高分子透明质酸钠预防椎板切除术后硬膜外粘连的实验研究

[目的]通过动物实验观察高分子透明质酸钠和几丁糖对预防椎板切除术后硬膜外瘢痕粘连的作用。[方法]45只纯种日本大耳白兔,随机分成A、B、C、三组,制作L3、4椎板损伤模型,A组硬膜外涂布生理盐水,B组硬膜外涂布几丁糖,C组硬膜外涂布高分子透明质酸钠。于术后12周分别对椎板切除部位进行大体形态、组织学观察及生化检查,比较各组间瘢痕形成和粘连情况。[结果]C组改良Rydell-Balazs、胶原含量及改良Nussvaum组织学评分均优于A组和B组(P0.05),A组与B组比较差异无统计学意义(P0.05)。[结论]高分子透明质酸钠可以减轻或者预防椎板切除术后硬膜外瘢痕粘连的形成。     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

几丁糖联合聚乳酸薄膜预防硬膜外粘连的研究

目的 观察几丁糖加聚乳酸薄膜联合运用对椎板切除术后预防硬膜外瘢痕粘连的效果.方法 80只成年家兔[体质量(2.0±0.2)kg]制作椎板切除模型,在椎板缺损处分别覆盖等渗盐水(A组)、聚乳酸薄膜(B组)、几丁糖(C组)及几丁糖加聚乳酸薄膜(D组),术后12周对椎板切除部位进行大体观察、组织学观察及透射电镜比较各组间瘢痕形成和粘连情况.结果 B、C、D组的Rydell-Balazs粘连度评分、Nussvaum组织学评分均优于A组(P<0.01),D组优于B组和C组(P<0.01),B组与C组间差异无统计学意义(P>0.05).结论 联合应用几丁糖加聚乳酸薄膜能有效预防硬膜外瘢痕粘连,比单独应用几丁糖或聚乳酸薄膜效果好.     

Effect of metoclopramide on pain on injection of propofol

We undertook a randomized, double-blind, placebo-controlled study to examine the efficacy of metoclopramide at three different doses (2.5 mg, 5 mg, 10 mg) for reducing pain on injection of propofol in 100 patients scheduled for elective surgery. Patients received intravenously the study drug, with venous occlusion for one minute, followed by propofol 2 mg/kg into a dorsal hand vein. The incidence of pain was significantly less in patients receiving metoclopramide 5 mg (32%) or 10 mg (28%) than in patients receiving placebo (80%) (P<0.01). No difference between metoclopramide 2.5 mg and the placebo groups was found. We conclude that pretreatment of a dorsal hand vein with metoclopramide in a dose of 5 or 10 mg, with venous occlusion for one minute, effectively decreases the incidence of pain caused by propofol injection.     

肾康宁对肾小球肾炎治疗作用的实验及临床研究

目的:观察中药肾康宁对家兔实验性肾炎黏附分子及细胞因子表达的影响,以及临床肾小球肾炎治疗前后尿蛋白的变化.方法:检测牛血清白蛋白所致急性实验性肾炎动物肾组织ICAM-1表达、血清IL-6水平的变化,以及临床肾小球肾炎肾康宁治疗前后血清IL-6水平、尿蛋白的变化.结果:肾康宁能明显降低实验动物血清IL-6含量,降低急性实验性肾炎模型中ICAM-1阳性细胞表达率,同时减轻肾小球基底膜(GBM)增厚及炎症细胞浸润,阻止毛细血管内微血栓的形成;在临床肾小球肾炎中,肾康宁能减少肾小球肾炎患者血清IL-6水平及24 h尿蛋白含量.结论:肾康宁通过降低细胞因子IL-6水平和黏附分子ICAM-1的表达,从而抑制免疫细胞的趋化、浸润、活化和增殖、减少免疫复合物的沉积,使肾小球炎症反应减轻,有效缓解家兔急性实验性和临床肾小球肾炎,使肾功能得以改善.     

离心对脂肪颗粒活性影响的研究

目的:明确离心对脂肪颗粒活性的影响,为脂肪移植术中纯化脂肪颗粒时是否采用离心以及选择最佳离心速率提供参考。方法:将脂肪颗粒经不同高速率(1　000、2　000、3　000、4　000rpm)及不同低速率(600、800、1　000rpm)离心后,即刻进行葡萄糖转移实验——即将每组脂肪颗粒样本分为 12 个标本,每个标本 5ml,置入 10ml 含糖 DMEM 中孵育,1h 后检测其葡萄糖转移量,此值代表各标本的活性,方差分析检验比较各组样本葡萄糖转移量即活性大小。将经不同速率 (600、1　000、2　000、3　000rpm)离心的脂肪颗粒放置 4.5h 后再进行葡萄糖转移实验(方法同上),方差分析检验比较各组脂肪颗粒葡萄糖转移量即活性变化。经静置、3　000rpm 离心的两组脂肪颗粒分别植入 6 只裸鼠背部皮下,每只注射 4 点,每点 0.2ml。15 周后取出移植物,测量残留体积、重量并比较之。每组取两个移植物送病理学检查。结果:脂肪颗粒经不同高、低离心速率处理后的即刻活性随离心速率的增大而显著降低(P<0.05),而经不同高、低离心速率处理再放置 4.5h 后,各离心组样本活性变得差异不显著(P>0.05),但仍较对照组(静置组)明显降低(P<0.05)。静置悬浮和 3　000rpm 离心的两组样本植入裸鼠背部皮下 15 周后,残留体积、重量差异不显著(P>0.05),　组织病理     

