海水浸泡兔脑挫伤后caspase-8及caspase-3表达的研究

目的建立海水浸泡颅脑挫裂伤模型,观察海水浸泡对实验性脑挫裂伤后创伤性脑水肿的影响及研究兔脑挫伤后不同时间caspase-8及caspase-3表达的变化。方法采用立体定向自由落体伤模型进行持续海水浸泡作为实验组,对照组采用同样的方法致伤后不进行海水浸泡。观察创伤组织的病理改变,并通过免疫组化染色和计算机图像分析技术用半定量化的方法检测不同干预不同时程caspase-8和caspase-3的活性表达强弱差异。结果实验组和对照组均发生了创伤性脑水肿,但水肿高峰期出现时间不一致,严重程度也不一致。实验组caspase-8和caspase-3活性表达强度均高于对照组。结论海水浸泡促进了挫裂伤周边缺血水肿区神经细胞凋亡的增加。     

L-丙酰肉碱对再灌注心肌损伤的保护及体外抗自由基作用

目的:观察L－丙酰肉碱对缺血再灌注心肌的保护作用，并探讨其机理。方法：采用大鼠在体心脏冠状动脉前降支阻断5min造成缺血再灌注模型，持续心电监护，观察心律失常与心功能指标；应用电子顺磁共振观察L－丙酰肉碱对Fenton体系及二甲基亚砜（DMSO）碱性有氧体系产生自由基的作用。结果：L－丙酰肉碱静脉给药明显减少再灌注时室性心动过速、室性纤维颤动的发生（P＜0．05），促进再灌注后左室收缩压、左室压最大上升速率、左室压最大下降速率、心力环面积的恢复，与对照组相比，各参数均明显增高（P＜0．05）；静脉注射L－丙酰肉碱100mmol／L时促进Fenton体系OH的产生，而500mmol／L时产生明显抑制作用，L－丙酰肉碱明显抑制DMSO碱性有氧体系OS的产生。结论：L－丙酰肉碱明显减少再灌注心律失常的发生，促进再灌注后心功能的恢复。推测它对自由基的作用可能是再灌注损伤保护机理之一。     

MISE AU POINT D'UNE TECHNIQUE D'ADMINISTRATION IN VIVO DES VECTEURS GENETIQUES DANS LEMUSCLE CARDIAQUE

Objective In order to improve the in vivo gene transfer into the heart muscle, we have designed a ECG-synchronized microinjection system that allows sequential gene delivery to the myocardium.Methods A cannula was introduced into the right carotid artery of the Wistar rat under general anesthesia.With the ECG-synchronized injection during diastole, the genetic vector (Ad CMV lacZ ) infusion was performed with various concentrations( l07 ～ l010pfu ) and different frequency ( the ratio of heart beats per injection from 1: 1 to 4: 1 ). The hearts of the rats were removed after 7 days for histological examination. Results Best results were obtained with a total vector amount of l09 pfu and a good ratio 3: 1 between heart frequency and injection frequency. The transfection efficiency was increased by use of vasodilators and by an increase of vascular permeability. No signs of myocardial ischemia or ventricular arrythmia were observed. Conclusion We have established a novel and safe method for in vivo gene transfer into the heart. Transgene expression suggests that this method may be useful technique to study cardiac function of treat cardiac diseases by means of gene theratpy.     

异丙酚与安氟醚或七氟醚静吸复合麻醉对心肌酶的影响

目的:观察异丙酚与安氟醚或七氟醚静吸复合麻醉对心肌酶的影响.方法:32例择期非心脏手术的全麻病人,随机分为4组(每组8例),分别给予安氟醚麻醉(A组)、七氟醚麻醉(B组)、异丙酚-安氟醚麻醉(C组)、异丙酚-七氟醚麻醉(D组).其中A、B组为对照组,C、D组为观察组.分别于麻醉前、麻醉诱导后2 h和术后3 d采集静脉血测血清磷酸肌酸激酶(CK)及其同功酶(CK-MB)、天门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、α-羟丁酸脱氢酶(HBDH).结果:麻醉诱导后2 h,A组CK、CK-MB值、LDH及HBDH值升高,与麻醉前比较差异有显著性(P<0.01或P<0.05);B组CK和CK-MB值升高,与麻醉前比较差异有显著性(P<0.05或P<0.01).术后3 d,A、B两组CK值升高,与麻醉前和麻醉诱导后2 h比较差异有显著性(P<0.01或P<0.05),AST值升高,与麻醉前比较差异有显著性(P<0.01或P<0.05).而且A、B两组相比较,A组的CK、LDH值升高幅度明显大于B组(P<0.05).C、D两组仅CK值在术后3 d与麻醉前比较差异均有显著性(P<0.01),但其升高幅度均明显低于A、B两组的同时值(P<0.01),其余各项心肌酶的变化在麻醉诱导后2 h及术后3 d差异均无显著性(P>0.05).与C组比较,A组在麻醉诱导后2 h CK、CK-MB、HBDH值升高(P<0.01),LDH值升高(P<0.05);在术后3 d CK值升高(P<0.01).与D组比较,B组CK值在麻醉诱导后2 h及术后3 d升高(P<0.01),CK-MB值在麻醉诱导后2 h升高(P<0.05).结论:安氟醚和七氟醚两者均能使心肌酶升高,但安氟醚所致的心肌酶升高幅度更明显;临床麻醉剂量的异丙酚能有效地防止安氟醚和七氟醚麻醉时心肌酶的升高.     

Die traumatische Pneumatocele — Ein Fallbericht

Zusammenfassung Die posttraumatische Pneumatocele ist eine seltene intrapulmonale Veränderung nach stumpfem Thoraxtrauma. Anhand eines gut dokumentierten Falles wird diese seltene Form der Lungenkontusion dargestellt und die klinisch bedeutsame Differentialdiagnose diskutiert.

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Traumatic pneumatocele — a case report

Summary The posttraumatic pneumatocele is a rare intrapulmonary lesion following blunt thoracic injury. By means of a well documented case report this rare form of lung contusion is demonstrated and the clinically important differential diagnosis is discussed.

     

幼兔缺血预处理在心肌保护第二窗期对未成熟心肌Bcl-2基因mRNA表达的影响

目的　观察幼兔心脏缺血预处理 2 4h对未成熟心肌缺血 /再灌注后Bcl -2mRNA表达的影响 ,探讨未成熟心肌保护第二窗形成的作用机理。方法　 18只 3～ 4周龄幼兔 ,随机分为 3组 ,每组 6只 :Ⅰ组 ,正常对照组 ;Ⅱ组 ,缺血 /再灌注损伤组 ;Ⅲ组 ,缺血预处理组。建立活体心脏缺血 /再灌注损伤模型 ,Maclab/8s系统监测左心室发展压 (LVDP)、左室压上升及下降最大速率 (+dp/dtmax,-dp/dtmax)变化 ,原位免疫杂交 (ISH)方法检测心肌细胞内Bcl-2mRNA的表达。结果　缺血再灌注前 ,各组间LVDP、±dp/dtmax无显著性差异 (P >0 .0 5) ;再灌注 1h后 ,Ⅱ组的LVDP、+dp/dtmax和 -dp/dtmax恢复率分别为 (42 .81± 12 .56) %、(3 0 .67± 16.2 2 ) %和 (2 9.49± 10 .13 ) % ;Ⅲ组LVDP、+dp/dtmax及 -dp/dtmax恢复率分别为 (84.15± 13 .56) %、(69.49± 10 .3 6) %和 (58.3 7± 12 .45) % ,两组间有显著性差异 (P <0 .0 1)。Ⅱ组、Ⅲ组Bcl -2mRNA表达阳性细胞面积百分数分别为 (8.3± 2 .5) %、(76.3±13 .5) % ,两组间有显著性差异 (P <0 .0 1)。结论　缺血预处理可上调Bcl -2mRNA表达 ,参与未成熟心肌保护第二窗的形成 ,促进未成熟心肌缺血 /再灌注后心室功能恢复     

应用门控SPECT测量左心室功能的方法学研究

目的：试用门控心肌显像测定左室功能并与心血池显像结果比较。材料和方法：61例受检者进行了Tc-99m—MIBI门控心肌显像及心血池显像．结果：门控断层心肌显像的短轴中间部左室功能结果与平衡法心血池显像有良好的相关性(r=0．82）。结论：门控心肌断层显像测定的左室功能结果方法简便可靠．能同时反映心肌直流及左室功能。     

The pathology of cardiac ischaemia: Cellular and molecular aspects

This study evaluates the morphological and phenotypic changes that occur in squamous cell carcinoma of the head and neck when local infusions of interleukin-2 (IL-2) are given. Twelve patients were treated with a range of doses of IL-2 (3 × 10³ to 3 × 10⁶ international units/day) by continuous intra-arterial infusion for 10 days. Biopsies of the tumour were taken pre- and 48 h post-therapy, snap-frozen, cut, and examined histologically and immunocytochemically. Local infusions of IL-2 increase the numbers of antigen-presenting Langerhans cells (CDIa-positive) and infiltrating lymphocytes, predominantly of the CD3 and CD4 (T-helper) phenotypes. Locally infused IL-2 results in the expression of MHC (major histocompatibility complex) class II antigens on the surface of the tumour cells, capillary and post-capillary endothelial cells, and peri-tumoural macrophages. Intratumoural NK (natural killer) cells and CD8-positive (T-cytotoxic) infiltrating lymphocytes were not increased by this therapy and CD25 (IL-2 receptor) was only increased in those patients treated at the lower does levels. The system of intra-arterial cytokine infusion into head and neck tumours developed in this study is a useful model to examine the biological effects of cytokines, since in vivo they are mainly produced and act locally, Furthermore, the infused tumours are easily accessible to biopsy. The results from studies such as this may influence the design of tumour-targeted cytokine gene therapy programmes.     

兔心肌挫伤心功能障碍与心肌细胞内Ca2+和线粒体ATP酶的变化

目的：探讨心肌细胞内游离钙([Ca^2 ]i)和心肌ATP酶变化在心肌挫伤（MC）后心功能障碍发生机制中的意义。方法：随机选取兔36只，分为6组：正常对照、伤后2、4、8、12、24h，每组6只。经右颈总动脉插管至左心室测左室压力。采用BIM-II型生物撞击机致成MC模型。在上述时相点测定左室压力，并测定心肌细胞内[Ca^2 ]i和心肌匀浆组织及线粒体ATP酶活力。结果：心脏收缩/舒张功能受到损害，心肌细胞内[Ca^2 ]i升高，心肌匀浆组织及线粒体ATP酶下降，相关分析表明心功能障碍与心肌细胞内[Ca^2 ]i含量升高呈明显负相关，与ATP酶活性降低呈明显正相关。结论：MC后心脏功能下降，心肌细胞内[Ca^2 ]i含量升高和ATP酶活性下降可能是其原因之一。