冠心病微循环白色小血栓的临床观察

冠心病外周微循环中白色微小血栓的研究,国内尚未见报导。我们对180例冠心病及120名正常人球结膜微循环对比观察,见23.9%的病例出现白色微小血栓(简称白色微栓),正常人无一例发现(P<0.01),白色微栓大小不一,但明显大于白细胞,呈絮状、团块或颗粒球状,在微静脉中漂摇而过,凡能引起血小板聚集和凝固     

机械通气致大鼠肺损伤时肺组织PPARγ表达的变化

目的观察PPARγ在通气相关性肺损伤大鼠肺组织中的表达,探讨PPARγ在通气相关性肺损伤中的作用。方法清洁雄性SD大鼠,随机分为大潮气量(Tidal volume,VT)组,Vt=12 m L;小潮气量组,Vt=6 m L;自主呼吸组。每组又分为3个亚组:即通气1 h、4 h、8 h组。于各时间段末放血处死动物,收集肺组织和肺灌洗液标本,测定肺灌洗液中蛋白总量、白细胞计数;测定肺组织湿/干重比(W/D);逆转录聚合酶链反应检测PPARγmRNA的表达;western blot检测PPARγ蛋白的变化。结果大潮气量组机械通气4 h、8 h后,与小潮气量组及自主呼吸组相比,肺灌洗液中白细胞计数、蛋白总量明显增加(P0.01),肺W/D增加(P0.01);肺组织出现明显病理组织学损伤;PPARγmRNA和PPARγ蛋白表达减少(P0.01)。通气1 h时,各组之间比较无显著差异(P0.05)。结论通气相关性肺损伤大鼠肺组织中PPARγ基因和蛋白表达下降,这可能与炎症损伤和持续有关。     

血液稀释对大鼠肺水肿保护作用的研究

本文观察等容血液稀释(HD)对大鼠氯化铵性肺水肿的防治作用。防治二组采用6%低分子右旋糖酐稀释。使血红蛋白值分别从130.5±1.2g/L,134.1±4.5g/L降至84.3±4.0g/L,88.6±4.5g/L。肺水肿组存活率为13.3%(2/15),预防组为42.1%(8/19),治疗组为60%(9/15),防治二组与肺水肿组比有非常显著差异(P<0.01)。肺系数肺水肿组为098±0.39,防治二组分别为0.70±0.16,0.69±0.07,与肺水肿组比有显著差异(P<0.05)。肺病理组织学与超微结构改变,防治二组均明显减轻。实验结果表明;HD对大鼠氯化铵引起的急性肺水肿有明显保护作用。     

小儿热性惊厥球结膜微循环监测的意义

目的探讨小儿热性惊厥后微循环微血管形态、血液流态、血管周围状态的变化.方法应用裂隙显微镜观测热性惊厥后球结膜微循环的变化,经计算机统计加权积分值,并与健康同龄组进行对比分析.结果热性惊厥组微循环细动脉收缩变细、细静脉舒张,血流减慢、红细胞聚集、白细胞增加、少量白色微栓,局部少量出血、水肿、渗出,惊厥组、对照组加权积分值经统计学处理有显著性差异(P＜0.01).结论热性惊厥后球结膜微循环有明显改变,微循环为轻度障碍.     

三七叶皂甙抗炎作用的实验研究

本文以角叉菜胶(Car)25mg·kg~(-1)诱导大鼠气囊滑膜炎模型为研究对象,观察了三七叶皂甙(PNGL)对Car诱导的气囊灌洗液中白细胞数及蛋白含量的影响,与此同时,还进一步观察了PNGL对灌洗液中PGE_2含量及PLA_2活性的影响。结果发现,Car致炎后气囊灌洗液中PLA_2活性明显升高,于12h达峰值(248.5±41.8 vs 38.4±9.2U·ml~(-1),P<0.01);PGE_2含量呈类似变化(1619±391 vs 397±41pg·mg~(-1),P<0.01);灌洗液中白细胞数及蛋白含量也显著升高(P均<0.     

