摘要
OBJECTIVE: To examine the microvascular pathological characteristics and changes in related injury factors in a rat model of acute blood stasis.METHODS: A total of 75 Sprague-Dawley rats were divided randomly and equally into a control group and four experimental groups assessed at different times after the induction of stasis(0, 1, 3 or 6 h after stasis)(n = 15). The acute blood stasis model was established through rat tail-vein injection of high-molecular-weight dextran. After Electrocardiograph(ECG) detection at predetermined times(0,1, 3 and 6 h after induction of stasis), the rats were sacrificed and blood and cardiac samples were harvested for analysis. Hematoxylin-eosin(HE) staining and transmission electron microscopy were used for histopathological detection; an enzyme linked immunosorbent assay(ELISA) was used to detect thromboxane B2(TXB2) and 6-keto-prostaglandin F1α(6-Keto-PGF1α) concentrations; a real-time polymerase chain reaction(PCR) reaction system was used to detect intercellular adhesion molecule1(ICAM-1) and vascular cell adhesion molecule1(VCAM-1) m RNA expression; western blotting was used to detect vascular endothelial cadherin(VE-cadherin) protein expression.RESULTS: The ST segment in the ECG showed gradual elevation after induction of stasis and continued elevation at a high level at 3 and 6 h. The HE staining showed changes in myocardial cell necrosis and tissue dissociation after the induction of stasis, along with inflammatory infiltration. Results of transmission electron microscopy showed immediate changes in blood stasis and lumen occlusion in the microvasculature, along with endothelial cell swelling. After the induction of stasis, TXB2 concentrations gradually increased while 6-Keto-PGF1αconcentrations were immediately significantly reduced. The TXB2/6-Keto-PGF1αratio was maintained at a high level. ICAM-1 m RNA expression showed an unstable elevation while VCAM-1 m RNA expression was significantly reduced after the induction of stasis. Compared with the control group, VE-cad
OBJECTIVE： To examine the microvascular patho- logical characteristics and changes in related injury factors in a rat model of acute blood stasis. METHODS： A total of 75 Sprague-Dawley rats were divided randomly and equally into a control group and four experimental groups assessed at different times after the induction of stasis （0, 1, 3 or 6 h af- ter stasis） （n = 15）. The acute blood stasis model was established through rat tail-vein injection of high-molecular-weight dextran. After Electrocardio- graph CECG） detection at predetermined times C0, 1, 3 and 6 h after induction of stasis）, the rats were sacrificed and blood and cardiac samples were har- vested for analysis. Hematoxylin-eosin （HE） staining and transmission electron microscopy were used for histopathological detection; an enzyme linked immunosorbent assay （ELISA） was used to detect thromboxane B2 （TXB2） and 6-keto-prostaglandin Fla （6-Keto-PGFla） concentrations; a real-time polymerase chain reaction （PCR） reaction system was used to detect intercellular adhesion molecule 1 （ICAM-1） and vascular cell adhesion molecule 1 （VCAM-1） mRNA expression; western blotting was used to detect vascular endothelial cadherin （VE-cadherin） protein expression. RESULTS： The ST segment in the ECG showed gradual elevation after induction of stasis and contin- ued elevation at a high level at 3 and 6 h. The HE staining showed changes in myocardial cell necrosis and tissue dissociation after the induction of sta- sis, along with inflammatory infiltration. Results of transmission electron microscopy showed immediate changes in blood stasis and lumen occlusion in the microvasculature, along with endothelial cell swelling. After the induction of stasis, TXB2 concen-trations gradually increased while 6-Keto-PGFlo con- centrations were immediately significantly re- duced. The TXBJ6-Keto-PGFlo ratio was maintained at a high level. ICAM-1 mRNA expression showed an unstable elevation while VCAM-1 mRNA expres- sion was significant
基金
the National Program on Key Basic Research Project(973 Program,No.2012CB518601)
