS complicated with AS.
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Objective To evaluate the effect of dexmedetomidine on autophagy in the hippocampal neurons of rats with traumatic brain injury (TBI).Methods Adult male Sprague-Dawley rats,aged 12-16 weeks,weighing 340-370 g,were randomly divided into 3 groups (n=80 each) using a random number table:sham operation group (group S),traumatic brain injury group (group TBI) and dexmedetomidine group (group Dex).The rats were subjected to a diffuse cortical impact injury caused by a modified weight-drop device to induce TBI.Dexmedetomidine 15 μg/kg was injected intravenously immediately after TBI in Dex group.At 24 and 48 h after TBI,neurological deficit score (NDS) was assessed,Morris water maze test was performed,and brains were removed for detection of brain water content in the brain tissue.At 6,12,24 and 48 h after TBI,the expression of hippocampal LC3]Ⅱ was determined using Western blot analysis.Results Compared with group S,brain water content and NDS were significantly increased at 24 and 48 h after TBI,the escape latency was prolonged,and the expression of hippocampal LC3 Ⅱ was upregulated at 6,12,24 and 48 h after TBI in TBI group.Compared with TBI group,brain water content and NDS were significantly decreased at 24 and 48 h after TBI,the escape latency was shortened,and the expression of hippocampal LC3 Ⅱ was down-regulated at 6,12,24 and 48 h after TBI in Dex group.Conclusion The mechanism by which dexmedetomidine reduces TBI is related to inhibition of autophagy in the hippocampal neurons of rats.
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ObjectiveTo study the pharmacokinetics of sufentanil in patients undergoing different cardiac surgeries with or without CPB.MethodsSixteen ASA Ⅱ or Ⅲ patients aged 56-64 yr weighing 52-78 kg undergoing cardiac surgery were divided into 2 groups ( n ＝ 8 each):group Ⅰ off-pump coronary artery bypass grafting and group Ⅱ valve replacement.Radial artery and peripheral vein were cannnlated.A bolus of sufentanil 5μg/kg was administered iv after induction of anesthesia.Blood samples were obtained from radial artery at 1,3,5,10,20,30,60,120,180,240,360 min after sufentanil injection.Plasma was immediately separated and stored at - 80 C for determination of plasma sufentanil concentration by liquid c hromatography-mass spectrometry.Pharmacokinetic parameters were calculated by 3P97 pharmacological program.ResultsThe pharmacokinetic profile of sufentanil was best described by a three-compartment open model.The 3 exponential equations in group Ⅰ,before and during CPB in group Ⅱ were:Cp(t) ＝ 11.7 e-0.47t + 1.9 e0.043t + 0.27 e-0.0032t ; Cp(t) ＝ 33.4 e-1.87t + 7.1e-0.103t +2.0 e-0.0248t and Cp(t) ＝ 23.8 e-0.54t + 5.2 e0.054t + 0.15 e-0.0017t respectively.There was significant difference in most of the pharmacokinetic parameters between the 2 groups.ConclusionsThe pharmacokinetics of sufentanil in patients undergoing different cardiac surgeries can be described by ~compartment open model.Low cardiac function and CPB can reduce its drug metabolism rate and prolong the duration of action.