术前CT指标对全胸腔镜肺叶切除手术中转开胸的预测价值

目的 探索术前CT指标与全胸腔镜肺叶切除手术中转开胸之间的关系,为临床医生更精确地选择适合全胸腔镜肺叶切除手术的病例提供影像学依据。方法 收集2016年6月至2018年10月期间在昆明医科大学第三附属医院行全胸腔镜肺叶切除手术的病例54例,回顾其术前CT资料并对CT指标进行分级,分析相关指标级别与是否实施中转开胸之间的关系。结果 共收集54例肺叶切除病例,其中38例施行了全胸腔镜肺叶切除术,16例施行了中转手术。全胸腔镜手术组与中转开胸手术组患者的年龄均值有统计学差异(P =0.047),中转组患者平均年龄较大。2组患者的性别及术后病理分布差异无统计学意义(P值分别为0.694、0.987)。2组患者术前CT指标中,病灶位置、肺门及纵隔淋巴结大小、肺门纵隔淋巴结钙化情况及胸膜增厚程度差异有统计学意义(P值分别为0.029、0.001、0.002、0.029),中转组术前CT显示病灶位于肺野中内带者较多,肺门、纵隔淋巴结较大,肺门纵隔淋巴结钙化出现率较高,胸膜增厚程度较重;而两组病灶的最大径差异无统计学意义(P值为0.817)。结论 拟行胸腔镜肺叶切除手术的患者,如果年龄较大,病灶靠近肺门,肺门及纵隔淋巴结明显肿大或伴有钙化,或术前CT显示胸膜较广泛增厚,则术中中转开胸的几率增高,这类患者可首先考虑胸腔镜辅助小切口手术或常规开胸手术。而患者的性别、病灶的性质及5 cm范围内病灶的大小对中转开胸没有预测作用。

γ-促分泌酶抑制剂对Notch1蛋白表达阳性的原代非小细胞肺癌细胞生长的抑制作用及其机制

目的探讨γ-促分泌酶抑制剂MW167Ⅱ对Notch1蛋白表达阳性的原代非小细胞肺癌细胞生长的抑制作用及其机制。方法收集11例非小细胞肺癌患者的癌组织标本,应用胶原酶消化法获取细胞后进行细胞培养,采用染色、免疫组化法鉴定为Notch1蛋白表达阳性非小细胞肺癌细胞。将细胞分为对照组、实验1组、实验2组、实验3组,分别加入生理盐水、0. 25μmol/L MW167Ⅱ、0. 50μmol/L MW167Ⅱ、0. 75μmol/L MW167Ⅱ,观察各组细胞周期分布情况、细胞存活率及Notch1 mRNA表达情况。结果与对照组比较,各实验组的G0/G1期细胞比例增高、细胞存活率及Notch1 mRNA表达量均降低(均P <0. 05)。G0/G1期的细胞比例与MW167Ⅱ的浓度呈正相关(P <0. 05)。培养24 h及48 h后,实验1组、实验2组、实验3组的细胞存活率及Notch1 mRNA表达量依次降低(均P <0. 05),且各实验组细胞培养48 h后的细胞存活率均低于培养24 h后(均P <0. 05)。结论γ-促分泌酶抑制剂可抑制Notch1蛋白表达阳性的非小细胞肺癌细胞的增殖分化,且呈浓度和时间双重依赖性,这可能与其抑制γ-促分泌酶的活性阻断Notch信号通路有关。

阿托品在保留自主呼吸无痛纤维支气管镜检查中的应用

目的研究阿托品在保留自主呼吸无痛纤维支气管镜(纤支镜)检查中的作用。方法40例拟行无痛纤支镜检查的患者,随机分为2组,每组20例。对照组(C组)依次给予舒芬太尼0.1μg/kg、右美托咪定0.2μg/kg、丙泊酚1 mg/kg、瑞芬太尼0.2μg/kg、丙泊酚1 mg/kg iv,然后再配合气管内表面麻醉行纤支镜检查,当出现呛咳、肢体活动,则追加丙泊酚0.4 mg/kg iv。观察组(S组)给于阿托品0.006 mg/kg iv后其余步骤同C组。记录2组患者不同时间点的生命体征变化情况、手术时间、苏醒时间、离室时间、麻醉效果评价、术中追加丙泊酚和使用血管活性药的例数、呼吸系统不良事件及术后不良事件的发生率。结果2组患者术前和术后3 min的心率(HR)、血压(MAP)、血氧饱和度(SpO_(2))组间比较无差异(P>0.05),C组患者T2的HR、MAP的显著低于T1(P<0.05),S组患者T2的HR、MAP、SpO_(2)显著高于C组(P<0.05),麻醉优良率明显高于C组(P<0.05),苏醒时间、离室时间显著低于C组(P<0.01)、术中追加丙泊酚和给于血管活性药的例数及术中不良事件的发生率明显低于C组(P<0.05)。结论阿托品可提高保留自主呼吸无痛纤支镜检查麻醉的安全性。

Decreased and dysfunctional circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease

Background It has been widely demonstrated that endothelial progenitor cells are involved in several diseases and that they have therapeutic implications. In order to define the altered pulmonary vascular homeostasis in chronic obstructive pulmonary disease, we sought to observe the level and functions of circulating endothelial progenitor calls in patients with chronic obstructive pulmonary disease. Methods The total study population included 20 patients with chronic obstructive pulmonary disease and 20 control subjects. The number of circulating endothelial progenitor cells （CD34＋/CD133＋/IVEGFR-2＋cells） was counted by flow cytometry. Circulating endothelial progenitor cells were also cultured in vitro and characterized by uptake of Dil- acLDL, combining with UEA-I, and expression of von Willebrand factor and endothelial nitric oxide synthase. Adhesion, proliferation, production of nitric oxide, and expression of endothelial nitric oxide synthase and phosphorylated-endothelial nitric oxide synthase were detected to determine functions of circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease. Results The number of circulating endothelial progenitor cells in the chronic obstructive pulmonary disease group was lower than in the control group： （0.54±0.16）% vs. （1.15±0.57）%, P 〈0.05. About 80% of adherent peripheral blood mononuclear cells cultured in vitro were double labeled with Dil-acLDL and UEA-I. The 92% and 91% of them were positive for von Willebrand factor and endothelial nitric oxide synthase, respectively. Compared with the control, there were significantly fewer adhering endothelial progenitor cells in chronic obstructive pulmonary disease patients： 18.7±4.8/field vs. 45.0±5.9/field, P 〈0.05. The proliferation assay showed that the proliferative capacity of circulating endothelial progenitor cells from chronic obstructive pulmonary disease patients was significantly impaired： 0.135±0.038 vs. 0.224±0.042, P 〈0.05. Furthermore, nitric oxide synthase （112.06±10.00 vs. 135.41±5.38, P 〈0.05）, phosphorylated endothelial nitric oxide synthase protein expression （88.89±4.98 vs. 117.98±16.49, P 〈0.05） and nitric oxide production （（25.11±5.27） Iμmol/L vs. （37.72±7.10） μmol/L, P 〈0.05） were remarkably lower in endothelial cells from the chronic obstructive pulmonary disease group than the control. Conclusion Circulating endothelial progenitor cells were decreased and functionally impaired in patients with chronic obstructive pulmonary disease.