Buja L M, Miller J C, Krueger G R
Department of Pathology and Laboratory Medicine, University of Texas Medical School, Houston 77030.
In Vivo. 1991 May-Jun;5(3):239-43.
The purpose of this study was to evaluate the effect of impaired high energy phosphate metabolism on the membrane fluidity of cardiac myocytes. Cultured neonatal rat cardiac myocytes were treated with the metabolic inhibitor, iodoacetic acid (IAA) (30 microM). Membrane lipid fluidity was assessed by the steady-state fluorescence polarization of 1,6-diphenyl 1-1,3,5-hexatriene (DPH). Metabolic inhibition with IAA resulted in a progressive decrease in fluorescence polarization and calculated microviscosity. Microviscosity was decreased by 11% after 60-90 minutes and by 21% after 120-210 minutes, respectively. These changes are consistent with a progressive increase in membrane fluidity. Pretreatment with the experimental phospholipase inhibitor, U26, 384 (5-10 microM) resulted in a slower onset and less change in membrane fluidity after treatment with IAA. Thus, a) metabolic inhibition in cardiac myocytes induces prominent alterations in membrane fluidity which probably contribute to the membrane dysfunction accompanying myocardial injury and b) phospholipid degradation may be a significant factor in the genesis of altered membrane fluidity.
本研究的目的是评估高能磷酸代谢受损对心肌细胞膜流动性的影响。用代谢抑制剂碘乙酸（IAA）（30微摩尔）处理培养的新生大鼠心肌细胞。通过1,6 - 二苯基 - 1,3,5 - 己三烯（DPH）的稳态荧光偏振评估膜脂质流动性。IAA导致的代谢抑制使荧光偏振和计算得到的微粘度逐渐降低。微粘度在60 - 90分钟后降低了11%，在120 - 210分钟后分别降低了21%。这些变化与膜流动性的逐渐增加一致。用实验性磷脂酶抑制剂U26,384（5 - 10微摩尔）预处理后，IAA处理后膜流动性的起始变化较慢且变化较小。因此，a）心肌细胞中的代谢抑制会引起膜流动性的显著改变，这可能导致伴随心肌损伤的膜功能障碍，并且b）磷脂降解可能是膜流动性改变发生过程中的一个重要因素。