家兔油酸中毒性肺水肿时血液流变性变化的动态观察

本文连续6 1/2小时观察了8只家兔油酸中毒性肺水肿的血液流变学变化。实验用新西兰白兔8只,1.5～2.5kg,耳缘静脉注入油酸0.1ml/kg,于注油酸前和注油酸后1/2h、1 1/2h、3 1/2h、6 1/2h分别采动脉血3ml。测量血液流变学指标的变化。发现注油酸后1 1/2h开始中切变率(46.0s~(-1))和高切变率(115.0s~(-1)和230.0s~(-1))的全血还粘度逐渐升高,与注油酸前相比有显著差异(P<0.05),至6 1/2h时升高更明显,与注油酸前相比有非常显著差异(P<0.01);同时,血浆粘度也逐渐升高,与注油酸前相比有显著差异(P<0.05)。此外,还测量到注油酸后血浆纤维蛋白原含量和全血血小板最大聚集率也呈逐渐升高趋势,但与注油酸前相比没有显著差异(P>0.05)。结果提示:家兔油酸中毒性肺水肿时血液呈高粘滞状态,这种血液流变学状态的改变对肺水肿的形成可能有一定的作用。     

伊文思蓝法测定小肠微循环通透性

本文讨论了伊文思蓝法测定小肠微循环通透性的影响因素。当小肠经生理盐水充分灌洗后可消除血液对测定的影响,灌洗压力应为8.0KPa以上,灌洗时间至少20分钟。猪回肠伊文思蓝渗出量为1.167±0.235μg/g湿组织,经乳酸林格氏液保存60分钟的移植小肠微循环通透性显著增加(7.543±0.22μg/gP<0.01)。     

中性白细胞消耗对大鼠油酸肺损伤时过氧化氢诱发化学发光…

大鼠油酸肺损伤时，血浆过氧化氢诱发化学发光峰值和总光强均显著升高且逐渐加重。用盐酸氮芥消耗大鼠９０％左右的白细胞以后，可以显著减轻油酸肺损伤时ＩＣＬ的升高程度，同时其支气管肺泡灌洗液中蛋白含量和ＩＣＬ水平也显著降低（Ｐ＜０．０５）。以上结果提示，白细胞在肺内聚集将加重肺损伤程度，而ＩＣＬ的升高与油酸肺损伤时肺内白细胞的作用有关。     

腹腔感染时肺毛细血管通透性变化

本研究通过静脉注射Evans蓝(20mg/kg)后测定肺组织中Evans蓝含量和肺血管外水(PEWV),观察了兔腹腔感染后肺毛细血管通透性改变及肺水肿情况。结果表明:盲肠结扎加戳孔(CLP)后6小时、12小时、24小时肺毛细血管通透性及PEWV明显增加(P<0.05和P<0.01),两者显著正相关(r=0.9232,P<0.05)。提示肺毛细血管通透性增加是肺水肿的主要原因。本实验同时检测了CLP后血清内毒素(ET),亦显示与PEWV呈正相关(r=0.8703,P<0.05)。     

