驱逐性脉络膜上腔出血2例

1　病例报告例 1　男 ,74岁。因右眼老年性白内障住院 ,入院后 BP180 /110 mm Hg,高血压病史 2 0 a,无出血性疾病及糖尿病 ,出凝血正常 ,住院后降血压治疗 ,血压降至 15 0 / 10 5 mm Hg后第 3天行白内障摘除植入人工晶体 ,术中球周注射 2 %利多卡因 0 .75 %布比卡因 5 ml,压迫眼球约 10 min,截囊膜时发现前房极浅无法进行截囊 ,前房注入粘弹剂 ,前房未能恢复 ,扩大切口6 mm准备剪开囊膜时 ,晶体玻璃体全部脱出 ,随之大量血液涌出 ,脉络膜嵌顿切口 ,经家属同意行球内容剜出。例 2　男 ,71岁。因右眼白内障继发青光眼 2 d住院 ,入院检查晶…     

动态APACHEⅡ评分在重症急性胰腺炎中的应用价值

目的:探讨动态APACHEⅡ评分在预测重症急性胰腺炎严重度及预后中的作用。方法:将34例重症急性胰腺炎患者分成两组。A组:胰腺感染组,动态观察该组患者的APACHEⅡ评分;B组:未继发胰腺感染组,观察其入院第一天的APACHEⅡ评分。结果:A组感染后的APACHEⅡ评分为21.10±4.52.明显高于发生胰腺感染前13.25±1.74及B组评分11.36±1.65(P<0.01);A组中死亡患者及存活患者在感染后同期的APACHEⅡ评分有差异(P<0.05)。结论:动态APACHEⅡ评分在预测重症急性胰腺炎严重度及预后中有重要作用。     

糖尿病视网膜病变的病理机制和新型药物研究进展

目前全球糖尿病视网膜病变(DR)患者约9 300万,其中增殖性DR(PDR)患者1 700万,糖尿病性黄斑水肿患者2 100万,威胁视力的DR患者2 800万〔1〕。DR属于糖尿病引起的微血管病变,是一种涉及多种细胞、分子的非常复杂的视网膜疾病。     

Protective Effect of Sodium Tanshinone ⅡA Sulfonate on Injury of Small Intestine in Rats with Sepsis and Its Mechanism

Objective:To explore the protective effect of sodium tanshinoneⅡA sulfonate(STS) on small intestine injury in rats with sepsis and its possible mechanism.Methods:According to a random number table, 24 Tats were randomly divided into 3 groups:sham operation group(sham group),sepsis model group(model group) and STS treatment group(STS group),with 8 Tats in each group.A rat model of sepsis was induced by cecal ligation and puncture(CLP) for 5 h.STS(1 mg/kg) was slowly injected through the right external jugular vein after CLP.The histopathologic changes in the intestine tissue were observed under a light microscope,and the intestinal epithelial cell apoptosis was evaluated by terminal deoxynucleoddyl transferase(TdT)-mediated dUTP nick-end labeling(TUNEL) method.The expressions of Bcl-2,Bax and nuclear factorκB(NF-κB) p65 in the intestinal tissue was determined by Western blot.The levels of tumor necrosis factorα(TNF-α) and interleukin 6(IL-6) in the intestinal tissue were determined using enzyme-linked immuno-sorbent assay(ELISA). Results:Obvious injuries were observed in the intestinal tissue in the CLP group compared with the sham group. The expression of NF-κB p65 and the levels of TNF-αand IL-6 were up-regulated after CLP,the apoptosis of intestinal epithelial cells was increased after CLP,and the ratio of Bcl-2 to Bax was decreased.STS posttreatment could attenuate the injury on the intestinal tissue induced by CLP,decrease the apoptosis of intestinal epithelial cells and the levels of NF-κB p65,TNF-αand IL-6,and increase the ratio of Bcl-2 to Bax.Conclusion: STS can protect the small intestine in rats with sepsis,and the mechanism may be associated with the inhibition of intestinal epithelial apoptosis and the reduction of activation of inflammatory cytokines.     

Protective effect of diallyl trisulfide on liver in rats with sepsis and the mechanism

The protective effects of diallyl trisulfide on liver were examined in rats with sepsis. Sepsis was reproduced in rats by cecum ligation and puncture (CLP). Fifty-six male Wistar rats were randomly divided into sham-operated group (group S, n=8), sepsis model group (group C, n=24), diallyl trisulfide (DATS)-treated group (group D, n=24). Animals in groups C and D were further divided into three subgroups according to different observation time points, with 8 rats in each sub-group.Rats in group D and C were intravenously injected with normal saline or DATS respectively at a dose of 20 mg/kg after the establishment of sepsis model. Eight rats in groups C and D were sacrificed at 3, 6 and 24 h post-CLP and their livers were harvested for detection of interleukin (IL)-1 receptor associated kinase-4 (IRAK-4), nuclear factor-κB (NF-κB), c-fos, c-jun, malondialdehydethhe (MDA) and superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α) and for pathological examination. The results showed that the levels of serum IRAK-4, NF-κB and TNF-α in hepatic tissues were higher in group C than group S (control group) (P<0.05). After DATS treatment, the levels of IRAK-4 and NF-κB in the hepatic tissues and serum TNF-α in group D were lower than those in group C (P<0.05). The levels of c-fos and c-jun and MDA in the hepatic tissues were higher in group C than in group S (P<0.05). After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P<0.05). When compared with group S group, concentration of SOD in the hepatic tissues in group C was significantly lower (P<0.05). After DATS treatment, the concentration of SOD in the hepatic tissues was higher in group D than in group C (P<0.05). These findings suggested that treatment with DATS could ameliorate sepsis-induced liver injury in rats. The protective effect might be related to its ability to inhibit the signal pathway of IRAK-4 and NF-κB, thereby decreasing the production o     

