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Aim To observe the neuroprotective effect of different doses of propofol on ischemic fetal rat brain.Methods Eighteen healthy pregnant SD rats were randomly allocated into the following six groups with three rats in each.Group S: sham operation group, Group IR: ischemia/reperfusion group, Group P1~P3: different doses of propofol groups, Group B: bicuculline group.In group S and group IR, 1 ml saline solution was administered via caudal vein.In group P1~P3, 10, 30, 50 mg·kg-1 of propofol was administered via caudal vein respectively.In group B, when 50 mg·kg-1 propfol was administered via caudal vein, 5 mg·kg-1 bicuculline was injected intraperitoneally at the same time.Bilateral uterine ovarian arteries were clamped for 11 mins to make intrauterine distress model of the fetal rats.The brains of fetal rats were removed after 3 days of reperfusion.Brain sections(5 μm thick) were mounted and stained with Hematoxylin and eosin(HE).The profile of the hippocampus CA1 was evaluated under a light microscope and neuronal Lesion-index(LI) was calculated.MDA content of fetal rat brain was detected by thiobarbituric acid reaction method to determine the lipid peroxidation degree of brain.Results LI was (7.2±0.9) and MDA was (3.86±0.20) μmol·g-1 in group S.LI was 71.9±2.8 and the content of MDA was (9.10±0.45) μmol·g-1 in group IR, which increased significantly compared with those in group S(P<0.01).LI was (40.8±2.6), (21.4±1.4), (20.1±1.3) and the content of MDA was (7.32±0.41), (5.65±0.27), (5.44±0.28) μmol·g-1 in propofol groups, which decreased significantly compared with those in group IR(P<0.05).LI and the content of MDA was (51.2±2.3), (7.54±0.31) μmol·g-1 in group B,respectively, reversing partly the neuroprotevtive effect of propofl.Conclusion Propofol could protect the neurons in hippocampus CA1 region of fetal rat against intrauterine distress by reducing the concentration of MDA in the brain.
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Objective To investigate the radiation doses for the patients undergoing interventional radiology and to analyze the dose - influencing factors.MethodsThe clinical data of 461 patients undergoing interventional radiology,including cerebral angiography ( CEA ),cerebral aneurysm embolism ( CAE ),superselective hepatic arterial chemoembolization ( SHAG ),coronary angiography ( COA ),percutaneous intracoronary stent implantation ( PIS1 ),cardiac radiofrequency catheter ablation ( RFCA ),and permanent cardiac pacemaker implantation(PCPI) were collected to observe the cumulative air kerma (CAK),dose area product (DAP),and fluoroscopy time,and effective dose was estimated using the conversion factors.Results The effective doses for CEA,CAE,SHAG,COA,PISI,RFCA,and PCPI were (0.33 ±0.20),(0.49 ±0.35),(6.92 ±4.19),(0.76 ±0.91),(2.35 ± 1.47),(0.50 ±0.74),and (0.67 ±0.70) Sv,respectively.In 126 of the 416 patients (26%),the effective doses were greater than 1 Sv,and the effective doses of 10 person-times were greater than 10 Sv,all of which were observed in the patients undergoing SHAG.The CAK values for CEA,CAE,SHAG,COA,PISI,RFCA,and PCPIwere (0.55 ±0.43),(1.34 ± 1.11),(0.95 ±0.57),(0.32 ±0.31),(0.91 ±0.33),(0.16 ±0.22),and (0.15 ±0.14) Gy,respectively.The CAK values were greater than 1 Gy in 59 of the 461 patients ( 12.8% ),greater than 2 Gy in 11 cases (2.4%) ,and greater than 3 Gy in 1 CEA cases and 1 CEA case,respectively.Conclusions There is a wide variation range in radiation dose for different procedures.As most interventional radiology procedure can result in clinically significant radiation dose to the patient,stricter dose control should be carried out.
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Objective To explore the optimum exposure factors in digital chest radiography.Methods Chest phantom was exposed under auto exposure control model with 73, 90, 125kV and S200,400,800 plus or minor 4 micro-adjust for each sensitivity grade. Meanwhile dose area product (DAP) was recorded and the value of IQFinv was analyzed automatically by Artinis CDRAD Analyzer 1.1. Ten volunteers were exposed with 73 kV, S800 - 2; 90 kV, S800 + 2 and 125 kV, S400 + 2. Two radiologists evaluated and scored image quality. Statistical analysis was performed using one way ANOVA test by SPSS 12. 0. Results ( 1 ) The quality scores of volunteers' images obtained with three combinations of exposure factors were 2. 7 ± 0. 5 for 73 kV group, 2. 9 ± 0. 3 for 90 kV group and 2. 8 ± 0. 4 for 125 kV group. The difference among them was not statistically significant ( F = 0. 587, P ＞ 0. 05 ). Whereas the DAP values were (29. 1 ± 7.9) mGy · cm2 for 73 kV group, ( 30. 5 ± 4. 5 ) mGy ·cm2 for 90 kV group and (40. 4 ±7.6) mGy · cm2 for 125 kV group, with statistically significant difference among them ( F = 9. 803, P ＜0. 01 ). (2) In all three kV conditions, DAP value of phantom declined when sensitivity increased. There was a difference of DAP value by 11％ between two successive sensitivity grades. Under the condition of same sensitivity, DAP value changed with kV in the following order: 73 kV ＞90 kV ＞ 125 kV. (3) The value of IQFinv decreased when sensitivity increased. Under the condition of same sensitivity, IQFinv changed with kV as follow: 73 kV ＞90 kV ＞ 125 kV. Conclusion The combination of exposure factors of 90 kV and S800 + 2-S800 +4 is optimum for digital chest radiography.
