地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

心肺脑复苏药物治疗新进展

单纯的心肺脑复苏（ＣＰＣＲ）技术，胸外按压，口对口人工呼吸，只能维持重要脏器暂时的血供，要彻底维持自主呼吸、血流动力学以及正常的心律，必须依靠进一步药物治疗和电除颤。长期以来，药物的使用及其疗效存在较大的争论［１］。复苏中常用药物：肾上腺素、阿托品、...     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

急性醋氨酚中毒致肝损伤及维拉帕米预处理的作用

目的　通过观察 [Ca2 + ]i、MDA、SOD、LDH在急性醋氨酚 (APAP)致肝损伤中的变化 ,探讨APAP致肝损伤机制 ,并且观察维拉帕米预处理是否可以预防。方法　采用两步灌流法分离肝细胞进行原代培养 ,观察加入 10mmol/LAPAP后 30min、 1h、 2h、 4h、 8h各时点[Ca2 + ]i、MDA、SOD、LDH的变化 ;另在加入APAP前 2h用不同浓度 (2 0、 40、 80 μg/ml)的维拉帕米预处理 ,4h后观察上述指标的变化。结果　在 10mmol/LAPAP处理后 ,30min出现[Ca2 + ]i 升高 ,1h后出现MDA升高 ,SOD和LDH在第 2～ 4h升高 (以上均 P <0 0 5 ) ;终浓度为2 0 μg/ml、 40 μg/ml的维拉帕米预处理明显使各值下降 (P <0 0 5 ) ,而 80 μg/ml使各数值不变或上升。结论　 [Ca2 + ]i 的显著性升高是急性醋氨酚中毒肝损伤的始动因素 ;一定浓度的维拉帕米预处理对这种肝损伤有保护作用     

地塞米松对大鼠颅脑创伤保护作用的实验研究

目的 观察地塞米松治疗大鼠创伤性脑损伤(traumatic brain injury, TBI)后大鼠脑组织中核因子κB(NF-κB)的变化,探讨地塞米松对大鼠 TBI 后继发性炎症反应的影响.方法 建立气体冲击致大鼠重度脑创伤模型;实验大鼠随机分为两组,脑损伤组和脑损伤十地塞米松治疗组各20只,每组又分为6 h组、24 h组、72 h组、120 h组,每组各5只;HE染色观察脑组织病理学变化;免疫组织化学检测脑组织中 NF-κB 水平.结果 脑组织中 NF-κB表达在大鼠TBI后 6 h即显著升高(P<0.05),伤后24 h达到峰值(P<0.01),之后有所回降,但仍持续维持较高水平至120 h(P<0.05);TBI大鼠经地塞米松治疗后,脑组织中NF-κB有明显降低(P<0.05).结论 地塞米松可抑制TBI大鼠脑组织中NF-κB的表达,减轻紊乱的炎性细胞因子所致的继发性损伤,起到治疗与保护作用.     

静脉注射地尔硫(艹卓)控制新发房颤患者心室率的疗效观察

目的观察静脉注射地尔硫革控制新发房颠患者心室率的疗效和安全性。方法19例新发房颠患者，心室率≥120次／min，在常规治疗的基础上，予地尔硫革0、25mg,／kg静脉注射，继以10mg／h静脉滴注维持，记录给药前及给药后5，15，30，60min时的心室率以及治疗过程中的不良反应。结果给药前及给药后5，15，30，60min时的心室率分别为（141±10）、（127±80）、（103±13）、（104±13）、（104±15）次／min，给药治疗前后具有统计学意义，P〈0．01，用药过程中无严重不良反应发生。结论静脉注射地尔硫革控制新发房颠的快速心室率安全有效，起效迅速，对无需紧急复律和无地尔硫革使用禁忌的患者，可作为首选药物使用。     

双水平正压通气治疗AECOPD的疗效观察

目的:探讨双水平正压通气(BiPAP)治疗AECOPD(慢性阻塞性肺病急性加重期)的效果.方法:26例AECOPD的患者,在综合治疗的基础上,应用BiPAP辅助通气治疗,观察其治疗前后生命体征和血气变化情况的变化.结论:AECOPD应用BiPAP辅助通气治疗效果显著.     

急性百草枯中毒大鼠肺间质成纤维细胞中MMP-9表达的研究

目的观察急性百草枯（PQ）中毒大鼠肺间质成纤维细胞中基质金属蛋白酶-9（MMP-9）的表达变化，探讨其在PQ中毒致肺纤维化中的意义。方法SD大鼠50只，随机分为染毒组和对照组，染毒组用PQ 50mg／kg灌胃染毒，对照组代以等剂量生理盐水灌胃，灌胃后1、3、7、14和28d分离和提取肺间质成纤维细胞，应用免疫细胞化学和逆转录多聚酶链式反应（RT-PCR）观察MMP-9蛋白及其mRNA的动态变化。结果PQ灌胃后1d，肺间质成纤维细胞MMP-9蛋白及其mRNA表达即增高，7d达到峰值，以后逐渐下降。MMP-9蛋白及其mRNA在PQ灌胃后1、3、7d与对照组比较升高（P〈0．05）。MMP-9蛋白在28d、MMP-9 mRNA在14d恢复到对照组水平。结论PQ灌胃后，肺间质成纤维细胞MMP-9的表达上调，损伤肺泡基底膜，启动肺纤维的发生。