低血压对颈动脉中度狭窄兔脑损伤的作用
发布时间:2019-02-22 07:43
【摘要】:目的:观察不同干预所致低血压时双侧颈动脉中度狭窄家兔模型血浆神经元特异性烯醇化酶(neuron-specific enolase, NSE)及S-100β蛋白浓度的变化,探讨围术期低血压对颈动脉狭窄兔脑组织的损伤作用。 方法:选择成年家兔建立双侧颈动脉中度狭窄家兔模型,采用完全随机法分为四组,除对照组外,其他三组分别采用放血,硝酸甘油,丙泊酚使血压降低20%-30%并维持20分钟后分别采用相对应的方法恢复血压,分别于恢复血压后7.5、24h取血液标本,离心取上清液,用酶联免疫吸附测定法(ELISA法)测定血清中NSE、S-100β蛋白,将脑损伤的程度做比较。 结果:与对照组比较3个降压组的血液标本中NSE及S-100β在各个观测时间点的值均升高,差别有统计学意义(P0.05)。丙泊酚组在降压7.5h的NSE及S-100β的表达值分别为(1487±19)μg/L和(592±10)μg/L,与放血组、硝酸甘油组相比较各时间点NSE蛋白表达指标的升高值较小,差异有统计学意义(P0.05),S-100β蛋白的表达7.5h较其余两个实验组低,差异有统计学意义(P0.05)。 结论:对于双侧颈动脉中度狭窄兔模型,放血、硝酸甘油及麻醉药物引起的血压降低20%-30%均引起NSE及S-100β蛋白的表达升高,其中丙泊酚组的升高程度相对较低,可能与丙泊酚的脑保护作用有关。
[Abstract]:Objective: to observe the changes of plasma neuron-specific enolase (neuron-specific enolase, NSE) and S-100 尾 protein levels in bilateral carotid artery stenosis model of rabbits induced by hypotension induced by different interventions. To investigate the effect of perioperative hypotension on brain tissue injury in carotid stenosis rabbits. Methods: the bilateral carotid artery stenosis model was established in adult rabbits. The rabbits were randomly divided into four groups, except the control group, the other three groups were treated with bloodletting and nitroglycerin respectively. Propofol reduced blood pressure by 20% to 30% and maintained it for 20 minutes. Blood samples were collected at 7.5h 24 hours after restoration of blood pressure, and supernatants were obtained by centrifugation. Serum NSE,S-100 尾 protein was determined by enzyme linked immunosorbent assay (ELISA), and the degree of brain injury was compared. Results: compared with the control group, the values of NSE and S-100 尾 in blood samples of three hypotensive groups were all increased at each observation time point, the difference was statistically significant (P0.05). The expression of NSE and S-100 尾 in propofol group were (1487 卤19) 渭 g / L and (592 卤10) 渭 g / L at 7.5 h after hypotension, respectively. The expression of S-100 尾 protein was significantly lower than that of the other two experimental groups at 7.5 h (P0.05). Conclusion: blood letting, nitroglycerin and anesthetic drugs can increase the expression of NSE and S-100 尾 protein in bilateral carotid artery stenosis model, especially in propofol group. It may be related to the brain protection of propofol.
【学位授予单位】:山西医科大学
【学位级别】:硕士
【学位授予年份】:2013
【分类号】:R651.15
本文编号:2427984
[Abstract]:Objective: to observe the changes of plasma neuron-specific enolase (neuron-specific enolase, NSE) and S-100 尾 protein levels in bilateral carotid artery stenosis model of rabbits induced by hypotension induced by different interventions. To investigate the effect of perioperative hypotension on brain tissue injury in carotid stenosis rabbits. Methods: the bilateral carotid artery stenosis model was established in adult rabbits. The rabbits were randomly divided into four groups, except the control group, the other three groups were treated with bloodletting and nitroglycerin respectively. Propofol reduced blood pressure by 20% to 30% and maintained it for 20 minutes. Blood samples were collected at 7.5h 24 hours after restoration of blood pressure, and supernatants were obtained by centrifugation. Serum NSE,S-100 尾 protein was determined by enzyme linked immunosorbent assay (ELISA), and the degree of brain injury was compared. Results: compared with the control group, the values of NSE and S-100 尾 in blood samples of three hypotensive groups were all increased at each observation time point, the difference was statistically significant (P0.05). The expression of NSE and S-100 尾 in propofol group were (1487 卤19) 渭 g / L and (592 卤10) 渭 g / L at 7.5 h after hypotension, respectively. The expression of S-100 尾 protein was significantly lower than that of the other two experimental groups at 7.5 h (P0.05). Conclusion: blood letting, nitroglycerin and anesthetic drugs can increase the expression of NSE and S-100 尾 protein in bilateral carotid artery stenosis model, especially in propofol group. It may be related to the brain protection of propofol.
【学位授予单位】:山西医科大学
【学位级别】:硕士
【学位授予年份】:2013
【分类号】:R651.15
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