中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2007年
5期
868-873
,共6页
周宇宏%王玲%单宏丽%张妍%孙宏丽%杨宝峰
週宇宏%王玲%單宏麗%張妍%孫宏麗%楊寶峰
주우굉%왕령%단굉려%장연%손굉려%양보봉
高胆固醇血症%钾电流%钙电流%膜片钳术%心肌细胞
高膽固醇血癥%鉀電流%鈣電流%膜片鉗術%心肌細胞
고담고순혈증%갑전류%개전류%막편겸술%심기세포
Hypercholesterolemia%Potassium current%Calcium current%Patch - clamp techniques%Cardiomyocytes
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.
目的:觀察高膽固醇血癥對大鼠心室肌細胞離子電流的作用.方法:通過全細胞膜片鉗技術記錄用酶解法分離的正常和高膽固醇飲食的大鼠心室肌細胞離子電流.結果:高膽固醇組(組Ⅱ)血清總膽固醇水平明顯高于正常組(組Ⅰ)[(3.10±0.62)mmol·L-1vs(1.18±0.37)mmol·L-1,P<0.01,n=20].組Ⅱ血清甘油三酯也明顯高于組Ⅰ[(1.51±0.30)mmol·L-1vs(0.43±0.15)mmol·L-1,P<0.01,n=20].組Ⅱ大鼠心室肌細胞動作電位時程(APD)與組Ⅰ相比明顯延長,APD50從(70.86±8.12)ms延長至(116.16±6.90)ms(n=10,P<0.01);APD90從(95.10±7.27)ms延長至(144.04±7.39)ms(n=10,P<0.01);在實驗電壓-120 mV,Ik1從(-16.98±4.54)pA/pF(組Ⅰ)增加到(-19.92±4.08)pA/pF(組Ⅱ)(n=12,P<0.05);在實驗電壓0 mV,Ica-L從(-8.56±1.29)pA/pF(組Ⅰ)減少到(-5.24±0.90)pA/pF(組Ⅱ)(n=10,P<0.01);在實驗電壓+60 mV,Ito從(13.20±1.97)pA/pF(組Ⅰ)減少到(10.30±1.97)pA/pF(組Ⅱ)(n=8,P<0.05).結論:高膽固醇血癥可顯著改變心肌細胞離子電流密度的大小,對心髒具有毒性作用.
목적:관찰고담고순혈증대대서심실기세포리자전류적작용.방법:통과전세포막편겸기술기록용매해법분리적정상화고담고순음식적대서심실기세포리자전류.결과:고담고순조(조Ⅱ)혈청총담고순수평명현고우정상조(조Ⅰ)[(3.10±0.62)mmol·L-1vs(1.18±0.37)mmol·L-1,P<0.01,n=20].조Ⅱ혈청감유삼지야명현고우조Ⅰ[(1.51±0.30)mmol·L-1vs(0.43±0.15)mmol·L-1,P<0.01,n=20].조Ⅱ대서심실기세포동작전위시정(APD)여조Ⅰ상비명현연장,APD50종(70.86±8.12)ms연장지(116.16±6.90)ms(n=10,P<0.01);APD90종(95.10±7.27)ms연장지(144.04±7.39)ms(n=10,P<0.01);재실험전압-120 mV,Ik1종(-16.98±4.54)pA/pF(조Ⅰ)증가도(-19.92±4.08)pA/pF(조Ⅱ)(n=12,P<0.05);재실험전압0 mV,Ica-L종(-8.56±1.29)pA/pF(조Ⅰ)감소도(-5.24±0.90)pA/pF(조Ⅱ)(n=10,P<0.01);재실험전압+60 mV,Ito종(13.20±1.97)pA/pF(조Ⅰ)감소도(10.30±1.97)pA/pF(조Ⅱ)(n=8,P<0.05).결론:고담고순혈증가현저개변심기세포리자전류밀도적대소,대심장구유독성작용.
AIM: To determine whether chronic hypercholesterolemia affects ionic currents on cardiac ventricular myocytes of rats. METHODS: Whole - cell patch - clamp technique was used to record the ionic currents in single cardiac myocytes isolated from normal cholesterolemia and hypercholesterolemia rats. RESULTS: In the hypercholesterol group (group Ⅱ ), serum total - cholesterol level was significantly higher than that of normal group (group Ⅰ) [ (3. 10 ±tricular myocytes 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); APD90 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, Ik1 increased from ( - 16. 98 ±4. 54) pA/pF(group Ⅰ ) to ( - 19.92 ±4.08) pA/pF (group Ⅱ ) (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). CON-CLUSION: Hypercholesterolemia affects the ionic currents on cardiomyocytes of rats greatly, which may be the ionic mechanism of cardiac toxicity induced by hypercholesterolemia.