右肺动脉叶间干的应用解剖学

在30例成尸标本上对右肺门角顶点的位置和右肺动脉叶间干进行了观测。右肺门角顶点位于右中叶动脉起始部者占67%,位于起始部以上者占23%,位于右肺动脉叶间干末端者占10%。右肺动脉叶间干长约21.3mm,上、中1/3段交界处:中、下1/3段交界处及末端的外径分别是11.7mm、11.1mm 和8.9mm。     

大鼠心导管留置术对器官功能影响的初步研究

目的：观察心导管留置术后大鼠血培养和各个器官功能的变化，为临床前药理研究建立稳定可靠的动物模型。方法：采用改良的心导管留置术建立大鼠模型，定期采血作血培养并检测血白细胞(WBC)和丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、尿素氮(BUN)、肌酐(Cr)、肌酸磷酸激酶(CK)等各项生化指标。     

野百合碱诱导大鼠肺动脉高压模型的建立

背景：目前尚缺乏简单易行、实用、操作性强的肺动脉高压动物模型。 目的：建立一种实用的注射野百合碱诱导的肺动脉高压动物模型。 方法：采用一次性皮下注射野百合碱60 mg/kg的方法制备SD大鼠肺动脉高压模型。 结果与结论：野百合碱注射后第1,2,3,4周,大鼠平均肺动脉压明显升高,右心室肥厚明显。光镜下可见肺小血管肌化程度增强,相对中膜厚度增加,肺血管密度减少,以上症状均随野百合碱注射时间的延长逐渐加重。证实此方法建立的大鼠肺动脉高压模型造模成功。     

不同方法培养大鼠肺动脉平滑肌细胞的性状

高血压、动脉粥样硬化、肺动脉高压等疾病均以血管平滑肌细胞的异常增生和迁移为特征。为此 ,近几年来 ,血管平滑肌细胞的培养已经成为研究工作的基础。目前 ,仍然多采用贴块片[1 ] 。因其方便经济、技术难度低 ,但贴块片确有不足之处 ,如细胞容易出现“去分化”或“调整”现象。故我们采用单纯胶原酶法 (Ａ)和复合胶原酶法 (Ｂ ,包括胶原酶弹性蛋白酶和胰蛋白酶抑制剂 )培养肺动脉平滑肌细胞 (ｐｕｌｍｏｎａｒｙａｒｔｅｒｉａｌｓｍｏｏｔｈｍｕｓｃｌｅｃｅｌｌ,ＰＡＳＭＣ) ,并初步观察两种方法培养的ＰＡＳＭＣ生长状况。材　料　和　…     

西拉普利对大鼠缺氧性肺动脉高压血管内皮保护作用的研究

目的：观察西拉普利对大鼠缺氧性肺动脉高压血管内皮的保护作用。方法：运用血液动力学方法、观察循环内皮细胞及血管紧张素转化酶、丙二醛的测定。结果：缺氧性肺动脉高压时右室压、肺动脉平均压升高（P＜0．01）,循环内皮细胞数量增加（P＜0．01）,丙二醛升高（P＜0．01）,西拉普利治疗后各值下降（P＜0．01）;缺氧时血管紧张素转化酶下降（P＜0．01）,西拉普利治疗后有上升（P＜0．01）。结论：西拉普利能降低肺动脉压,清除氧自由基,减少血CEC,对血管内皮细胞有保护作用。     

改良的大鼠心肌微血管内皮细胞培养方法

目的:改良大鼠心肌微血管内皮细胞(MMVECs)培养方法,提高细胞收获量和细胞纯度。方法:选择6～8周龄Wistar雄性大鼠,腹腔内注射200U肝素,摘取左心室剪成若干2mm3小块接种于培养皿中,待其贴壁后,加入含有肝素的DMEM高糖培养液,换液、去除组织块、消化、传代,取第二代MMVECs进行细胞形态学和免疫组化、免疫荧光染色鉴定。结果:贴块法培养48h可见组织块周围有细胞长出,70h长出较多,去组织块后再培养36h,细胞生长至80%～90%融合,呈典型铺路石样。免疫组化和免疫荧光染色证实培养细胞CD31、CD34和Ⅷ因子相关抗原染色均呈阳性,且纯度较高。结论:采用心肌组织贴块及培养液中加入肝素培养的方法可获得高纯度的MMVECs,方法简单,结果可靠。     

