摘要
目的研究肾上腺髓质素(ADM)对脓毒性休克大鼠心肌细胞外向钾电流的影响。方法成年大鼠腹腔注射脂多糖(LPS,10 mg/kg)4 h后,分离心室肌细胞。用全细胞膜片钳的方法记录瞬时外向钾电流(Ito),稳态钾电流(Iss)和ATP敏感钾电流(IK,ATP)。结果LPS处理对Ito和Iss无影响。休克心肌细胞IK,ATP密度[(2.66±0.56)pA/pF(n=12)]较正常心肌细胞值[(0.27±0.08)pA/pF(n=14)]明显增加(P<0.01)。ADM受体拮抗剂ADM-(22-52)可使增加的IK,ATP得到明显的恢复[(0.69±0.21)pA/pF(n=11),P<0.01 vs LPS组]。而ADM-(22-52)与100μmol/L氨基胍联合处理几乎可完全取消IK,ATP的增加。结论脓毒性休克大鼠心肌细胞IK,ATP被激活。ADM与NO共同参与了脓毒性休克大鼠心肌细胞IK,ATP的激活。
Objective To study the outward potassium current in myocytes from septic shock rats and the effects of adrenomedullin（ADM）. Methods Ventricular myocytes were isolated from adult rats 4 h after an intraperitoneal injection of lipopolysaccharide（LPS, 10 mg/kg）. Transient outward K- current（ Ito）, steady-state K^＋ current （ Iss ） and ATP sensitive potassium current（IK.ATP）were recorded using whole cell patch clamp methods. Results LPS treatment had no effect on Ito and Lss. The IK,ATP density in septic shock group [（2.66±0.56） pA/pF, n = 12] was significantly higher than that in control group [（0.27±0.08） pA/pF.n= 14 ,P〈0,01]. The ADM antagonist ADM-（22-52）significantly reversed the increased IK.ATP[（0.69±0. 21 ） pA/pF, n = 11, P〈0.01 vs LPS group] in shock myoeytes. IK.ATP density was lower in LPS plus aminoguanidine myocytes[（0. 77±0. 18） pA/pF,n= 10,P〈0. 01 vs LPS group]than that in LPS myocytes. ADM （22-52）and 100 gmol/L aminoguanidine could completely abolish the increase in IK.ATP . Conclusion IK.ATP was activated in myocytes from septic shock rats. Adrenomedullin along with NO precipitated activation of the IK.ATP in rat ventricular myocytes during septic shock.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2010年第1期42-46,共5页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
The Committee on Research and Conference Grant of the University of Hong Kong and from Research Grant Council of Hong Kong(No. HKU 7492/06)
