Besides local neuronal damage caused by the primary insult, central nervous system injuries may secondarily cause a progressive cascade of related events including brain edema, ischemia, oxida- tive stress, excitotoxi...Besides local neuronal damage caused by the primary insult, central nervous system injuries may secondarily cause a progressive cascade of related events including brain edema, ischemia, oxida- tive stress, excitotoxicity, and dysregulation of calcium homeostasis. Hypothermia is a beneficial strategy in a variety of acute central nervous system injuries. Mild hypothermia can treat high in- tracranial pressure following traumatic brain injuries in adults. It is a new treatment that increases survival and quality of life for patients suffering from ischemic insults such as cardiac arrest, stroke, and neurogenic fever following brain trauma. Therapeutic hypothermia decreases free radical pro- duction, inflammation, excitotoxicity and intracranial pressure, and improves cerebral metabolism after traumatic brain injury and cerebral ischemia, thus protecting against central nervous system damage. Although a series of pathological and physiological changes as well as potential side ef- fects are observed during hypothermia treatment, it remains a potential therapeutic strategy for central nervous system injuries and deserves further study.展开更多
Previous studies have reported a neuroprotective effect of 8-hydroxy-2-（di-n-propylamino）tetralin （8-OH-DPAT） against traumatic brain injury. In accordance with the Marmarou method, rat models of diffuse axonal in...Previous studies have reported a neuroprotective effect of 8-hydroxy-2-（di-n-propylamino）tetralin （8-OH-DPAT） against traumatic brain injury. In accordance with the Marmarou method, rat models of diffuse axonal injury were established. 8-OH-DPAT was intraperitoneally injected into model rats. 8-OH-DPAT treated rats maintained at constant temperature served as normal temperature controls TUNEL results revealed that neural cell swelling, brain tissue necrosis and cell apoptosis occurred around the injured tissue. Moreover, the number of Bax-, Bcl-2- and caspase-3-positive cells increased at 6 hours after diffuse axonal injury, and peaked at 24 hours. However, brain injury was attenuated, the number of apoptotic cells reduced, Bax and caspase-3 expression decreased, and Bcl-2 expression increased at 6, 12, 24, 72 and 168 hours after diffuse axonal injury in normal temperature control and in 8-OH-DPAT-intervention rats. The difference was most significant at 24 hours. All indices in 8-OH-DPAT-intervention rats were better than those in the constant temperature group. These results suggest that 8-OH-DPAT inhibits Bax and caspase-3 expression, increases Bcl-2 expression, and reduces neural cell apoptosis, resulting in neuroprotection against diffuse axonal injury. This effect is associated with a decrease in brain temperature.展开更多