重型颅脑损伤患者肌钙蛋白和心电图的变化及意义

目的：探讨重型颅脑损伤后肌钙蛋白及心电图的变化,了解隐匿性心肌损伤的发生率。方法：监测89例重型颅脑损伤患者血清心肌肌钙蛋白（cTnI）的水平,分析患者血清cTnI与心肌损伤、GCS评分、病死率的关系。结果：89例重型颅脑损伤患者有68例（76．4％）存在cTnI的升高,cTnI水平与（X2S评分成正相关,cTnI值越高,病死率越高,74例（83．15％）出现心电图异常。结论：重型颅脑损伤患者可出现不同程度的心肌损害,cTnI比心电图更能反映脑外伤患者的心肌损伤。     

内毒素预处理对内毒素血症大鼠肝TLR-4、NF-κB和ICAM-1表达的影响

目的 观察内毒素预处理对内毒素血症大鼠肝Toll样受体4(TLR-4)、核因子-κB(NF-κB)和白细胞间粘附分子-1(ICAM-1)表达的影响,探讨内毒素预处理对内毒素血症肝损伤的保护作用及机制.方法 采用直接注射内毒素脂多糖(LPS,10 mg/kg体重)的方法建立大鼠急性内毒素血症模型,实验动物随机分成3组:生理盐水对照组(N组);内毒素脂多糖(LPS)组(L组)和LPS预处理组(P组),其中P组在制模前分别经腹腔注射LPS 0.25、0.50 mg/kg体重.逆转录聚合酶链反应(RT-PCR)检测肝组织TLR-4 mRNA表达,免疫印迹法(Western blot)检测肝组织NF-κB表达,免疫组化法检测肝组织ICAM-1表达,取肝脏(肝左上叶)用10%的中性甲醛固定观察肝脏病理形态.结果 内毒素血症时,肝脏组织TLR-4、NF-κB和ICAM-1水平明显增加,显著高于N组(P＜0.05),而经内毒素预处理的模型动物肝脏组织TLR-4、NF-κB和ICAM-1水平明显降低(P＜0.05),P组肝脏组织病理学改变较L组减轻.结论 内毒素预处理能够减轻内毒素血症导致的肝损伤,其机制可能与抑制TLR-4信号传导通路及减少单核巨噬细胞内NF-κB和ICAM-1的表达有关.     

小剂量胰岛素持续滴注治疗小儿糖尿病酮症酸中毒24例临床分析

小儿糖尿病酮症酸中毒(Diabetic ketoacidosis,DKA),为小儿糖尿病最常见的严重并发症,尤多见于年幼患儿。国内资料表明,50%～70%的小儿糖尿病发生过一次或多次酮症酸中毒,死亡率高,目前尚无可靠、有效的治疗方法。我院自1998年1月至2005年10月应用小剂量胰岛素持续静脉滴注治疗     

原代培养的皮质神经元缺血性损伤模型的建立

目的建立方便有效的神经元拟缺血性损伤的离体模型。方法以原代培养Wistar大鼠乳鼠大脑皮层神经元为研究对象,不同浓度H2O2及Glu与细胞作用24h后,检测细胞活力,LDH漏出量及细胞形态学改变。结果6．25μmol/L～200μmol/L H2O2及12．5μmol/L～50μmol/L Glu均可降低神经元生长能力,增加乳酸脱氢酶漏出量；细胞形态有不同程度病理变化。结论H2O2与Glu引起的细胞损伤模型是两种方便有效的神经元拟缺血性损伤模型。     

内毒素预处理对内毒素血症大鼠肝损伤的保护作用

目的 探讨内毒素预处理对内毒素血症大鼠肝损伤的保护作用.方法 采用直接注射内毒素的方法建市大鼠急性内毒素血症模型.雄性Wistar人鼠72只,随机分成三组:生理盐水对照组(N组,n=24只)、内素脂多糖(IPS)(L组,n=24只)和LPS预处理组(P组,n=24只),每组义按时间分为2 h组、4 h组、6 h组、12 h组4个亚组,每个亚组6只.P组:首次经腹腔注射LPS 0.25mg/kg;24 h后再经腹腔注射IPSO.5 mg/kg,其余两组给予等容量生理盐水.第二次腹腔注射72 h后,L组和P组经尾静脉一次注射LPS 10 mg/kg,N组给予等量生理盐水,L组和P组在注射LPS后2,4,6,12 h,N组在注射最后一次NS后2,4,6,12 h,各取6只取肝组织制成匀浆检测Toll样受体4(Toll likereceptor-4,TLR-4)、核因子-кB(nuclear factor kappa B,NF-кB)、肿瘤坏死因子-α(tulnor necrosis factor-a,TNF-α)和丙二醛(malondiahtehyde,MDA),抽血检测谷丙转氨酶(ALT),谷草转氨酶(ASF),取肝脏(肝左上叶)用10%的中性甲醛固定.采用SPSS 13.0统汁软件进行单因素方差分析.结果 内毒素血症时符时间点肝脏组织TLR-4,NF-кB和TNF-α浓度较对照组显著升高,而内毒素预处理后则有明显下降,其中内毒素血症时4 h组肝脏组织TLR-4,NF-кB和TNF-α分别为(38.76±0.67),(170.82±31.40),(293.16±49.49)和(6.263±0.351),显著高于对照组(P＜0.05),而内毒素预处理后上述指标降至(22.32±1.35),(135.55±26.44)和(234.23±44.96),差异有统计学意义(P＜0.05).结论 内毒素预处理可减轻内毒素血症时的肝损伤,其机理可能与肝组织TLR-4,NF-кB和TNF-α的表达减少有关.