摘要
对兔出血症的凝血象和组织病理学变化进行了动态研究。结果表明：兔出血症伴有弥漫性血管内凝血（ＤＩＣ）病理过程，并呈动态发展规律。凝血象检测发现：感染后６ｈ凝血酶原时间（ＰＴ）、白陶土部分凝血活酶时间（ＫＰＴＴ）缩短或正常，为高凝期，该期短，很快进入低凝期。感染后１８ｈＰＴ、ＫＰＴＴ显著延长，死前更明显。血小板数（ＰＣ）呈渐进性降低，纤维蛋白（原）降解产物（ＦＤＰ）在感染后６ｈ显著增加（Ｐ＜０．０１），感染后１８ｈ达高峰值。组织病理学观察表明：肺的病变严重而且有规律，感染后１２ｈ肺的微血栓检出率最高，同时在心、肝、肾、脑等器官也见微血栓。感染后２４ｈ或死兔的肺出血严重，血栓少见，表现为纤溶亢进的特征性变化。此外，患出血症的兔血管壁早期损伤明显，先于高凝期，可能是ＤＩＣ的启动因素之一。
Selected coagulation assays were conducted and histopathologic changes were monitored on 38 rabbitsinoculated with rabbit hemorrhagic disease virus (RHDV) at different intervals from inoculation to death. The resultswere showed that disseminated intravascular coagulation (DIC) was a anthologic mechanism in this disease. The hypercoagulable Period began at hour 6 postinoculation (HPI ), then prothrombin time (PT ) and koalin partiathrombonplastin time (KPTT) were shorter or normal, compared with those before inoculation. The coagulation assay was charactered by evidently prolonged PT and KPTT at HPI 18, indicating that the blood had gone to thehypocoagulable Period. Blood plateletS count (PC) decreased progressively during the infection. Fibrinolytic degradation products (FDP) increased significently (P<0. 01 ) at HPI 6, and reached its Peak at HPI 18. In histopethologicinvestigation, a high number of microthrombins were found in lungs and a low number in other organs at HPI 12,but at HPI 24 or after death, rare microthrombins and severe hemorrhage were observed in lungs. It was discoveredthat endothelium was damaged before the hypercoagulable period, the endothelial damages might be initial cause ofDIC in RHD.
出处
《南京农业大学学报》
CAS
CSCD
北大核心
1994年第4期83-86,共4页
Journal of Nanjing Agricultural University
关键词
出血症
弥漫性
血管内凝血
兔病
rabbit hemorrhagic disease
disseminated intravascular coagulation
coagulation figure: histopathology
dynamical change
