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目的采用β1肾上腺素能受体抗体(anti-ADRβ1)模拟自身抗体,研究其对小鼠心室肌细胞钾离子通道的作用。方法酶解法分离小鼠心室肌细胞,以不同稀释比例anti-ADRβ1灌流心肌细胞,膜片钳电生理技术记录钾离子通道电流的变化。结果不同稀释比例anti-ADRβ11/500、1/100、1/50的细胞外液灌流5min后,Ito电流密度无明显变化(P>0.05);与正常外液时(4.7±0.24)pA/pF比较,anti-ADRβ11/500时Iss电流密度(3.6±0.18)pA/pF降低,但差异无统计学意义(P>0.05),anti-ADRβ11/100和1/50时Iss电流密度明显降低,分别为(3.5±0.18)pA/pF和(3.1±0.15)pA/pF(P均<0.05),并且具有明显的剂量依赖性。结论β1肾上腺素能受体抗体可以抑制小鼠心肌细胞Iss通道而对Ito无影响,其作用可能类似激动剂样效应,该结论为进一步研究心衰患者β1肾上腺素能受体自身抗体的作用机制提供了实验依据。
Objective To study the effect of β1 adrenergic receptor antibody (anti-ADRβ1) on potassium channel in mouse ventricular myocytes. Methods The ventricular myocytes of mice were isolated by enzyme digestion and the cardiomyocytes were perfused with different dilutions of anti-ADRβ1. The changes of potassium channel currents were recorded by patch-clamp electrophysiological techniques. Results The Ito current density did not change significantly after 5 min of anti-ADRβ11 / 500, 1/100, 1/50 extracellular fluid perfusion (P> 0.05). Compared with normal external fluid (4.7 ± 0.24) pA / Compared with the anti-ADRβ11 / 500, the iss current density (3.6 ± 0.18) pA / pF was decreased, but the difference was not statistically significant (P> 0.05) (3.5 ± 0.18) pA / pF and (3.1 ± 0.15) pA / pF (all P <0.05), with significant dose-dependent. Conclusion The β1 adrenergic receptor antibody can inhibit the Iss channel in mouse cardiomyocytes without affecting Ito, and its effect may be similar to that of agonist-like effect. This conclusion is a further study on the mechanism of β1 adrenergic receptor autoantibodies in patients with heart failure Provided experimental basis.