Lysophosphoglycerides in ischemic myocardium effluents and potentiation of their arrhythmogenic effects.
Lysophosphoglycerides in ischemic myocardium effluents and potentiation of their arrhythmogenic effects.
复制标题
缺血心肌流出物中的溶血磷酸甘油酯及其致心律失常作用的增强。
DOI：
10.1152/ajpheart.1981.241.5.h700
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Corr,PB
中科院分区：
文献类型：
--
作者：
Snyder,DW;CraffordJr,WA;Glashow,JL;Rankin,D;Sobel,BE;Corr,PB
溶血磷酸甘油酯在缺血心肌中蓄积。为了确定细胞外液中溶血磷脂酰胆碱（LPC）浓度是否增加，并可能是致炎性的，开胸猫（n = 12）的冠状动脉前降支灌注Krebs-白蛋白溶液后10分钟的缺血和测定LPC的流出物。观察到LPC增加两倍（0.097 +/- 0.02至0.170 +/- 0.03 mM）。微电极细胞内记录从正常的猫endocellular在pH值7.4在体外显示动作电位变化不大，尽管增加LPC与猫血浆灌流时，正常水平的两倍（0.74毫米）。然而，在pH 6.7时，富含LPC的血浆引起显著变化，包括静息膜电位降低（-96 +/- 1至-35 +/- 7 mV），振幅（102 +/- 3至36 +/- 8 mV），0相的最大上升速率（Vmax）（178 +/- 24至26 +/- 11 V/s），以及动作电位分级的传导速度。酸化对照血浆仅降低Vmax（从161 V/s降至57 V/s）。因此，缺血10分钟后，体内猫心肌流出物中的LPC增加了两倍，再加上缺血诱导的酸中毒，足以在体外诱导明显的电生理紊乱。
Lysophosphoglycerides accumulate in ischemic myocardium. To determine whether lysophosphatidylcholine (LPC) concentrations increase in extracellular fluid and may be arrhythmogenic, the anterior descending coronary artery of the open-chest cat (n = 12) was perfused with a Krebs-albumin solution after 10 min of ischemia and the effluent assayed for LPC. A twofold increase in LPC (0.097 +/- 0.02 to 0.170 +/- 0.03 mM) was observed. Microelectrode intracellular recordings from from normal feline endocardium at pH 7.4 in vitro revealed little change in action potentials when superfused with feline plasma despite augmented LPC to twice normal levels (0.74 mM). However, at pH 6.7, marked changes were elicited by LPC-enriched plasma including diminished resting membrane potential (-96 +/- 1 to -35 +/- 7 mV), amplitude (102 +/- 3 to 36 +/- 8 mV), maximum rate of rise (Vmax) of phase 0 (178 +/- 24 to 26 +/- 11 V/s), and conduction velocity with fractionation of the action potential. Acidified control plasma decreased only Vmax (from 161 to 57 V/s). Thus LPC increases twofold in effluents from cat myocardium in vivo after 10 min of ischemia and, coupled with ischemia-induced acidosis, is sufficient to induce marked electrophysiological derangements in vitro.