丙泊酚制剂引起注射部位疼痛的机制研究进展

背景 丙泊酚是目前临床常用的静脉麻醉药,其具有起效快、作用时间短及安全性高的特点.但是30%～70%患者会出现注射疼痛的副作用,对患者机体和精神造成了严重影响.目的 为减轻丙泊酚临床给药疼痛提供有效的解决策略,为新制剂研发提供思路.内容 对近年来国内外学者关于丙泊酚注射疼痛机理的研究进展进行分析评述,概括导致丙泊酚注射...     

二氢青蒿素对胰腺癌生长的抑制作用

Objective To investigate the anti-tumor activity of dihydroartemisinin in pancreatic cancer in vitro and in vivo. Methods For cultured cells,cell growth was determined by the MTT assay and apoptosis was evaluated by flow cytometry analysis stained with Annexin V-FITG/PI. The protein expression in BxPC-3 cells was analyzed by Western blot assay. BxPC-3 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors and the tumor volume was monitored after exposure to dihydroartemisinin. Ki-67 staining and TUNEL assay were used to assess tumor cell proliferation and apoptosis in tumor tissue. Results After treatment by dihydroartemisinin in vitro, the proliferative inhibition rates of pancreatic cancer cells BxPC-3 and AsPC-1 reached up to (76.2 ± 3.5) % and (79.5 ± 2.9) %, and the apoptosis rates were up to (55.5 ± 3.2)% and (40.0 ± 3.5)%, the differences were significantly (P ＜ 0.01) compared with control [(2.0 ± 1.3) % and (0.9 ± 0.4) %]. Dihydroartemisinin inhibited the growth of pancreatic xenograft tumors in nude mice. The proliferation index and apoptusis index were (49.1 ± 3.9)% and (50.2 ± 4.4)% respectively in dihydroarternisinin 50 mg/kg treatment group, compared to those of (72.1 ± 3.3) % and (9.4 ± 2.9) % in control, the differences were significantly (P ＜0.01). Western blot assay indicated that dihydroartemisinin up-regulates expression of proliferation-associated protein p21WAF1 and down-regulates expression of PCNA, increases expression of apoptosis-associated protein Bax and decreases expression of Bcl-2 and activates caspase-9 in BxPC-3 cells. Conclusions Dihydroartemisinin exerts anti-tumor activity in pancreatic cancer both in vitro and in vivo by proliferation inhibition and apoptusis induction. Dihydroartemisinin can be used as a potential anti-tumor drug in pancreatic cancer.     

二氢青蒿素对胰腺癌生长的抑制作用

Objective To investigate the anti-tumor activity of dihydroartemisinin in pancreatic cancer in vitro and in vivo. Methods For cultured cells,cell growth was determined by the MTT assay and apoptosis was evaluated by flow cytometry analysis stained with Annexin V-FITG/PI. The protein expression in BxPC-3 cells was analyzed by Western blot assay. BxPC-3 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors and the tumor volume was monitored after exposure to dihydroartemisinin. Ki-67 staining and TUNEL assay were used to assess tumor cell proliferation and apoptosis in tumor tissue. Results After treatment by dihydroartemisinin in vitro, the proliferative inhibition rates of pancreatic cancer cells BxPC-3 and AsPC-1 reached up to (76.2 ± 3.5) % and (79.5 ± 2.9) %, and the apoptosis rates were up to (55.5 ± 3.2)% and (40.0 ± 3.5)%, the differences were significantly (P ＜ 0.01) compared with control [(2.0 ± 1.3) % and (0.9 ± 0.4) %]. Dihydroartemisinin inhibited the growth of pancreatic xenograft tumors in nude mice. The proliferation index and apoptusis index were (49.1 ± 3.9)% and (50.2 ± 4.4)% respectively in dihydroarternisinin 50 mg/kg treatment group, compared to those of (72.1 ± 3.3) % and (9.4 ± 2.9) % in control, the differences were significantly (P ＜0.01). Western blot assay indicated that dihydroartemisinin up-regulates expression of proliferation-associated protein p21WAF1 and down-regulates expression of PCNA, increases expression of apoptosis-associated protein Bax and decreases expression of Bcl-2 and activates caspase-9 in BxPC-3 cells. Conclusions Dihydroartemisinin exerts anti-tumor activity in pancreatic cancer both in vitro and in vivo by proliferation inhibition and apoptusis induction. Dihydroartemisinin can be used as a potential anti-tumor drug in pancreatic cancer.