目的 研究亚低温联合依达拉奉治疗急性脑梗死的疗效及对血清超敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)、神经元特异性烯醇化酶(Neuron-specific enolase ,NSE)、S100钙结合蛋白β(S100 calcium binding protein β,S1...目的 研究亚低温联合依达拉奉治疗急性脑梗死的疗效及对血清超敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)、神经元特异性烯醇化酶(Neuron-specific enolase ,NSE)、S100钙结合蛋白β(S100 calcium binding protein β,S100-β)水平的影响。方法 选取郑州大学附属郑州中心医院收治的急性脑梗死病人96例,随机分为对照组和研究组,各48例。对照组单纯予以依达拉奉治疗,研究组在此基础上施加亚低温治疗。比较两组治疗总有效率、不良反应情况等。记录治疗前后两组神经功能缺损(National Lnstitute of Health Stroke Scale, NHISS)评分和日常生活活动能力(Ability of Daily Life, ADL)评分。采集病人治疗前后血液样本,检测血清hs-CRP、NSE、S100-β蛋白水平及血浆超氧化物歧化酶(su-peroxidedismutase, SOD)和丙二醛(malondialdehyde,MDA)水平。结果 研究组治疗总有效率(91.67%)明显高于对照组(75.00%,χ2=4.80, P =0.03);治疗后,研究组血清学指标hs-CRP、S100-β、NSE均明显低于对照组(均 P <0.01);研究组SOD水平高于对照组( P <0.01),而MDA低于对照组( P <0.01);研究组ADL评分高于对照组( P <0.01),而NHISS评分低于对照组( P <0.01);两组不良反应发生率比较差异无统计学意义( P >0.05)。结论 亚低温联合依达拉奉治疗急性脑梗死疗效显著,可有效改善相关血清学指标,减轻体内氧化应激反应,改善病人神经功能及预后,且较安全可靠。展开更多
目的探讨缺血期亚低温对常温再灌注后心肌细胞的保护作用及其可能机制。方法本实验在中山大学心肺脑复苏研究所完成。取50只SD新生1—2d乳鼠心脏，建立心肌细胞体外模型，利用氧糖剥夺（oxygen and glncose deprivation，OGD）和氧糖恢...目的探讨缺血期亚低温对常温再灌注后心肌细胞的保护作用及其可能机制。方法本实验在中山大学心肺脑复苏研究所完成。取50只SD新生1—2d乳鼠心脏，建立心肌细胞体外模型，利用氧糖剥夺（oxygen and glncose deprivation，OGD）和氧糖恢复（oxygen and glucoserestoration，OGR）模拟缺血一再灌注过程。将细胞随机（随机数字法）分入常温对照组、32℃ OGD-37℃OGR组（低温组）、37℃ OGD—OGR组（常温组），并在OGR0，0．5，1．0，1．5，2．0h分别测定心肌细胞收缩频率和平均收缩速率；在OGR0，2h分别收集细胞进行透射电镜观察超微结构以及线粒体变化，同时采取差速离心法制备心肌细胞线粒体匀浆液，使用Clark氧电极测定上述两个检测时点的线粒体呼吸控制率（respiratory control rate，RCR）。采用SPSSl3．0统计软件分析结果。结果低温组和常温组在OGD1h后都出现收缩频率和收缩速率下降，但是常温组下降更明显（P=0．000）。随着OGR时间延长，两组的收缩参数都呈上升趋势，但低温组在1h后收缩功能接近正常，而常温组在观测时点始终低于对照组和低温组（P=0．000）。心肌细胞超微结果提示，常温组的线粒体肿胀明显，基质密度降低。线粒体RCR测定提示，低温组和常温组在OGR0h都明显降低，但后者损伤效应显著延长，持续到OGR2h。结论单纯缺血期亚低温可以减轻细胞线粒体的损伤，并有助于心肌细胞早期恢复收缩功能。展开更多
文摘Besides local neuronal damage caused by the primary insult, central nervous system injuries may secondarily cause a progressive cascade of related events including brain edema, ischemia, oxida- tive stress, excitotoxicity, and dysregulation of calcium homeostasis. Hypothermia is a beneficial strategy in a variety of acute central nervous system injuries. Mild hypothermia can treat high in- tracranial pressure following traumatic brain injuries in adults. It is a new treatment that increases survival and quality of life for patients suffering from ischemic insults such as cardiac arrest, stroke, and neurogenic fever following brain trauma. Therapeutic hypothermia decreases free radical pro- duction, inflammation, excitotoxicity and intracranial pressure, and improves cerebral metabolism after traumatic brain injury and cerebral ischemia, thus protecting against central nervous system damage. Although a series of pathological and physiological changes as well as potential side ef- fects are observed during hypothermia treatment, it remains a potential therapeutic strategy for central nervous system injuries and deserves further study.