一氧化氮诱导大鼠肺动脉平滑肌细胞凋亡机制研究

目的:研究一氧化氮(NO)诱导大鼠肺动脉平滑肌细胞(PASMC)凋亡的作用机制。方法:体外培养Wistar大鼠PASMC,加入NO供体硝普钠(SNP)于常氧和低氧条件下孵育12h或24h,通过流式细胞术碘化丙啶染色法观察PASMC细胞周期时段及凋亡亚二倍体峰变化,应用细胞免疫化学法检测PASMCcaspase-3和NF-κB的表达,同时行DNA断裂琼脂糖凝胶电泳。结果:SNP作用后PASMC出现剂量-依赖性促凋亡作用(P＜0.01),表现为凋亡指数与caspase-3表达的不同程度的增强。随凋亡的进展,出现PASMC凋亡核小体DNAladder,同时PASMCNF-κB阳性核表达较对照组少(P＜0.01)。结论:外源性NO诱导大鼠PASMC凋亡,caspase-3与NF-κB可能涉及PASMC凋亡的调控信号途径。     

碱性成纤维细胞生长因子在低氧大鼠肺动脉的表达及其对肺动脉张力的影响

目的:观察碱性成纤维细胞生长因子(bFGF)在低氧性肺动脉高压发病中的可能作用。方法:应用逆转录多聚酶联反应(RT-PCR)技术观察低氧大鼠肺动脉bFGF的表达水平,并观察bFGF对离体大鼠肺动脉环收缩功能的影响。结果:①低氧时,肺动脉bFGFmRNA表达明显增加,bFGF与β-actin的RT-PCR反应产物的放射强度(counts·min^-1)之比由对照的0.5074上升到0.9182(低氧1周)和0.7812(低氧2周)(P均＜0.05)。②bFGF能收缩离体大鼠肺血管环,收缩强度与剂量相关(r=0.695,P＜0.05),其EC₅₀为2.62×10^-7mol/L。结论:提示bFGF可能参与低氧性肺动脉高压的发病过程。     

A single open sea air dive increases pulmonary artery pressure and reduces right ventricular function in professional divers

After decompression from dives, bubbles are frequently observed in the right ventricular outflow tract and may lead to vascular damage, pulmonary arterial hypertension and right ventricular overload. No data exist on the effect of open sea diving on the pulmonary artery pressure (PAP). Eight professional divers performed an open sea air dive to 30 msw. Before and postdive a Doppler echocardiographic study was undertaken. Systolic pulmonary artery pressure (SPAP) was estimated from measurement of peak flow velocity of the tricuspid regurgitant jet; the ratio between pulmonary artery acceleration times (AccT) and right ventricular ejection time (RVET) was used as an estimate of the mean PAP. No evidence of either patent foramen ovale or intra-pulmonary shunt was found in any subject postdive after performing a Valsalva maneuver. SPAP increased from 25 ± 3 to 33 ± 2 mmHg and AccT/RVET ratio decreased from 0.44 ± 0.04 to 0.3 ± 0.02 20 min after the dive, respectively. Pulmonary vascular resistance increased from 1.2 ± 0.1 to 1.4 ± 0.1 Woods Units. Postdive right ventricle end-diastolic and end-systolic volumes were increased for about 19% (P = 0.001) and 33% (P = 0.001) and right ejection fraction decreased about for 6% (P = 0.001). Cardiac output decreased from 4.8 ± 0.9 (l min⁻¹) to 4.0 ± 0.6 at 40 min postdive due to decreases in heart rate and stroke volume. This study shows that a single open sea dive may be associated with right heart overload due to increased pressure in the pulmonary artery.     

Pinacidil对低氧性肺动脉高压大鼠肺动脉压和血浆内皮素-1的影响

目的：探讨钾通道开放剂pinacidil对低氧性肺动脉高压（HPH）及对血浆内皮素-1（ET-1）含量的影响。方法：将45只雄性Wistar大鼠分为3组：①对照组;②低氧组,每天低氧8 h,共4周;③治疗组,每天低氧前半小时腹腔注射pinacidil 3 mg/kg,共4周,4周后观察3组平均肺动脉压（mPAP）,右心室肥厚指标、血浆中ET-1的水平。结果：低氧组大鼠mPAP明显高于对照组。右心室肥厚显著,血浆中ET-1含量明显高于对照组;治疗组mPAP明显低于低氧组,右心室肥厚轻于低氧组,血浆中ET-1含量明显低于低氧组。结论：pinacidil能有效降低HPH中肺动脉压力、阻抑右心室肥厚,并影响血浆中ET-1的水平。     

新生儿肺炎期间肺动脉压力、心腔内径及心脏功能变化的研究

目的探讨新生儿肺炎期间及肺炎合并心衰时肺动脉压力、心腔内径及心功能变化规律。方法用彩色多谱勒超声TR压差法检测肺炎期间及肺炎合并心衰时肺动脉压力、心腔内径及心脏功能,同时做血气及心肌酶谱检查,并与正常新生儿比较,找出变化规律。结论新生儿肺炎期间肺动脉压力增高、肺动脉内径增宽、血气及心肌酶谱均有不同程度改变。肺炎合并心衰时左心室内径及右心室内径均有不同程度的增大。同时也证明肺炎合并心衰时是肺动脉压力增高及毒素等作用的结果。     

A refined radio-telemetry technique to monitor right ventricle or pulmonary artery pressures in rats: a useful tool in pulmonary hypertension research

Implantable radio-telemetry methodology, allowing for continuous recording of pulmonary haemodynamics, has previously been used to assess effects of therapy on development and treatment of pulmonary hypertension. In the original procedure, rats were subjected to invasive thoracic surgery, which imposes significant stress that may disturb critical aspects of the cardiovascular system and delay recovery. In the present study, we describe and compare the original trans-thoracic approach with a new, simpler trans-diaphragm approach for catheter placement, which avoids the need for surgical invasion of the thorax. Satisfactory overall success rates up to 75% were achieved in both approaches, and right ventricular pressures and heart and respiratory rates normalised within 2 weeks. However, recovery was significantly faster in trans-diaphragm than in trans-thoracic operated animals (6.4 ± 0.5 vs 9.5 ± 1.1 days, respectively; p < 0.05). Stable right ventricular pressures were recorded for more than 4 months, and pressure changes, induced by monocrotaline or pulmonary embolisms, were readily detected. The data demonstrate that right ventricular telemetry is a practicable procedure and a useful tool in pulmonary hypertension research in rats, especially when used in combination with echocardiography. We conclude that the described trans-diaphragm approach should be considered as the method of choice, for it is less invasive and simpler to perform. Electronic supplementary material The online version of this article (doi: ) contains supplementary material, which is available to authorized users.     

Diurnal variation in pulmonary artery pressure

SUMMARY  Previous observations have suggested that pulmonary artery pressure rises during sleep, whereas systemic artery pressure falls. A system has been developed for careful and accurate recording of pulmonary arterial pressure, and applied it to two groups of subjects: patients with heart failure, and patients with chronic stable angina. The results have largely confirmed the nocturnal pressure rise in pulmonary arterial pressure. Detailed analysis strongly suggests that the same physiological mechanisms producing a fall in systemic pressure are responsible for the rise in pulmonary pressure. The precise mechanism remains to be elucidated.     

