CAJ | 학술논문

目的探讨自发性蛛网膜下腔出血(SAH)是否对脑皮质动脉和穿支动脉电压依赖性钾通道(Kv)电流的抑制作用存在差异.方法制备大鼠SAH模型,72 h后用酶促消化法急性分离脑皮质动脉和穿支动脉的平滑肌细胞,运用膜片钳技术分别研究其静息电位和Kv电流.结果 SAH使皮质动脉[(45.63±1.18) mV]和穿支动脉[(41.55±1.19) mV]静息电位均减小且后者更为显著(F=8.24,P＜0.05; F=9.36,P＜0.01);1μmol/L 4-氨基吡啶(4AP)可使正常皮质动脉[(38.76±1.03) mV]、正常穿支动脉[(38.53±0.67) mV]、SAH皮质动脉[(36.87±1.49) mV]和SAH穿支动脉[(37.89±1.24)mV]平滑肌细胞静息电位下降至同一水平(F=3.08,P＞0.05).SAH使皮质动脉和穿支动脉脑动脉平滑肌细胞最大电流密度减小且后者更为显著(20.82±0.59与15.15±0.37,F=6.22,P＜0.05),1μmol/L 4AP均可使正常皮质动脉(9.15±0.16)、正常穿支动脉(9.04±0.36)、SAH皮质动脉(8.77±0.26)和SAH穿支动脉(9.12 ±0.17)的Kv电流最大密度下降至同一水平(F=2.96,P＞0.05).结论 SAH和Kv阻滞剂对Kv电流抑制作用的机制较接近,并且SAH对穿支动脉平滑肌细胞静息电位和Kv电流最大密度的抑制作用大于皮质动脉,推测该差异性可能与皮质动脉和穿支动脉对CVS的敏感性不同有关.
목적 탐토자발성주망막하강출혈(SAH)시부대뇌피질동맥화천지동맥전압의뢰성갑통도(Kv)전류적억제작용존재차이.방법 제비대서SAH모형,72 h후용매촉소화법급성분리뇌피질동맥화천지동맥적평활기세포,운용막편겸기술분별연구기정식전위화Kv전류.결과 SAH사피질동맥[(45.63±1.18) mV]화천지동맥[(41.55±1.19) mV]정식전위균감소차후자경위현저(F=8.24,P＜0.05; F=9.36,P＜0.01);1μmol/L 4-안기필정(4AP)가사정상피질동맥[(38.76±1.03) mV]、정상천지동맥[(38.53±0.67) mV]、SAH피질동맥[(36.87±1.49) mV]화SAH천지동맥[(37.89±1.24)mV]평활기세포정식전위하강지동일수평(F=3.08,P＞0.05).SAH사피질동맥화천지동맥뇌동맥평활기세포최대전류밀도감소차후자경위현저(20.82±0.59여15.15±0.37,F=6.22,P＜0.05),1μmol/L 4AP균가사정상피질동맥(9.15±0.16)、정상천지동맥(9.04±0.36)、SAH피질동맥(8.77±0.26)화SAH천지동맥(9.12 ±0.17)적Kv전류최대밀도하강지동일수평(F=2.96,P＞0.05).결론 SAH화Kv조체제대Kv전류억제작용적궤제교접근,병차SAH대천지동맥평활기세포정식전위화Kv전류최대밀도적억제작용대우피질동맥,추측해차이성가능여피질동맥화천지동맥대CVS적민감성불동유관.
Objective To study the effect of subarachnoid hemorrhage (SAH) on voltagedependent potassium channels (Kv) currents of smooth muscle cells,which is hypothesized to be different between cerebral pial arteries and penetrating arteries.Methods Smooth muscle cells from cerebral pial arteries and penetrating arteries in rats were enzymatically isolated 72 h after SAH,and patch clamp was used to test the relative cell size,resting potential and Kv currents.Results Resting potential of either pial ((45.63 ±1.18) mV) or penetrating artery ((41.55-± 1.19) mV) was shifted positively by SAH,even more significantly in latter (F =8.24,P ＜ 0.05 ; F =9.36,P ＜ 0.01) ; Resting potential of pial artery of control ((38.76 ± 1.03) mV),penetrating artery of control ((38.53 ± 0.67) mV),pial artery of SAH ((36.87 ± 1.49) mV) and penetrating artery of SAH((37.89 ± 1.24) mV) were shifted positively to the same level by 1 μmol/L 4-aminopyridine (4AP; F =3.08,P ＞0.05).Maximum Current Density (Imax) of either pial ((20.82 ±0.59) pA/pF) or penetrating artery ((15.15 ±0.37) pA/pF) was compromised by SAH,also more significantly in latter (F =6.22,P ＜ 0.05) ; Imax of pial artery of control (9.15 ± 0.16),penetrating artery of control (9.04 ± 0.36),pial artery of SAH (8.77 ± 0.26) and penetrating artery of SAH (9.12 ± 0.17) were decreased to the same level by 1 μmol/L 4AP (F =2.96,P ＞ 0.05).Conclusions SAH probably shares the similar pathway with Kv blocker (4AP) in Kv currents inhibition.Further,SAH differently inhibits smooth muscle cells Kv currents and resting potential of cerebral pial arteries and penetrating arteries,which may be related with their different sensitivity towards cerebral vasospasm following SAH.