【摘要】 目的　探讨组织胺及其 1型受体 (H1R)阻断剂、2型受体 (H2R)阻断剂对贮脂细胞收缩的影响。方法　采用肝脏离体胶原酶灌注消化及密度梯度离心的方法来分离培养贮脂细胞 ;用二甲基多聚硅烷烧制聚硅酮膜 ;传代后的贮脂细胞在聚硅酮膜上培养 3d后 ,随机分为 5组 :A组(对照组 ) ;B组 (组织胺 1× 10 -7mol/L组 ) ;C组 (组织胺 1× 10 -6mol/L组 ) ;D组 (H 1R阻断剂 +组织胺 1× 10 -6mol/L组 )和E组 (H2R阻断剂 +组织胺 1× 10 -6mol/L组 )。各组于加药前及加药后 2 0min摄相 ,在相片上分析同一视野细胞周围的聚硅酮膜皱纹变化 ,皱纹增多表明细胞收缩。结果　B组、C组的贮脂细胞收缩率分别为 2 1.0 %、34.2 % ,远高于A组的 3 .8% ,并呈量效依赖关系 (P <0 .0 0 1) ;D组的贮脂细胞收缩率为 17.7% ,低于C组 (P <0 .0 5 ) ;E组的贮脂细胞收缩率为2 6 .3 % ,与C组相比 ,差异无显著性 (P >0 .0 5 )。结论　组织胺通过H1R的介导促进贮脂细胞的收缩 ,可能在门静脉高压症的发生发展中起了一定的作更多还原

【Abstract】 Objective To investigate the effect of histamine and H1 receptor (H1R) antagonist, H2 receptor (H2R) antagonist on the contractility of rat fat storing cells. Methods Fat storing cells was isolated and purified from rat liver by collagenase IV perfusion and density gradient centrifugation with Nycodenz. Silicone rubber membrane was made of dimethylpolysiloxane by heating. Passaged fat storing cells were cultured on silicone rubber membrane for 3 days, then divided randomly into 5 groups: control group (group A), histamine 1×10 -7 mol/L treated group (group B), histamine 1×10 -6 mol/L treated group (group C), histamine 1×10 -6 mol/L plus H1R antagonist treated group (group D) and histamine 1×10 -6 mol/L plus H2R antagonist treated group (group E). The cells of all groups were photographed before and 20 min after the addition of agents. The change in the number of wrinkles of silicone rubber membrane around the cells from the same area was determined on photographs. An increased number of wrinkles indicated contractile responses. Results The percentage of contracted fat storing cells in group B and group C was 21.0 % and 34.2 % respectively, which were significantly higher than in the group A(3.8 %, P <0.001)in a dose dependent manner. The percentage of contracted fat storing cells in the group D (17.7 %) was lower than in the group C ( P <0.05). There was no significant difference in percentage of contracted fat storing cells between the group E (26.3 %) and group C ( P >0.05). Conclusion Histamine could induce contraction of fat storing cells through H1R, which might play a role in the pathogenesis of portal hypertension. [更多还原