目的：建立慢性间歇性低氧（CIH）新西兰兔模型，应用超声心动图观察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。方法健康雄性新西兰兔24只置于8%~21%氧浓度的CIH舱内，每天持续6 h，6 d/周，共8周。于CIH第0、1、2、4、6、8周超声心动图观察新西兰兔右心室结构和功能，同时随机处死1只，观察右心室心肌和肺组织的病理变化。采用混合效应模型分析比较制模后0、1、2、4、6、8周右心结构及功能参数。结果右心结构参数与CIH 0周比较，右心室前后径、长径、基底部横径、中部横径、右心室前壁厚度、右心室流出道内径、肺动脉内径、左肺动脉内径、右肺动脉内径、右心房前后径及右心房上下径8周时增大，但差异均无统计学意义（P均＞0.05）。右心室收缩功能参数：与CIH 0周相比，右心室心肌做功指数（RVMPI）于4周减小（F=3.46，P＜0.05），三尖瓣环平面收缩位移（TAPSE）于4、6、8周增大（F=3.11、3.41、3.86，P均＜0.05），右心室面积变化率（RVFAC）于8周增大（F=3.45，P＜0.05），心率校正的等容收缩时间（ICTc）于2、4周时缩短（F=3.13、3.33，P均＜0.05），8周时恢复至基础状态，肺动脉血流频谱射血时间（ET）于1、2周缩短（F=3.01、3.15，P均＜0.05），加速时间（AT）于1、2、4周缩短（F=3.13、3.15、3.32，P均＜0.05）。右心室舒张功能参数：与CIH 0周相比，心率（HR）于1周、2周、4周加快（F=3.06、3.12、3.30，P均＜0.05），心率矫正的等容舒张时间（IRTc）于1、2、4周缩短（F=3.15、3.31、3.17，P均＜0.05），三尖瓣口舒张早期峰值流速/组织多普勒右心室侧壁三尖瓣环舒张早期峰值速度（E/Eʹ）于1、2周时减小（F=3.13、3.44，P均＜0.05），三尖瓣口舒张早期峰值流速/三尖瓣口舒张晚期峰值流速（E/A）于4、6、8周时增大（F=4.01、3.82、3.37，P均＜0.05），组织多普勒右心室侧壁三尖瓣环舒张早期峰值速度/组织多普勒右心室侧壁三尖瓣舒张晚期峰值速度（Eʹ/Aʹ）于8周时增大（F=3.81，P＜0.05）。病理学检查：右心室心肌细胞CIH 4周心肌结构正常，心肌细胞细长；CIH 8周少部分出现细胞核肥大，染色加深，部分胞质疏松淡染。肺组织CIH 4周肺组织结构正常，肺泡腔无渗出；CIH 8周少部分出现炎性细胞浸润，毛细血管扩张充血，肺小动脉血管壁轻度增厚。结论 CIH早期新西兰兔右心室功能代偿性增强，且早于结构异常；右心室舒张功能代偿早于收缩功能，IRT和ICT是右心舒张及收缩功能代偿的敏感性指标。%ObjectiveTo observe right ventricle (RV) structure and function of New Zealand rabbits with chronic intermittent hypoxia (CIH) for short-term (0-8 weeks) by echocardiography. MethodsTwenty-four healthy male New Zealand rabbits were set up CIH animal model for 8 weeks. RV structureʹs systolic and diastolic function were measured by conventional and tissue Doppler echocardiography at 0, 1, 2, 4, 6 and 8 week and one rabbit was sacriifced randomly for RV myocytes and pulmonary tissue pathology examination. RV structure and function parameters at 0, 1, 2, 4, 6 and 8 week were analyzed by mixed effects model analysis.ResultsRV structure variables: RV, RA at 8 week increased compared with those at 0 week, but had no signiifcant difference (P>0.05); RV systolic function variables:RVFAC at 8 week increased compared with those at 0 week (F=3.45, P<0.05), TAPSE at 4, 6, 8 week increased compared with that at 0 week (F=3.11, 3.41 and 3.86, all P<0.05), RVMPI at 4 week decreased compared with that at 0 week (F=3.46, P<0.05), recovered to baseline at 6, 8 week. Isovolumetric relaxation time (IRTc) corrected by heart rate at 1, 2, 4 week decreased compared with that at 0 week (F=3.15, 3.31 and 3.17, all P<0.05), recovered to baseline at 8 week, ET of PA at 1, 2 week decreased compared with that at 0 week (F=3.01 and 3.15, both P<0.05), recovered to baseline at 4, 6, 8 week, AT of PA at 1, 2, 4 week decreased compared with that at 0 week (F=3.13, 3.15 and 3.32, all P<0.05), recovered to baseline at 6, 8 week. RV diastolic function variables: isovolumetric contraction time (ICTc) corrected by heart rate at 2, 4 week decreased compared with that at 0 week (F=3.13 and 3.33,both P<0.05), E/Eʹ at 1, 2 week decreased compared with that at 0 week (F=3.13 and 3.44,bothP<0.05), recovered to baseline at 4, 6, 8 week, E/A at 4, 6, 8 week increased compared with that at 0 week (F=4.01, 3.82 and 3.37, all P<0.05), Eʹ/Aʹ at 8 week increased compared with that at 0 week (F=3.81, P<0.05). The myocardial pathology showed that RV myocardial cell structure was normal at 4 week. Nuclei enlarged, stain darkened and some cytoplasms loosed when exposed to CIH for 8 weeks. The structure of lung tissues was normal when exposed to CIH for 4 weeks. Inflammatory cell inifltrated, capillary engorged as well as the wall of pulmonary arterioles thickened slightly at 8 week.ConclusionsRV diastolic and systolic function showed compensatory and structure was normal in early CIH (0-8 week). RV diastolic function compensated earlier than systolic function. IRT and ICT were sensitive indicators of RV systolic and diastolic function compensation.
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