Deng Chaosheng, Wu Dawen, Zhai Zhenguo, Lin Qichang, Zhong Zhanghua, Yang Yuanhua, Chen Qunlin, Lian Ningfang, Gao Shaoyong, Yang Minxia, Liu Kaixiong, Wang Chen
Division of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China.
Division of Respiratory and Critical Care Medicine, Beijing Institution of Respiratory Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China.
J Thromb Thrombolysis. 2016 May;41(4):581-91. doi: 10.1007/s11239-015-1268-5.
To investigate the pulmonary angiography and pathology in a canine model with chronic pulmonary thromboembolism (PTE). The cylindrical blood clots were selectively introduced into the left (n = 10) or right (n = 20) lower pulmonary arteries of dogs. Pulmonary arteriography (PA) was performed before or after embolization. The values after embolization and baseline of mean pulmonary arterial pressure, pulmonary vascular resistance, cardiac output had changed. After 1 or 2 weeks' embolization, local PA demonstrated the abrupt cut-off perfusion defects or webs, bands, and abrupt vascular narrowing. 2 weeks after embolization, the pathology showed that the fibrin networks of the thrombi had multiple recanalization channels, and pulmonary artery had the concentric, lamellar (onion-like) intimal hyperplasia, multilayered, irregular arrangements of endothelial cells, and the infiltration of inflammatory cells. After embolectomy-mediated reperfusion, 2 weeks' subgroup showed destroyed and incomplete alveolar structures, and a large number of exudative cells, primarily neutrophils, and exudate. There close concordance between pulmonary angiography and pathology in a canine model with chronic PTE. The LIRI mechanisms after embolectomy-mediated reperfusion involve the destroyed, incomplete alveolar structures, and infiltration of inflammatory cells, primarily neutrophils.
研究慢性肺血栓栓塞症(PTE)犬模型的肺血管造影及病理学表现。将圆柱形血凝块选择性地注入犬的左(n = 10)或右(n = 20)下肺动脉。在栓塞前或栓塞后进行肺血管造影(PA)。栓塞后平均肺动脉压、肺血管阻力、心输出量的值与基线相比发生了变化。栓塞1或2周后,局部PA显示出突然截断的灌注缺损或网状、条索状以及血管突然狭窄。栓塞2周后,病理学显示血栓的纤维蛋白网络有多个再通通道,肺动脉有同心、层状(洋葱样)内膜增生,内皮细胞多层、不规则排列以及炎症细胞浸润。在血栓切除术介导的再灌注后,2周亚组显示肺泡结构破坏且不完整,有大量渗出细胞,主要是中性粒细胞,还有渗出物。慢性PTE犬模型中肺血管造影与病理学表现密切一致。血栓切除术介导的再灌注后的肺缺血再灌注损伤机制涉及肺泡结构破坏、不完整以及炎症细胞(主要是中性粒细胞)浸润。