临床与实验病理学杂志
臨床與實驗病理學雜誌
림상여실험병이학잡지
Chinese Journal of Clinical and Experimental Pathology
2015年
10期
1135-1139
,共5页
许耀强%刘迎龙%苏俊武%李刚%朱耀斌
許耀彊%劉迎龍%囌俊武%李剛%硃耀斌
허요강%류영룡%소준무%리강%주요빈
肺动脉%发育不良%先天性心脏病%紫绀%形态定量分析
肺動脈%髮育不良%先天性心髒病%紫紺%形態定量分析
폐동맥%발육불량%선천성심장병%자감%형태정량분석
pulmonary artery%hypoplasia%congenital heart defects%cyanosis%quantitative morphometric technique
目的:建立紫绀型肺血少动物模型,对肺血减少时未成熟肺小血管进行形态观察和半定量分析,观察肺血减少时未成熟肺小血管的发育特点。方法取紫绀型肺血少动物肺组织,进行固定、制片及染色。光镜和透射电镜观察,形态半定量测量分析肺小动脉中膜厚度( media thickness, MT)及中膜厚度百分比( percentage of media thickness, MT%)、中膜面积( media section area, MS)及中膜面积百分比( percentage of media section area, MS%);计数单位面积肺小动脉数目( arterial numbers of per square centimeter, APSC)和单位面积肺泡数量( mean alveolar nunber, MAN);计算同一张切片所有泡内肺动脉( intraacinar pulmonary arteries, IAPA)中肌型动脉( circular muscular artery, CMA)、部分肌型动脉( partially muscular artery, PMA)和无肌型动脉( non-muscular artery, NMA)的比例。结果同对照组( C组)相比,光镜观察肺血减少组( D组)肺小动脉中层退化和发育不良,管腔扩大,形态不规则,管壁厚薄不均,部分弹力纤维层中断、缺失。 PMA和NMA比例较C组高,而CMA比例相对较低(P<0.001)。 D组肺小动脉MT、MT%及MS、MS%均显著小于C组(P均<0.001)。 D组APSC较C组减少(P<0.01),而MAN与C组差异无显著性(P>0.05)。电镜下显示D组肺小血管内皮细胞胞质肿胀,基膜变薄;弹力纤维排列不整齐,有的区域萎缩变薄或中断;血管中层平滑肌轻度萎缩;细胞器减少,线粒体空泡化;部分肺泡Ⅱ型上皮细胞增生明显,板层体丰富。结论肺血流减少时肺小血管发育不良或退化,形态结构异常影响器官的正常功能,尽早改善肺血少状态是促进肺血管发育和改善全身状况的关键。
目的:建立紫紺型肺血少動物模型,對肺血減少時未成熟肺小血管進行形態觀察和半定量分析,觀察肺血減少時未成熟肺小血管的髮育特點。方法取紫紺型肺血少動物肺組織,進行固定、製片及染色。光鏡和透射電鏡觀察,形態半定量測量分析肺小動脈中膜厚度( media thickness, MT)及中膜厚度百分比( percentage of media thickness, MT%)、中膜麵積( media section area, MS)及中膜麵積百分比( percentage of media section area, MS%);計數單位麵積肺小動脈數目( arterial numbers of per square centimeter, APSC)和單位麵積肺泡數量( mean alveolar nunber, MAN);計算同一張切片所有泡內肺動脈( intraacinar pulmonary arteries, IAPA)中肌型動脈( circular muscular artery, CMA)、部分肌型動脈( partially muscular artery, PMA)和無肌型動脈( non-muscular artery, NMA)的比例。結果同對照組( C組)相比,光鏡觀察肺血減少組( D組)肺小動脈中層退化和髮育不良,管腔擴大,形態不規則,管壁厚薄不均,部分彈力纖維層中斷、缺失。 PMA和NMA比例較C組高,而CMA比例相對較低(P<0.001)。 D組肺小動脈MT、MT%及MS、MS%均顯著小于C組(P均<0.001)。 D組APSC較C組減少(P<0.01),而MAN與C組差異無顯著性(P>0.05)。電鏡下顯示D組肺小血管內皮細胞胞質腫脹,基膜變薄;彈力纖維排列不整齊,有的區域萎縮變薄或中斷;血管中層平滑肌輕度萎縮;細胞器減少,線粒體空泡化;部分肺泡Ⅱ型上皮細胞增生明顯,闆層體豐富。結論肺血流減少時肺小血管髮育不良或退化,形態結構異常影響器官的正常功能,儘早改善肺血少狀態是促進肺血管髮育和改善全身狀況的關鍵。
목적:건립자감형폐혈소동물모형,대폐혈감소시미성숙폐소혈관진행형태관찰화반정량분석,관찰폐혈감소시미성숙폐소혈관적발육특점。방법취자감형폐혈소동물폐조직,진행고정、제편급염색。광경화투사전경관찰,형태반정량측량분석폐소동맥중막후도( media thickness, MT)급중막후도백분비( percentage of media thickness, MT%)、중막면적( media section area, MS)급중막면적백분비( percentage of media section area, MS%);계수단위면적폐소동맥수목( arterial numbers of per square centimeter, APSC)화단위면적폐포수량( mean alveolar nunber, MAN);계산동일장절편소유포내폐동맥( intraacinar pulmonary arteries, IAPA)중기형동맥( circular muscular artery, CMA)、부분기형동맥( partially muscular artery, PMA)화무기형동맥( non-muscular artery, NMA)적비례。