目前,肺移植是公认的治疗多种终末期肺疾病的唯一有效方法[1].然而,供肺资源短缺严重制约了肺移植的发展,为解决这一难题,已提出并临床实践的对应策略有:边缘供肺肺移植、心死亡供体肺移植、体外肺灌注( EVLP)体外肺修复肺移植、解剖和非解剖性肺减容肺移植、肺叶移植[2-3].对于身材矮小或者有限制性肺疾病的小胸腔患者来说,肺叶移植已成为扩大其供肺来源的重要方式之一[2-8].现对郑州大学第一附属医院完成的华中地区首例双侧肺叶移植治疗成人支气管扩张并感染的资料进行总结,并结合相关文献复习,报道如下.

目的：探索各医院间交叉培养医学全日制专业学位研究生的可行性，尝试解决目前医学生临床能力训练中存在的问题。方法研究对象来源于郑州大学第一附属医院和郑州大学第三附属医院（以下简称“郑大一附院”和“郑大三附院”）新入学的2013级临床医学硕士专业学位研究生，抽取的两院研究生专业构成相同，每院分别随机分为两组，一组（3-1组和1-1组）进行交叉培养，另一组（3-2组和1-2组）由本院单独培养。培养结束后由专业教师进行考核，并比较两组考核成绩的差异。结果共有94名研究生纳入本研究，进行交叉培养的3-1组和1-1组的平均成绩分别为88.96分和87.41分；本院单独培养的3-2组和1-2组的平均成绩分别为82.01分和81.14分。交叉培养组学生的平均成绩优于本院单独培养组，差异具有统计学意义（P约0.05）。结论医院间高标准的交叉培养教学模式对提高临床硕士专业研究生的临床综合技能是有益的。

Objective To explore whether hydrochloride penehyclidine can inhibit rat pulmonary hypertension induced by monocrotaline and prevent or relieve the remodeling of pulmonary vascular.Methods Thirty healthy male SD rats (aged 3-4 weeks,weighing 90-100 g)were randomly divided into normal control group (group C),monocrotaline pulmonary hypertension group (group M)and hydrochloride penehyclidine treatment group (group P,n = 10 each).Rat pulmonary hyper-tension model was established by abdominally injecting 60 mg/kg monocrotaline all at once;The con-trol group was abdominally injected equal volume of normal saline all at once;the treatment group P 2 mg/kg hydrochloric penehyclidine 1 5 minutes before model building 1 mg/kg hydrochloric penehyclid-ine two days after model building;while the other two groups received equal volume of normal saline as placebo at the same time of medicine injecting,which lasted consecutively for 3 weeks.21 days af-ter model building,the haemodynamics (pulmonary artery pressure and right ventricular pressure) test was performed for all groups;Venous blood was sampled for blood biochemical tests (using ELISA method to test the content of NO and ET-1 )before executing the rats.The left lung tissue was sliced to observe the pathological morphological changes of lung tissues.The right lung tissue was cryopreserved for other tests.Results Compared with the normal control group,the pulmonary artery pressure and right ventricular pressure of monocrotaline pulmonary hypertension group notably enhanced (P <0.05);The pulmonary arterioles strongly thickened;The lumen of pulmonary arteri-oles became narrow and even blocked;The inflammatory cells of lung tissues apparently infiltrated. When compared with the monocrotaline pulmonary hypertension group, the pulmonary artery pressure and right ventricular pressure of the hydrochloride penehyclidine treatment group greatly lowered (P <0.05);Both the thickening degree of pulmonary arterioles walls and the infiltrating de-gree of inflammation cells of lung tissues lessened.When compared with the normal control group, the NO content of other groups significantly lowered and the ET-1 content apparently increased;When compared with the monocrotaline pulmonary hypertension group,the NO content of hydrochlo-ride penehyclidine treatment group was higher and the ET-1 content was lower.The differences were statistically significant (P <0.05).Conclusion The rat pulmonary hypertension model has been suc-cessfully built with the help of monocrotaline.The reducing of NO content and increasing of ET-1 was relevant to the formation of rat pulmonary hypertension induced by monocrotaline;The fact that hy-drochloric penehyclidine lowered the pulmonary artery pressure of rat pulmonary hypertension model and improved the thickening degree of pulmonary arterioles walls might involve the increasing of NO cotent and reducing of ET-1 content.

Objective To investigate the role of RhoA /Rho-kinase pathway in rat models of left heart disease-as-sociated pulmonary hypertension ( PH-LHD) .Methods Twenty male SD rats (3-4 week-old, 90-100 g) were randomly divided into two groups (10 rats in each group):the group C ( control group) with sham operation, and group H ( pulmo-nary arterial hypertension) .The rat model of left heart disease-associated pulmonary hypertension was established by supra-coronary aortic banding in the group H, and the sham surgery was applied for the rats in the group C ( The titanium clip was&nbsp;fixed at the mediastinal tissue adjacent to the artery rather than the ascending aorta).On day 60 after the operation, the cardiac functions, including right ventricular systolic pressure and pulmonary artery pressure were evaluated.After that, all rats were sacrificed and treated with cardiopulmonary lavage in vivo until the lung became white.Then the left lung tissues were fixed in 4%paraformaldehyde for pathological observation while the right lung tissues were frozen for mRNA detec-tion.Results Compared with the group C, both ventricular systolic pressure and pulmonary artery pressure in the group H were increased significantly (P<0.01).Pathological data demonstrated that the pulmonary artery walls in H group were much thicker than that in the group C.Moreover, vascular wall hypertrophy index in the group H was increased greatly compared with that in the group C (P<0.01).QPCR data showed that mRNA levels of Rho kinase, RhoA and ET-A R in the group H were up-regulated compared with the group C ( P<0.01) .Conclusions Rat model of left heart disease-asso-ciated pulmonary arterial hypertension can be successfully established by supracoronary aortic banding.Rho-kinase-media-ted pathway may contribute to the pathogenesis and progress of left heart disease-associated pulmonary arterial hypertension.

Objective To evaluate the effect of alprostadil on acute lung injury in septic rats. Methods Thirty adult male Sprague?Dawley rats, weighing 200-250 g, were randomly divided into 3 groups (n=10 each) using a random number table: sham operation group (group S), acute lung injury group ( group ALI) , and alprostadil group ( group Q) . The animals were anesthetized with intraperitoneal 1% pentobarbital sodium 5 ml∕100 g. Sepsis was induced by cecal ligation and puncture. In group Q, al?prostadil ( 10 μg∕2 ml) 2 ml∕kg was injected via the tail vein at 30 min before cecal ligation and puncture. The equal volume of normal saline was given in S and ALI groups. At 24 h after operation, blood samples were taken for determination of serum tumor necrosis factor?alpha ( TNF?α) and interleukin?6 ( IL?6) con?centrations by enzyme?linked immunosorbent assay. The animals were then sacrificed. The left lungs were immediately removed for microscopic examination, and the right lungs were immediately removed for deter?mination of wet∕dry lung weight ratio ( W∕D ratio ) , and expression of TNF?α mRNA and high mobility group box?1 ( HMGB1) using real?time reverse transcriptase?polymerase chain reaction. Results Com?pared with group S, the concentrations of serum TNF?α and IL?6 were significantly increased, and the ex?pression of TNF?α mRNA and HMGB1 mRNA was up?regulated, and W∕D ratio was increased in ALI and Q groups ( P<0?05) . Compared with group ALI, the concentrations of serum TNF?αand IL?6 were signifi? cantly decreased, and the expression of TNF?α mRNA and HMGB1 mRNA was down?regulated, and W∕D ratio was decreased in group Q ( P<0?05) . The pathological changes of left lungs were significantly attenua?ted in group Q as compared with group ALI. Conclusion Alprostadil can reduce acute lung injury in septic rats, and the mechanism may be related to down?regulation of HMGB1 expression and inhibition of inflam?matory responses.

目的 探讨盐酸戊乙奎醚对内毒素(LPS)所致新生大鼠肾损伤的保护作用及可能机制.方法 取健康7日龄SD大鼠72只,体重15～18 g,采用随机数字表法分为三组,每组24只.L组和P组采用腹腔注射LPS 5 mg/kg制备急性肾损伤模型,C组腹腔注射等量生理盐水.P组在注射LPS前30 min腹腔注射盐酸戊乙奎醚2mg/kg.各组分别在制模后6h随机抽取8只大鼠进行麻醉,用ELISA法检测IL-6、TNF-α、缺氧诱导因子(HIF)-1α和谷氨酰胺(Gln)血清浓度和肾组织含量,测定肾组织的干/湿重比(W/D),并行HE染色观察组织病理学变化.用RT-PCR法检测肾组织中HIF-1α mRNA的表达.各组剩余的16只大鼠用于观察生存状态.结果 与C组比较,L组和P组大鼠血清IL-6和TNF-α含量明显升高(P＜0.05),且L组明显高于P组(P＜0.05);L组和P组大鼠肾组织中IL-6、TNF-α、HIF1α、HIF-1α mRNA的表达、Gln的含量和W/D明显升高(P＜0.05),且L组明显高于P组(P＜0.05).P组肾组织病理学损伤程度较L组轻.P组存活大鼠明显多于L组且生存状态更好.结论 盐酸戊乙奎醚预处理可减轻LPS所致大鼠急性肾损伤,其机制与下调肾组织HIF-1α的表达,降低炎症反应有关;与保护其Gln含量,维持其能量代谢有关.