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作 者:周宇宏[1] 王玲[1] 单宏丽[1] 张妍[1] 孙宏丽[1] 杨宝峰[1]
机构地区:[1]哈尔滨医科大学药理教研室,黑龙江哈尔滨150086
出 处:《中国病理生理杂志》2007年第5期868-873,共6页Chinese Journal of Pathophysiology
基 金:Supported by the National Nature Science Foundation of China (No.30271599)
摘 要:目的:观察高胆固醇血症对大鼠心室肌细胞离子电流的作用。方法:通过全细胞膜片钳技术记录用酶解法分离的正常和高胆固醇饮食的大鼠心室肌细胞离子电流。结果:高胆固醇组(组Ⅱ)血清总胆固醇水平明显高于正常组(组Ⅰ)[(3.10±0.62)mmol.L-1vs(1.18±0.37)mmol.L-1,P<0.01, n=20]。组Ⅱ血清甘油三酯也明显高于组Ⅰ[(1.51±0.30)mmol.L-1vs(0.43±0.15)mmol.L-1,P<0.01, n=20]。组Ⅱ大鼠心室肌细胞动作电位时程(APD)与组I相比明显延长,APD50从(70.86±8.12) ms延长至(116.16±6.90) ms (n=10, P<0.01); APD90从(95.10±7.27) ms延长至(144.04±7.39) ms (n=10, P<0.01);在实验电压-120 mV, Ik1从( -16.98±4.54) pA/pF(组I)增加到( -19.92±4.08) pA/pF(组Ⅱ)(n=12, P<0.05);在实验电压0 mV, ICa -L从( -8.56±1.29) pA/pF(组Ⅰ)减少到( -5.24±0.90) pA/pF(组Ⅱ)(n=10, P<0.01);在实验电压+60 mV,Ito从(13.20±1.97) pA/pF(组I)减少到(10.30±1.97) pA/pF(组Ⅱ)(n=8, P<0.05)。结论:高胆固醇血症可显著改变心肌细胞离子电流密度的大小,对心脏具有毒性作用。AIM: To determine whether chronic hypercholesterolemia affects ionic currents on cardiac ventricular myoeytes of rats. METHODS : Whole - cell patch - clamp technique was used to record the ionic currents in single cardiac myoeytes isolated from normal cholesterolemia and hypercholesterolemia rats. RESULTS: In the hypereholesterol group (groupⅡ ), serum total -cholesterol level was significantly higher than that of normal group (group Ⅰ) [ (3. 10 ± 0. 62) mmol·L-1 vs (1.18 ±0. 37)mmol ·L-1, P〈0. 01, n =20]. The serum triglyceride content of group Ⅱ was remark- ably higher than that of group Ⅰ ( 1.51 ± 0. 30) mmol ·L-1vs (0. 43 ±0. 15) mmol ·L-1, p 〈 0. 01, n = 20 ]. In ventricular myoeytes of rats, 50% repolarization of action potential duration ( APD50 ) prolonged from ( 70. 86 ±8. 12 ) ms ( group I ) to ( 116. 16 ±6. 90) ms ( group Ⅱ ) ( n = 10 in each group, P 〈 0. 01 ) ; APDgo prolonged from ( 95. 10±7.27)ms (group Ⅰ ) to (144.04±7.39)ms (group Ⅱ) (n =10 in each group, P〈0.01); at the test potential of - 120 mV, Iki increased from ( - 16. 98± 4. 54) pA/pF( group Ⅰ ) to ( - 19. 92±4. 08) pA/pF (groupⅡ) (n = 12 in each group, P 〈0. 05) ; at the test potential of 0 mV, ICa-L decreased from ( -8.56±1.29) pA/pF (group Ⅰ) to ( - 5.24±0. 90) pA/pF ( group Ⅱ ) ( n = 10 in each group, P 〈 0. 01 ) ; at the test potential of + 60 mV, Ito decreased from (13.20±1.97) pA/pF (group Ⅰ) to (10.30±1.97) pA/pF (group Ⅱ) (n=8 in each group, P〈0.05). CONCLUSION: Hypercholesterolemia affects the ionic currents on cardiomyoeytes of rats greatly, which may be the ionic mechanism of cardiac toxicity induced by hypercholesterolemia.
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