title: [Related research between acute inflammatory reaction and hemodynamic changes of pulmonary embolism rabbit with hyperhomocysteinemia].
abstract: OBJECTIVE
  To explore the association between acute inflammatory reaction and hemodynamic changes of acute pulmonary embolism rabbit with hyperhomocysteinemia.
  
  
  METHODS
  A total of 30 Japanese white rabbits were randomly divided into homocysteine group and control group according to the random number table, which were treated with 2% methionine and normal saline, respectively. Rabbit model of acute pulmonary embolism was established by autologous blood clots reinfusion after 8 weeks, then the level of serum tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), right ventricular systolic pressure (RVSP), right atria systolic pressure (RASP), pulmonary artery pressure (PAP) were checked before and after thrombosis at different time points. At last, area of embolism, degree of lung congestion and incidence of lung infarction were evaluated after the rabbits were sacrificed.
  
  
  RESULTS
  Both homocysteine group and control group serum TNF-α, IL-1β increased at 30, 60, 120 min after embolism, and serum TNF-α, IL-1β of homocysteine group [(12.4 ± 1.0), (15.7 ± 1.1), (23.2 ± 1.4) and (7.6 ± 1.0), (10.2 ± 2.1), (18.8 ± 1.3) pg/ml] increased more obviously than control group [(10.2 ± 1.0), (11.7 ± 1.4), (12.1 ± 1 .2) and (6.4 ± 1.1), (8.5 ± 1.9), (10.0 ± 2.1) pg/ml] (all P<0.05). All of RVSP, RASP, and PAP increased in each group after embolism, while homocysteine group RVSP [(52.8 ± 3.3), (54.7 ± 4.5), (46.4 ± 4.4) mmHg], RASP [(3.9 ± 1.2), (4.5 ± 2.0), (4.5 ± 1.9) mmHg] and PAP[(52.9 ± 3.3), (55.1 ± 2.9), (47.5 ± 3.6) mmHg] increased more obviously compared with control group [(39.4 ± 2.5), (39.4 ± 3.3), (34.5 ± 3.9) mmHg, (2.3 ± 1.1), (3.3 ± 1.1), (3.3 ± 1.2) mmHg and (37.7 ± 2.7), (40.2 ± 2.9), (33.7 ± 4.2) mmHg] (all P<0.05).
  
  
  CONCLUSIONS
  Inflammatory response of acute pulmonary embolism rabbit increases in hyperhomocysteinemia and the degree of embolism increases as well, which may lead to increase of hemodynamic instability.
authors: Department of Respiratory, the First Affiliated Hospital of Henan University of Science and Technology, Luoyang 471003, China.
authors: Xuegai
authors: X
authors: He
authors: Department of Respiratory, the First Affiliated Hospital of Henan University of Science and Technology, Luoyang 471003, China; Email: yimin6107@sina.com.
authors: Yimin
authors: Y
authors: Mao
authors: Department of Respiratory, the First Affiliated Hospital of Henan University of Science and Technology, Luoyang 471003, China.
authors: Jun
authors: J
authors: He
mesh_terms: D000818:Animals; D006439:Hemodynamics; D020138:Hyperhomocysteinemia; D007249:Inflammation; D053583:Interleukin-1beta; D008168:Lung; D011654:Pulmonary Edema; D011655:Pulmonary Embolism; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha
chemical_list: D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha