title: [Effect of activating blood circulation or activating blood circulation and detoxication on platelet activation, inflammation, and coagulation status in acute myocardial infarction rats].
abstract: OBJECTIVE
  To observe the effect of activating blood circulation drugs or activating blood circulation and detoxication drugs on indices of platelet activation, inflammation, and coagulation status correlated with blood-stasis and toxin in acute myocardial infarction rats.
  
  
  METHODS
  Totally 100 male SD rats were randomly divided into the sham-operation group, the model group, the activating blood circulation group, the activating blood circulation and detoxication group, and the metoprolol group, 20 in each group. Rats in the activating blood circulation group were administered with Xiongshao Capsule at the daily dose of 0.39 g/kg. Rats in the activating blood circulation and detoxication group were administered with Xiongshao Capsule (at the daily dose of 0.39 g/kg) and Huanglian Capsule (at the daily dose of 0.135 g/kg). Rats in the metoprolol group received metoprolol at the daily dose of 2.25 mg/kg. And rats in the rest two groups were administered with normal saline. All medication lasted for 3 successive weeks. After the last administration, the rat model of acute myocardial infarction was prepared by ligation of left anterior descending artery. No ligation was given to rats in the sham-operation group. Animals were sacrificed 24 h after modeling. Tumor necrosis factor-α (TNF-α), β-thromboglobulin (β-TG), platelet α granule membrane protein-140 (GMP-140), 11 dehydro-thromboxane B2 (11-DH-TXB2), fibrinopeptide A (FPA), antithrombin III (AT-III), and D-dimer (DD) were detected by ELISA. The mRNA expression of TNF-α was tested by RT-PCR.
  
  
  RESULTS
  Platelet activation parameters were significantly increased in the model group, when compared with the sham-operation group (P < 0.01). Compared with the model group, all indices (except GMP-140 in the metoprolol group) obviously decreased in each medicated group (P < 0.01, P < 0.05). Besides, β-TG and 11-DH-TXB2 were superior in the activating blood circulation and detoxication group to that of the metoprolol group (P < 0.05). But 11-DH-TXB2 was also obviously superior in the activating blood circulation and detoxication group to that of the activating blood circulation group (P < 0.05). Compared with the sham-operation group, an obviously hypercoagulable state was obviously shown in the AMI model group, with significantly increased FPA and DD (P < 0.05 or 0.01) and significantly decreased AT III (P < 0.01). Compared with the model group, the FPA level significantly decreased in each medicated group (P < 0.01), and the AT III level significantly increased in the activating blood circulation group and the activating blood circulation and detoxication group (both P < 0.01). The level of DD obviously decreased in the activating blood circulation and detoxication group (P < 0.01). Besides, the 3 indices were superior in the activating blood circulation and detoxication group to those of the metoprolol group (P < 0.05). Compared with the sham-operation group, the serum TNF-α level and myocardial TNF-α mRNA expression were significantly increased in the model group (P < 0.05, P < 0.01). Compared with the model group, not only the serum TNF-α level was significantly decreased, but also the TNF-α gene expression in the myocardial tissue was improved in the activating blood circulation and detoxication group (P < 0.01).
  
  
  CONCLUSIONS
  Combined use of activating blood circulation and detoxication drugs could play an effective role in treatment of coronary heart disease by fighting against platelet activation, improving the hypercoagulable state, and inhibiting inflammation, which was significantly better than using activating blood circulation and removing stasis drugs alone.
authors.affiliation: Xiyuan Hospital,  Chinese Academy of Medical Sciences, Beijing, China
authors.forename: Xiao-Juan
authors.initials: XJ
authors.lastname: Ma
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Guo
authors.forename: Hui-Jun
authors.initials: HJ
authors.lastname: Yin
authors.forename: Yue
authors.initials: Y
authors.lastname: Liu
authors.forename: Da-Zhuo
authors.initials: DZ
authors.lastname: Shi
mesh_terms: D000818:Animals; D004365:Drugs, Chinese Herbal / Q000494:pharmacology; D005338:Fibrin Fibrinogen Degradation Products; D007249:Inflammation / Q000378:metabolism; D008297:Male; D008516:Medicine, Chinese Traditional; D009203:Myocardial Infarction / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D015539:Platelet Activation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004365:Drugs, Chinese Herbal; D005338:Fibrin Fibrinogen Degradation Products; D014409:Tumor Necrosis Factor-alpha; C036309:fibrin fragment D; C494417:huanglian; C528128:xiongshao