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作 者:张孝勇[1] 马进[2] 杜滂[1] 马克军[1] 王亚蓉[1] 魏经国[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
出 处:《世界华人消化杂志》2007年第3期216-220,共5页World Chinese Journal of Digestology
基 金:国家自然科学基金资助项目;No.30470787~~
摘 要:目的:研究高胆固醇血症(hypercholesterolemia,HC)兔胆管Oddi括约肌(SO)收缩反应及钾离子通道活性的变化情况,并探讨其机制.方法:将24只新西兰雌兔随机分成两组,HC模型组和对照组各12只,分别取两组SO组织制备成离体肌环,观察SO肌环对KCl及钾离子通道阻断剂盐酸四乙铵(TEA)和4-氨基吡啶(4-AP)的收缩反应,并采用Western blot技术,检测两组兔SO组织中钾离子通道的表达情况.结果:60mmol/LKCl所诱发的HC组和对照组SO肌环的收缩力分别为1.23±0.08g和1.52±0.11g,HC组的收缩反应明显高于对照组(t=5.89,P<0.05).以1mmol/L为浓度梯度累积加入TEA,从3mmol/L至8mmol/L,HC组SO肌环对TEA的相对收缩反应在各个浓度点均明显低于对照组(t=2.72,P<0.05).以2mmol/L为浓度梯度累积加入4-AP,从8至18mmol/L,HC组SO肌环对4-AP的相对收缩反应在各个浓度点均较对照组显著降低(t=4.71,P<0.05).蛋白免疫印迹半定量分析显示HC组SO组织BKCa通道相对光密度为0.36±0.06,对照组为0.84±0.03,HC组BKCa通道蛋白表达量明显降低(t=3.18,P<0.05).结论:HC兔SO肌环的收缩反应增强,SO细胞BKCa及KV通道活性降低,BKCa通道蛋白表达量降低,这可能是导致HC兔发生SO功能紊乱的原因之一.AIM To study the changes of the contractile responses and potassium ion channel activity in sphincter of Oddi (SO) from rabbits with hypercholesterolemia (HC), and elucidate the underlying mechanisms responsible for these changes. METHODS: A total of 24 New Zealand female rabbits were divided randomly into control group (n = 12) and HC group (n = 12). SO muscle rings were dissociated from the rabbits in both groups in vitro. The contractile responses of SO to potassium chloride (KCl) was observed firstly. Then the contractile responses evoked by tetraethylammonium (TEA) and 4-aminopyri- dine (4-AP) were measured. Western blot was employed to examine the expression of potassium ion channels in tissues of HC and control group. RESULTS: The contractile forces (induced by 60 mmol/L KCl) of SO tissues from HC and control group were 1.23 ± 0.08 and 1.52 ± 0.11 g, respectively. HC group showed a markedly increased contractile response (t = 5.89, P 〈 0.05). Compared with that in control group, the ratio of contractile responses induced by TEA (3-8 mmol/L) or 4-AP (8-18 mmol/L) to those induced by 60 mmol/L KC1 was decreased significantly in HC group (t = 2.72, P 〈 0.05; t = 4.71, P 〈 0.05). Western blot indicated that the protein expression of potassium ion channels of SO tissue was significantly reduced in HC group in comparison with that in control group (0.36 ± 0.06 vs 0.84 ±0.03, t = 3.18, P 〈 0.05). CONCLUSION: The contractile response of SO to KC1 increases while the activities of BKCa and Kv in SO cells decrease in HC rabbits, which might be one of the reasons why SO dysfunction is caused in the condition of HC.
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