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Objective To investigate the changes of neuroglobin (Ngb) expression in the CA1 hippocampus after cerebral ischemia and the effect of limb ischemic preconditioning (LIP) on it in young and aged rats. Methods SD rats aged 3 months and 21-23 months with permanently occluding bilateral vertebral arteries were randomly divided into cerebral ischemic group and LIP + cerebral ischemic group, respectively. The expression of Ngb mRNA and protein in the hippocampus were investigated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot methods. The profile of delayed neuronal death (DND) of pyramidal neurons in the hippocampus CA1 was evaluated by using thionin staining under light microscope by determining the neuronal density (ND) and histological grade (HG). Results Ngb mRNA and protein expressions were 0.16±0.02 and 0.32±0.07, 0.52±0.04 and 0.91±0.06, 0.09±0.01 and 0.22±0.08, 0.21±0.01 and 0.66± 0. 06 in young cerebral ischemia group, LIP + young cerebral ischemia group, aged cerebral ischemia group and LIP + aged cerebral ischemia group, respectively. The expressions of Ngb mRNA and protein after cerebral ischemia for 8 minutes in aged rats were decreased compared with those in the young rats which suffered an identical cerebral ischemia with the aged rats (P<0.05). LIP up-regulated Ngb mRNA and protein expressions in both young and aged rats which suffered cerebral ischemia (P<0.05). However, the up-regulation of Ngb expression in aged rats was significantly less than that in young rats (P<0.05). Neuropathological evaluation showed that ND was 38.8±10.9, 171.5±16.9, 21.2±12.2 and 102.7±15.4 in young cerebral ischemic group, LIP + young cerebral ischemic group, aged cerebral ischemic group and LIP + aged cerebral ischemic group, respectively. It showed that obvious DND of pyramidal neurons was found in young and aged rats after cerebral ischemia. Although LIP effectively protected the pyramidal neurons in the CA1 hippocampus against DND normally induced by ischemic insult, the neuroprotection of LIP for aged rats was less effective than that for young rats. Conclusions The expression of Ngb and the up-regulation effect of LIP on the expression in aged rats are significantly decreased compared to those in young rats when the rats suffer cerebral ischemia. These differences may be one of underlying reasons why the aged rats exhibit severe DND after cerebral ischemia and why the neuroprotective effect of LIP is less in the aged rats than that in the young rats.
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AIM To observe whether limb ischemic preconditioning (LIP) could attenuate pyramidal neuronal apoptosis of the CA1 hippocampus and brain edema evoked by brain ischemia in rats. METHODSSeventy-two rats whose bilateral vertebral arteries occluded permanently were randomly assigned into 6 groups: sham, LIP(bilateral femoral arteries were clamped for 10 min, 3 times, in a 10-min interval), brain ischemic insult, LIP+brain ischemic insult, DMSO+LIP+brain ischemic insult and SB 203580+LIP+brain ischemic insult groups. Assays for neuronal apoptosis were performed using TUNEL staining. The percentage of wet over dry tissue weight of the brain was measured by weighing method. RESULTS There were almost no TUNEL-positive cells in the CA1 hippocampus in either sham or LIP group. Clear TUNEL-positive pyramidal neurons of the CA1 hippocampus and increase in brain water content were detected in rats subjected to brain ischemic insult. But the number of TUNEL-positive cells and the increase in brain water content were significantly decreased in LIP+brain ischemic insult group compared with that in brain ischemic insult group, indicated that LIP prevented the occurrence of apoptosis of pyramidal neurons of the CA1 hippocampus and brain edema induced by brain ischemic insult. Pretreatment with SB 203580, an inhibitor of mitogen activated protein kinase p38(p38 MAPK), significantly increased the number of TUNEL-positive cells and brain water in SB 203580+LIP+brain ischemic insult group compared with that in DMSO+LIP+brain ischemic insult group, indicated that SB 203580 blocked the protection of LIP against neuronal apoptosis in the CA1 hippocampus and brain edema. CONCLUSION LIP could attenuate pyramidal neurons apoptosis of the CA1 hippocampus and brain edema evoked by brain ischemia, which maybe related to the activation of p38 MAPK.
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AIM To explore the role of superoxide dismutase (SOD) in the p38 mitogen-activated protein kinase (MAPK) mediated brain ischemic tolerance induced by limb ischemic preconditioning (LIP). METHODS The Wistar rats with permanent occlusion of the bilateral vertebral arteries were subjected to occlude the bilateral femoral arteries for 10 min, 3 times, at an interval of 10 min to get the LIP, then global brain ischemia was induced immediately by occluding the bilateral common carotid arteries for 8 min. SB 203580 (100 μmol·L-1, in a volume of 25 μL), an inhibitor of p38 MAPK, was intraventricularly injected 30 min before LIP in SB 203580+LIP+brain ischemia group. Xanthinoxidase and thiomalonylurea methods were used to determine SOD activity and malondialdehyde (MDA) content of the hippocampus, respectively. Thionin staining was used for observing histological changes of the hippocampus. RESULTS LIP significantly prevented the decrease of SOD activity, the increase of MDA content and the delayed neuronal death in the CA1 hippocampus induced by the brain ischemia. SB 203580 pretreatment evidently blocked the protective effect of LIP against the delayed neuronal death and the modulation on SOD activity and MDA content. CONCLUSIONSOD may play an important role served as a downstream molecule of p38 MAPK in the induction of brain ischemic tolerance by LIP.