甲萘硫脲水毒性肺水肿时肺循环中PMN和微血栓的变化

目的进一步观察甲萘硫脲中毒性肺水肿时肺循环中中性粒细胞(PMN)和微血栓的变化。方法选用健康家兔24只,雌雄不限。肺循环灌流液37℃的灭菌生理盐水。将24只家兔随机分成三组,每组8只。第一组于实验的前三天开始,每天注射1％盐酸氮芥1mL／只,实验时每只家兔经耳静脉注射0.25％甲萘硫脲1mL／kg体重;第二组不经任何处理,实验时经耳静脉注射0.03％甲萘硫脲1mL／kg体重;第三组经耳静脉注射等量的灭菌生理盐水作为对照。各组于注射甲萘硫脲后2h放血处死动物。动物处死后,完整的分离出心脏肺,结扎主动脉,肺动脉插管,然后将灌流液从左心房注入,经过肺静脉,肺微血管,从肺动脉插管中收集灌流液。灌流液压力为50cm水柱。显微镜下计数每毫升下层液中PMN及微血栓数,同时用下层液涂片,作白细胞分类计数。结果第一组8只动物中仅有5只出现肉眼可见的肺水肿;肺循环灌流液中PMN高于对照组并有一定差异,而微血栓数却明显高于对照组动物,差异极显著(P<0.01)。第二组8只动物都出现不同程度的肺水肿,肺循环灌流液中PMN和微血栓数都明显高于对照组,差异极显著(P<0.01)。结论甲萘硫脲中毒性肺水肿的发生可能与肺循环中有大量的PMN和微血栓的滞留有关。外周血液中的PMN减少可能降低肺水肿的发病率。     

肺部超声对重症肺部感染患者肺通气的评估价值

目的:探讨肺部超声评价重症肺部感染患者通气情况的应用价值。方法:选取88例重症肺部感染患者,采用半定量方法对肺部超声征象进行评分,以CT检查结果为金标准,分析肺部超声评分与患者肺通气的关系;同时分析存活和死亡患者临床资料、肺部超声评分的差异,以及肺部超声评分预测患者死亡的价值。结果:88例患者全肺超声评分平均为（18.50±2.12）分,全肺CT值平均为（-620.50±88.13） HU,不通气/低通气肺组织比例平均为（10.41±3.35）%,正常通气肺组织比例平均为（71.54±6.69）%,过度通气肺组织比例平均为（17.65±4.11）%;患者肺部超声评分与全肺CT值、不通气/低通气肺组织比例呈正相关（r=0.775、0.648, P<0.05）,与正常通气肺组织比例、过度通气肺组织比例无明显相关性（r=-0.170、0.046, P>0.05）;死亡组患者年龄、糖尿病比例、APACHEⅡ评分、肺泡-动脉氧分压差、机械通气治疗和肺部超声评分分别为（59.28±8.12）岁、44.83%、（22.19±2.40）分、（344.40±82.29） mmHg、72.41%和（20.20±1.72）分,明显高于存活组（P<0.05）,而氧合指数为（104.42±21.18）,明显低于存活组（P<0.05）;Logistic回归分析结果显示:年龄、APACHEⅡ、肺部超声评分是重症肺部感染患者死亡的影响因素（OR=1.758、2.841、2.440, P<0.05）;肺部超声评分预测重症肺部感染患者死亡的ROC曲线下面积为0.901（95%CI:0.836~0.966）,截断值为20分,灵敏性和特异性分别为82.80%和84.70%。结论:肺部超声可以作为重症肺部感染患者肺通气的评估指标,同时其在预测患者预后方面有一定应用价值。     

Reversal of pulmonary vascular remodeling in pulmonary hypertensive rats

Pulmonary hypertension is responsible for significant mortality and morbidity among newborns and infants. The pathology is characterized by pulmonary vascular remodeling with medial hypertrophy and adventitial thickening, leading to decreased gas exchange. Since it is unknown if these abnormalities are reversible, we analyzed these vascular changes in pulmonary hypertensive rats. Exposure of rats to hypobaric hypoxia for 4 weeks induced clinical signs of pulmonary hypertension, such as increased right ventricular systolic pressure, increased right ventricular weight and considerable pulmonary vascular remodeling. The vascular changes were associated with the expression of Non -Muscle Myosin Heavy Chain B in the pre-acinar vessels and an increased expression of alpha Smooth Muscle Actin, Smooth Muscle Myosin Heavy Chain 2 and Calponin in the intra-acinar vessels. The right ventricular systolic pressure and right ventricular weight gradually decreased after specific periods of recovery in normoxia, although this reversal did not reach baseline levels after six weeks at normoxia. However, the cellular changes in the pulmonary vasculature were completely reversed. Development of pulmonary hypertension is associated with an increase of synthetic perivascular cells in the pre-acinar arteries and an aberrant differentiation of perivascular cells in the smallest intra-acinar arteries. These cellular and structural changes in the pulmonary vasculature are completely reversible after recovery in normoxia.     

A case of pulmonary capillary hemangiomatosis with pulmonary fibrosis associated with MMP-9 related pulmonary remodeling

Pulmonary capillary hemangiomatosis (PCH) is a rare cause of pulmonary hypertension. It is characterized capillary proliferation within the alveolar septa. Here, we report a case of PCH with extensive pulmonary fibrosis. A 52-year-old man with a clinical diagnosis of non-specific interstitial pneumonia died of respiratory failure with severe pulmonary hypertension. Autopsy revealed pronounced right ventricle hypertrophy and pulmonary fibrosis. Consistent with clinical diagnosis, histological examination revealed diffuse pulmonary fibrosis, in addition, it also disclosed marked capillary proliferation within the alveolar septa as well as the fibrotic pulmonary stroma, suggesting the presence of PCH. Hemosiderin-laden macrophages had accumulated in the capillary proliferative area, and bronchiolar-type metaplasia was conspicuous in the fibrotic lesion. Proliferated capillaries were surrounded by fine collagen and α-smooth muscle actin-positive myofibroblasts. Immunohistochemistry revealed that type IV collagen around capillaries in the area of the PCH without inflammation disappeared in the area with inflammation. In addition, the PCH lesion contained significant numbers of macrophages expressing matrix metalloproteinase (MMP) 9 and type II pneumocytes positive for vascular endothelial growth factor. Although pulmonary fibrosis is a distinctive disease entity, different from PCH, MMP-9-driven destruction of the basement membrane may promote unusual pulmonary remodeling, which, in this case, resulted in extensive pulmonary fibrosis.     

Pathogenesis of pulmonary edema: learning from high-altitude pulmonary edema

Pulmonary edema is a problem of major clinical importance resulting from a persistent imbalance between forces that drive water into the airspace of the lung and the biological mechanisms for its removal. Here, we will review the fundamental mechanisms implicated in the regulation of alveolar fluid homeostasis. We will then describe the perturbations of pulmonary fluid homeostasis implicated in the pathogenesis of pulmonary edema in conditions associated with increased pulmonary capillary pressure, namely cardiogenic pulmonary edema and high-altitude pulmonary edema (HAPE), with particular emphasis on the latter that has provided important new insight into underlying mechanisms of pulmonary edema. We will provide evidence that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent a central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction, and, in turn, capillary stress failure and alveolar fluid flooding. We will then demonstrate that exaggerated pulmonary hypertension, while possibly a prerequisite, may not always be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we will outline, how this new insight gained from studies in HAPE, may be translated into the management of pulmonary edema and hypoxemia related disease states in general.     

肺结核病与非结核分枝杆菌肺病互相继发4例报告并文献复习

目的分析非结核分枝杆菌(Nontuberculous Mycobacteria,NTM)肺病及肺结核病与NTM肺病互相继发(或并发)的临床表现特点,提高认识,减少误诊。方法收集4例肺结核病与NTM肺病互相继发病例的有关资料,并文献资料一起分析。结果①NTM肺病的性别分布男多于女,发病年龄多见于40岁以上;②主要症状:咳嗽、咳痰、咯血(或血痰)、发热,③病程长,最长达50年,④多数患者有慢性病史,⑤X线胸片表现两侧达68%、单侧30%、空洞54%、胸膜累及40%,⑦对异烟肼(H)、利福平(R)、链霉素(S)、乙胺丁醇(E)的耐药性分别为:95%、73%、79%和74%。结论NTM肺病多见于有慢性病史,病程长,以咳嗽、咳痰、咯血(或血痰)、发热为主要症状,X线胸片,病灶分布两侧为多、多有空洞并累及胸膜,对常用的抗痨药物有高度耐药性;而患者病情较重与患肺结核或NTM肺病后容易互相继发(或并发)有一定关系。