人肺动脉干、右肺动脉和左肺动脉多层螺旋CT成像的基础研究

目的利用多层螺旋CT对人肺动脉干、右肺动脉和左肺动脉成像,测量评价肺动脉干、右肺动脉和左肺动脉。方法选取正常人340例,胸部多层螺旋CT增强扫描,将图像传至工作站进行三维重建,观察测量肺动脉干、右肺动脉和左肺动脉,然后对肺动脉干、右肺动脉和左肺动脉进行比较分析。结果①螺旋CT扫描成像测量的肺动脉的管径明显小于X线测量的肺动脉的管径,有统计学意义(P0.05);②男、女性别之间的肺动脉管径也有显著差异(P0.05);③不同年龄组别之间的肺动脉也有差异(P0.05);④右、左肺动脉之间比较也有显著性统计学意义(P0.01);⑤不同的重建方法各有其优越性,其中,MIP重建能较好的显示肺动脉干、右肺动脉左肺动脉,并且其测量值比其它重建方法测量较为准确。结论多层螺旋CT胸部增强扫描,通过工作站三维重建能较好的显示肺动脉干、右肺动脉和左肺动脉,并对其进行科学的评价,这种方法优于传统的尸体解剖方法,其数据可靠,此方法可以对活体人的器官进行大样本的形态学研究。     

肺癌侵犯肺动脉干19例

目的 观察肺癌侵犯肺动脉干的病理解剖,ＣＴ征象,为手术提供参考。方法 对１９例肺癌侵犯肺动脉干的切除标本进行病理解剖。与术前ＣＴ比较。结果 肿瘤包绕肺动脉全周８例,部分包绕１１例。肿瘤侵犯以管壁外膜和中膜为主,尤其局限在中膜的外弹性膜周围,内膜未受侵。管壁炎性浸润,水肿或肉芽及结缔组织增生突出。ＣＴ表现管周脂肪异常１０例,肿块与肺动脉干肾密相贴或包绕１６例,压迫及移位２例,低肺血流灌注３例。     

15-HETE与ERK1/2在大鼠缺氧性肺动脉收缩中的作用

目的:为揭示缺氧性肺血管收缩机制,探讨细胞外信号调节激酶1/2 (ERK1/2)是否参与15-羟基二十碳四烯酸（15-HETE）收缩缺氧大鼠肺动脉的过程以及15-HETE对 ERK1/2活性的影响。 方法: 将大鼠置于氧气分数为12.0％的低氧箱中连续9 d形成缺氧模型。完整取出心肺，在显微镜下分离直径0.8-1.0 mm肺动脉剪为3 mm长的动脉环在组织浴槽内进行张力研究。比较15-HETE给药前后肺动脉环张力变化；用ERK1/2上游激酶抑制剂U0126孵育肺动脉环，比较U0126孵育前后15-HETE对缺氧性肺动脉环的收缩作用；机械法去除动脉环内皮，再比较U0126孵育前后15-HETE的收缩作用。酶法分离培养大鼠肺动脉平滑肌细胞。Western blotting方法检测15-HETE作用时间（5-90 min）及浓度（10^-9-10^-6 mol/L）对 ERK1/2 的表达及活性的影响。 结果: 15-HETE对缺氧大鼠肺动脉环有收缩作用，呈浓度-效应关系，与正常对照组比较差异显著（P<0.05）；内皮完整和内皮去除的肺动脉环，U0126孵育前后，15-HETE的缩血管作用都受到抑制，差异显著（均为P<0.05）。Western bloting结果显示，15-HETE明显增强肺动脉血管平滑肌细胞ERK1/2的活性，随时间延长而降低，随浓度增加而增加，但对ERK1/2的蛋白表达无影响。 结论:15-HETE能上调大鼠肺动脉血管平滑肌细胞ERK1/2的活性，提示ERK1/2的活化是15-HETE收缩慢性缺氧大鼠肺动脉的一个重要环节。