高胆固醇血症兔Oddi括约肌张力的变化机制  

Mechanisms of tension changes of the sphincter of Oddi from hypercholesterolemic rabbits

作　　者：张孝勇[1] 魏经国[1] 马进[2] 王莎[3] 马孝武[2] 马克军[1] 王亚蓉[1] 

机构地区：[1]中国人民解放军第四军医大学唐都医院放射科,陕西省西安市710038 [2]中国人民解放军第四军医大学航空航天生理学教研室,陕西省西安市710032 [3]中国人民解放军第四军医大学西京医院血液科,陕西省西安市710032

出　　处：《世界华人消化杂志》2004年第5期1114-1118,共5页World Chinese Journal of Digestology

基　　金：陕西省自然科学基金资助项目;No.2002C2-19~~

摘　　要：目的:观察高胆固醇血症(hypercholesterolemia,HC)兔离体Oddi括约肌(sphincter of oddi,SO)张力的变化,探讨其作用机制. 方法:新西兰雌兔24只随机分成两组:对照组和HC模型组各12只,分别取两组SO制备成离体肌环,观察SO的自主收缩运动及其对KCl和Ca2+的收缩反应,以及对硝普钠(sodium nitroprusside,SNP)和硝苯吡啶(nifedipine, Nif)的舒张反应. 结果:HC组的自主收缩频率高于对照组(P<0.05,t=2.86), 自主收缩波幅较对照组降低(P<0.05,t=2.48).以10 mmoL/L 为浓度梯度累积加入KCI至90 mmoL/L,HC组对中低浓度KCl(10-40 mmoL/L)收缩反应高于对照组(P<0.01, t=4.01);两组最大收缩力无显著差异,且均可被3 μmoL/L Nif完全缓解.用60 mmoL/L KCl预收缩SO肌环后加入SNP (0.1 nmoL/L-1 mmoL/L),在各个浓度点HC组的舒张反应均明显低于对照组(P<0.01,t=5.12).SO肌环在无钙Krebs液中温育5 min后复钙引起两组明显收缩反应所需的Ca2+浓度分别为0.1和1.0 mmoL/L,HC组显著低于对照组(P<0.01,t=4.91);复钙2.5 mmoL/L诱发两组肌环的收缩反应均可被3μmoL/LNif完全缓解.用60mmoL/L KCl预收缩SO肌环后加入Nif,两组对Nif(0.1 nmoL/L-3 μmoL/L) 的舒张反应在各个浓度点均无明显差别.在Krebs液中先加入3μmoL/L Nif,再加入KCl,CaCl2,两组肌环均未发生收缩反应. 结论:在离体条件下,HC可导致SO张力异常,SO处于易激惹状态,其机制与SO细胞内钙离子浓度([Ca2+]i)过载有关,而该过载状态与L型电压依赖性钙通道(L-type Voltage-dependent calcium channels,L-VDCs)无关.AIM: To observe the effects of hypercholesterolemia (HC) on tension of sphincter of Oddi (SO) in rabbits and to study the mechanisms of the sphincter of Oddi dysfunction (SOD). METHODS: Twenty-four New Zealand female rabbits were divided randomly into control group and HC group (12 rabbits each). Sphincter of Oddi muscle rings were dissociated from both groups in vitro. Automatic contractility was observed firstly. Then the contraction responses evoked by KCI and CaCl2 and relaxation responses caused by sodium nitroprusside (SNP) and nifedipine (Nif) were measured. RESULTS: Compared with control group, the automatic contractile frequency of HC group was increased (P<0.05), and the automatic contractile amplitude of HC group was decreased (P<0.05). The tension of SO rings evoked by KCI at low and moderate concentrations (10-40 mmol/L) was significantly higher in HC group than in control group (P<0.01). The maximum tension was not found difference between two groups, and both could be completely relaxed by Nif (3 μmol/L). Compared with the control group, relaxation responses of SO rings in HC group to SNP (0.1 nmoL/L-1 mmoL/L) were markedly decreased after the administration of KCI (60 mmoL/L) in HC group (P<0.01). The minimum solution value (0.1 mmoL/L) of Ca2+ evoking contraction in HC group was evidently lower than that of the control group (1.0 mmoL/L) (P<0.001). Tensions of SO rings evoked by Ca2+ (2.5 mmoL/L) were entirely relaxed by Nif (3 μmoL/L) both in HC group and control group. After the administration of KCI (60 mmoL/L) relaxation responses of rabbit SO rings to Nif (0.1 nmoL/L-3 μmoL/L) were not found difference between in the two groups. Nif (3 μmoL/L) could completely inhibit the contraction responses evoked by KCI or CaCl2 in both groups. CONCLUSION: Hypercholesterolemia can lead to SO dysfunction and increase the sensitivity of SO to KCI at low and moderate concentrations in vitro. The overloading of intracellular Ca2+ is an important reason for these phenomena, which has no direct relation wi

关 键 词：高胆固醇血症 兔 ODDI括约肌 HC SO 肌张力 胆系疾病 

分 类 号：R575.6[医药卫生—消化系统]