결과동대조조( C조)상비,광경관찰폐혈감소조( D조)폐소동맥중층퇴화화발육불량,관강확대,형태불규칙,관벽후박불균,부분탄력섬유층중단、결실。 PMA화NMA비례교C조고,이CMA비례상대교저(P<0.001)。 D조폐소동맥MT、MT%급MS、MS%균현저소우C조(P균<0.001)。 D조APSC교C조감소(P<0.01),이MAN여C조차이무현저성(P>0.05)。전경하현시D조폐소혈관내피세포포질종창,기막변박;탄력섬유배렬불정제,유적구역위축변박혹중단;혈관중층평활기경도위축;세포기감소,선립체공포화;부분폐포Ⅱ형상피세포증생명현,판층체봉부。결론폐혈류감소시폐소혈관발육불량혹퇴화,형태결구이상영향기관적정상공능,진조개선폐혈소상태시촉진폐혈관발육화개선전신상황적관건。
Purpose Using quantitative morphometric techniques, To analyzse the developmental characteristics of pulmonary arterial and alveolar with a porcine model of cyanotic congenital heart defect with decreased pulmonary blood flow that we had established. Methods Lung biopsy specimens were taken from animals of control ( C) and cyanosis ( D) groups and than sectioned and stained. The morphological observation and the method of half-quantitative morphometric technique were applied to measure the following char-acteristics:the media thickness ( MT) and the percentage of media thickness ( MT%) , the media section area ( MS%) and the per-centage of media section area ( MS) , the numbers of micro-arteries per square centimeter ( APSC) . In addition, we calculated the ratio of CMA, PMA and NMA in the same section of lung biopsy specimens. Results There showed universally distended, irregular and thin-walled vessels in the lung biopsy specimens of group D under the light microscope. There was an increased number of pulmonary arteries whose media were hypoplastic. The MT, MT% and MS, MS% in group D were significantly less than those of group C ( all P<0. 001), the APSC was also less in group D than in group C (P<0. 01), but MAN were not significantly different between two groups (P>0. 05). Electron microscopy revealed endothelial swell and irregularity, a thinned basement membrane, a disorganized or disrupted elastic fibers layer. The smooth muscle of vascular media shrunk. In addition to these, other changes included the mitochon-drion vacuolization, a diminished cellular organelle and type Ⅱ alveolar epithelial hyperplasia. Conclusion The pulmonary vessels are evidently hypoplastic or degenerated in cyanotic congenital heart defect with decreased pulmonary blood flow, and the function is thought to be influenced by the morphological changes. To promote the pulmonary artery growth and improve this pathophysiological state, it is critical to increase the pulmonary blood flow.