超声心动图观察慢性间歇性低氧新西兰兔右心结构和功能的实验研究

发布时间：2018-04-01 05:34

本文选题：慢性间歇性低氧　切入点：模型　出处：《山西医科大学》2014年硕士论文

【摘要】：目的：本研究意在建立慢性间歇性低氧（CIH）兔模型，用二维、血流及组织多普勒超声心动图观察CIH早期（0～8周）新西兰兔右心结构、功能及血流动力学的动态变化。方法：选用健康雄性新西兰大白兔24只，建立CIH动物模型，实验持续8周。于CIH模型制作开始0、1、2、4、6、8周应用常规及组织多普勒超声心动图测量右室结构、收缩及舒张功能参数，分析其动态变化趋势。并于每次超声检查后随机处死1只兔，分离心脏、右室，进行HE染色，观察右室心肌、肺动脉、肺组织结构的变化。结果：右心结构参数变化：与0周相比，RV、RA8周增大（P＜0.05），PA主干、RVWd各周无明显变化（P＞0.05）；RV收缩功能参数：与0周相比，RVFAC8周增大（P＜0.05），TAPSE4、6、8周均增大（P＜0.05），RMPI4周减小（P＜0.05），6、8周恢复至基础状态，ICT2、4周缩短（P＜0.05），6、8周恢复至基础状态，肺动脉血流频谱ET1、2周缩短（P＜0.05），4、6、8周恢复至基础状态，肺动脉血流频谱AT1、2、4周缩短（P＜0.05），6、8周恢复至基础状态；RV舒张功能参数变化：与0周相比，IRT于1、2周均缩短（P＜0.05），E/E’1、2周均减小（P＜0.05），4、6、8周均恢复至基础状态，E/A4、6、8周增大（P＜0.05），E’/A’8周增大（P＜0.05）；④病理学变化:心肌细胞病理变化：细胞核肥大，染色加深，部分胞浆疏松淡染，呈水肿样，，肌纤维有灶性坏死及溶解,心肌间质增宽,局部细胞增多,其形态与成纤维细胞相似；肺组织病理变化：可见炎性细胞浸润，毛细血管壁扩张充血，大量浆液、纤维素渗出，肺小动脉横切面平滑肌细胞数增加，肺小动脉血管壁略增厚，管腔略变窄。结论：CIH早期新西兰兔右室功能代偿性增强，右心功能异常早于结构异常；右室舒张功能代偿早于收缩功能，IRT和ICT变化早于其它舒张及收缩功能参数。
[Abstract]:Objective: to establish a chronic intermittent hypoxia rabbit model and to observe the dynamic changes of the right heart structure, function and hemodynamics in New Zealand rabbits at the early stage of CIH by two-dimensional, flow and tissue Doppler echocardiography. Methods: 24 healthy male New Zealand white rabbits were used to establish CIH animal model for 8 weeks. The right ventricular structure, systolic and diastolic function parameters were measured by routine and tissue Doppler echocardiography at the beginning of CIH model making. After each ultrasound examination, a rabbit was killed at random to separate the heart and the right ventricle and stained with HE to observe the changes of the tissue structure of the right ventricle, pulmonary artery and lung. Results: compared with 0 week, the RV RV RA8 weeks increased P < 0.05 and PA trunk RVWd showed no significant change (P > 0.05). Compared with 0 week, RVFAC 8 weeks increased P < 0.05% TAPSE468 weeks increased P < 0.05% RMPI 4 weeks decreased P < 0.05 weeks, and recovered to the basic state ICT2 / 4 weeks, respectively (P < 0.05), P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05%, P < 0. 05, P > 0. 05%, respectively. Shortened P < 0.05 and restored to the basic state in 8 weeks. The pulmonary artery blood flow spectrum et _ (1) was shortened in 2 weeks, P < 0.05, and recovered to the basic state in 8 weeks. Pulmonary artery blood flow spectrum AT1 / 2 ~ 2 ~ 4 weeks shortened P < 0. 05 ~ 0. 05 ~ 6 ~ 8 weeks to return to basic state and RV diastolic function parameters changed: compared with 0 ~ (th) week, IRT was shortened at 12 ~ 2 weeks (P < 0. 05), P < 0. 05% E / E ~ (1 +) decreased in 2 ~ 2 weeks, P < 0. 05 ~ 0. 05 ~ 0. 05% EA4 / A ~ 6 ~ 8 weeks increased, P < 0. 05% E / A / A ~ (8) week increased, P < 0. 05% P < 0. 05% E / A ~ (8) week increased, P < 0. 05% P < 0. 05% P < 0. 05% P < 0. 05% P < 0. 05%. Cardiac myocyte pathological changes: nuclear hypertrophy, The staining deepened, some of the cytoplasm were loose and light stained, showing edema, focal necrosis and dissolution of muscle fibers, widening of myocardial interstitial cells and increasing of local cells, their morphology was similar to that of fibroblasts, pathological changes of lung tissue: inflammatory cell infiltration was observed. Capillary wall dilatation hyperemia, a large amount of serous, cellulose exudate, pulmonary arteriole cross-sectional smooth muscle cells increased, pulmonary arteriole wall slightly thickened, the lumen slightly narrow. Conclusion right ventricular function compensatory enhancement, right ventricular dysfunction is earlier than structural abnormality, right ventricular diastolic function compensation is earlier than systolic function, IRT and ICT changes are earlier than other parameters of diastolic and systolic function.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R540.45

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