基金funded by the Natural Science Foundation of Technology Department of Liaoning Province, No.20032047
文摘Previous studies have reported a neuroprotective effect of 8-hydroxy-2-（di-n-propylamino）tetralin （8-OH-DPAT） against traumatic brain injury. In accordance with the Marmarou method, rat models of diffuse axonal injury were established. 8-OH-DPAT was intraperitoneally injected into model rats. 8-OH-DPAT treated rats maintained at constant temperature served as normal temperature controls TUNEL results revealed that neural cell swelling, brain tissue necrosis and cell apoptosis occurred around the injured tissue. Moreover, the number of Bax-, Bcl-2- and caspase-3-positive cells increased at 6 hours after diffuse axonal injury, and peaked at 24 hours. However, brain injury was attenuated, the number of apoptotic cells reduced, Bax and caspase-3 expression decreased, and Bcl-2 expression increased at 6, 12, 24, 72 and 168 hours after diffuse axonal injury in normal temperature control and in 8-OH-DPAT-intervention rats. The difference was most significant at 24 hours. All indices in 8-OH-DPAT-intervention rats were better than those in the constant temperature group. These results suggest that 8-OH-DPAT inhibits Bax and caspase-3 expression, increases Bcl-2 expression, and reduces neural cell apoptosis, resulting in neuroprotection against diffuse axonal injury. This effect is associated with a decrease in brain temperature.
文摘目的 研究亚低温联合依达拉奉治疗急性脑梗死的疗效及对血清超敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)、神经元特异性烯醇化酶(Neuron-specific enolase ,NSE)、S100钙结合蛋白β(S100 calcium binding protein β,S100-β)水平的影响。方法 选取郑州大学附属郑州中心医院收治的急性脑梗死病人96例,随机分为对照组和研究组,各48例。对照组单纯予以依达拉奉治疗,研究组在此基础上施加亚低温治疗。比较两组治疗总有效率、不良反应情况等。记录治疗前后两组神经功能缺损(National Lnstitute of Health Stroke Scale, NHISS)评分和日常生活活动能力(Ability of Daily Life, ADL)评分。采集病人治疗前后血液样本,检测血清hs-CRP、NSE、S100-β蛋白水平及血浆超氧化物歧化酶(su-peroxidedismutase, SOD)和丙二醛(malondialdehyde,MDA)水平。结果 研究组治疗总有效率(91.67%)明显高于对照组(75.00%,χ2=4.80, P =0.03);治疗后,研究组血清学指标hs-CRP、S100-β、NSE均明显低于对照组(均 P <0.01);研究组SOD水平高于对照组( P <0.01),而MDA低于对照组( P <0.01);研究组ADL评分高于对照组( P <0.01),而NHISS评分低于对照组( P <0.01);两组不良反应发生率比较差异无统计学意义( P >0.05)。结论 亚低温联合依达拉奉治疗急性脑梗死疗效显著,可有效改善相关血清学指标,减轻体内氧化应激反应,改善病人神经功能及预后,且较安全可靠。
文摘目的探讨缺血期亚低温对常温再灌注后心肌细胞的保护作用及其可能机制。方法本实验在中山大学心肺脑复苏研究所完成。取50只SD新生1—2d乳鼠心脏，建立心肌细胞体外模型，利用氧糖剥夺（oxygen and glncose deprivation，OGD）和氧糖恢复（oxygen and glucoserestoration，OGR）模拟缺血一再灌注过程。将细胞随机（随机数字法）分入常温对照组、32℃ OGD-37℃OGR组（低温组）、37℃ OGD—OGR组（常温组），并在OGR0，0．5，1．0，1．5，2．0h分别测定心肌细胞收缩频率和平均收缩速率；在OGR0，2h分别收集细胞进行透射电镜观察超微结构以及线粒体变化，同时采取差速离心法制备心肌细胞线粒体匀浆液，使用Clark氧电极测定上述两个检测时点的线粒体呼吸控制率（respiratory control rate，RCR）。采用SPSSl3．0统计软件分析结果。结果低温组和常温组在OGD1h后都出现收缩频率和收缩速率下降，但是常温组下降更明显（P=0．000）。随着OGR时间延长，两组的收缩参数都呈上升趋势，但低温组在1h后收缩功能接近正常，而常温组在观测时点始终低于对照组和低温组（P=0．000）。心肌细胞超微结果提示，常温组的线粒体肿胀明显，基质密度降低。线粒体RCR测定提示，低温组和常温组在OGR0h都明显降低，但后者损伤效应显著延长，持续到OGR2h。结论单纯缺血期亚低温可以减轻细胞线粒体的损伤，并有助于心肌细胞早期恢复收缩功能。
