Burt J M, Massey K D, Minnich B N
Department of Physiology, University of Arizona, Tucson 85724.
Am J Physiol. 1991 Mar;260(3 Pt 1):C439-48. doi: 10.1152/ajpcell.1991.260.3.C439.
The permeability and conductance of gap junctions between pairs of neonatal rat heart cells were rapidly and reversibly decreased by oleic acid in a dose- and time-dependent manner. Other unsaturated fatty acids (C-18: cis 6, 9, or 11, and C-18, 16, and 14, cis 9), saturated fatty acids (C-10, 12, and 14), and saturated fatty alcohols (C-8, 10, and 12) also caused uncoupling. The most effective compounds of the unsaturated and saturated fatty acid and saturated fatty alcohol series caused essentially complete uncoupling at comparable aqueous concentrations. However, oleic acid uncoupled cells at membrane concentrations as low as 1 mol%, whereas decanoic acid required upwards of 35 mol%. The channels that support the action potential remained functional at these same membrane concentrations. The data are discussed in terms of the possible mechanism by which these compounds cause uncoupling and the possible role of uncoupling by nonesterified free fatty acids in the initiation of arrhythmias during and after ischemic insults.
新生大鼠心脏细胞对之间的间隙连接的通透性和电导,会被油酸以剂量和时间依赖的方式迅速且可逆地降低。其他不饱和脂肪酸(C-18:顺式6、9或11,以及C-18、16和14,顺式9)、饱和脂肪酸(C-10、12和14)和饱和脂肪醇(C-8、10和12)也会导致解偶联。不饱和脂肪酸系列、饱和脂肪酸系列和饱和脂肪醇系列中最有效的化合物,在相当的水相浓度下会导致基本完全解偶联。然而,油酸在低至1摩尔%的膜浓度下就能使细胞解偶联,而癸酸则需要超过35摩尔%。支持动作电位的通道在这些相同的膜浓度下仍保持功能。本文根据这些化合物导致解偶联的可能机制,以及非酯化游离脂肪酸解偶联在缺血性损伤期间和之后心律失常发生中的可能作用,对这些数据进行了讨论。