| Objective: To explore the effect of angiotensin(Ang)II induced acute blood pressure elevation on the cognitive function of rats,to explore the effect of acute blood pressure elevation on the permeability of the blood-brain barrier and the internal relationship among them.Methods: Sixteen adult male Lister-Hooded rats were randomly divided into experimental group(n=8)and control group(n=8).Six adult male SD rats were randomly divided into experimental group(n=3)and control group(n=3).3 SD rats in the experimental group and 3 SD rats in the control group were taken and measured their blood pressure with the tail cuff.Blood pressure was measured once every minute,after 5consecutive measurements,the experimental group was injected with Ang II at a dose of60 μg /kg intraperitoneally,the control group was injected with an equal volume of normal saline intraperitoneally.At the end of the injection,blood pressure was continuously measured for 15 minutes.5 Lister-Hooded rats in the experimental group and 5 ListerHooded rats in the control group were selected,they were performed acute electrophysiological experiments in vivo.Rats were deeply anesthetized with 30%urethane at a dose of 1.5g/kg,incised the scalp to expose the craniofacial area,drilled at the top of the skull,placed electrodes in the hippocampus CA1 area on the right side of the brain,fixed the electrodes with dental cement,and recorded f EPSP after resting for 30 minutes.The baseline was recorded for 30 minutes,the rats in the experimental group were injected with Ang II via the left femoral vein at a dose of 60 μg /kg,and the rats in the control group were injected with an equal volume of normal saline via the left femoral vein.It took about 5 minutes and continued recording for 50 minutes.The rats were given450 Low Frequency Stimulation(LFS)to induce Long-Term Depression(LTD),and the recording was continued for 3 hours.Three Lister-Hooded rats in the experimental group and three Lister-Hooded rats in the control group were selected,at the end of 30%urethane intraperitoneal injection anesthesia,the rats in the experimental group were injected with Ang II through the left femoral vein at a dose of 60μg/kg,the control group Rats were injected with an equal volume of normal saline through the left femoral vein.After injection,wait for 10 minutes,the rats in the experimental group and the rats in the control group were given a dose of 10 mg/kg to continue to inject 4.4k-Da TRITC-Dextran via the left femoral vein.After 40 minutes,the rats in the experimental group and the rats in the control group were perfused through the heart,and the whole brain tissue was taken out,fixed with 4% paraformaldehyde,stored at 4°C overnight,and dehydrated at 4°C with30% sucrose for 3 days.The dehydrated brain was sliced into 40μm thick brain slices by frozen section machine at-20℃.The slices were made on site and observed under a Leica SP8 gated sted fluorescence microscope and the whole brain slices were photographed.The Image J software was used to process the acquired pictures and measure the fluorescence intensity of the whole image.Results: One rat at control group died during the acute electrophysiological experiment in vivo,and the rest of the rats completed the experiment successfully.1.During the experiment,in the control group,the average arterial pressure of the rats was relatively stable and fluctuated from 79.10±2.14 mm Hg to 84.93±5.06 mm Hg.In the experimental group,the average arterial pressure of the rats increased to138.80±6.15 mm Hg after using Ang II,and then they slowly decreased.There were statistical differences in mean arterial pressure between the two groups of rats at the 6th minute,the 7th minute,the 8th minute,and the 11 th minute(P < 0.01).2.After 450 times of LFS,the experimental group f EPSP% decreased slightly,then increased rapidly,and finally stabilized near the baseline,the f EPSP% was 83.68±7.38%(n=5,p>0.05).After450 times of LFS,f EPSP% of the control group was 83.68±7.38%(n=5,p>0.05);f EPSP%decreased significantly,and then rose slightly,f EPSP% stabilized at 59.93±3.3%(n=4,p<0.05).Acute elevation of blood pressure can inhibit the LTD in hippocampal CA1 region of rats,resulting in the damage of synaptic plasticity.3.There was no statistical difference in the permeability of the blood-brain barrier between the experimental group and the control group.Conclusion: 1.Acute blood pressure elevation can damage the synaptic plasticity in the CA1 region of the hippocampus in rats and then may impair their cognitive function.2.Acute blood pressure elevation may not increase the permeability of the blood-brain barrier in rats,and more sensitive experimental methods may be needed to detect subtle differences. |
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