Electrophysiologic effects of intracellular lysophosphoglycerides and their accumulation in cardiac lymph with myocardial ischemia in dogs.
Electrophysiologic effects of intracellular lysophosphoglycerides and their accumulation in cardiac lymph with myocardial ischemia in dogs.
复制标题
犬心肌缺血时细胞内溶血磷酸甘油酯的电生理效应及其在心脏淋巴液中的积累。
DOI：
10.1172/jci112561
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Corr,PB
中科院分区：
文献类型：
--
作者：
Akita,H;Creer,MH;Yamada,KA;Sobel,BE;Corr,PB
溶血磷脂酰胆碱 (LPC) 在缺血组织中积聚，外源性 LPC (20-100 microM) 可在体外诱导电生理改变。然而，为了确定区室化是否至关重要，我们对 LPC 进行了细胞内压力显微注射，同时记录了跨膜动作电位。根据注射液体积和细胞体积的校准计算，细胞内 LPC 浓度高达 500 µM (n = 18)，不会引起电生理改变。评估从麻醉狗心上淋巴管获得的淋巴液中磷脂和溶血磷脂的浓度和流出，以评估细胞外积累的程度。缺血之前，磷脂酰胆碱 (PC) 是淋巴中的主要磷脂 (79 +/- 2%)，并含有大量的鞘磷脂 (11 +/- 2%) 和 LPC (6 +/- 1%)。缺血时，LPC 浓度增加 18%，LPC 净流出增加 24%（P 小于 0.01），而 PC 或其他测定的磷脂没有净流出。缺血区域内淋巴液中 LPC 的计算浓度从 84 微摩尔增加到 197 微摩尔，该浓度足以诱发电生理紊乱。
Lysophosphatidylcholine (LPC) accumulates in ischemic tissue, and exogenous LPC (20-100 microM) induces electrophysiologic alterations in vitro. However, to determine whether compartmentalization is critical, intracellular pressure microinjection of LPC was performed with simultaneous recording of the transmembrane action potential. Intracellular LPC in concentrations as high as 500 microM (n = 18), calculated based on calibration of injectate volume and cellular volume, did not induce electrophysiologic alterations. The concentrations and efflux of phospholipids and lysophospholipids were assessed in lymph obtained from the supracardiac lymph vessel in anesthetized dogs to assess the extent of extracellular accumulation. Prior to ischemia, phosphatidylcholine (PC) was the major phospholipid in lymph (79 +/- 2%) with substantial quantities of sphingomyelin (11 +/- 2%) and LPC (6 +/- 1%). With ischemia, the concentration of LPC increased by 18%, and net efflux of LPC increased by 24% (P less than 0.01) with no net efflux of PC or other assayed phospholipids. The calculated concentration of LPC increased from 84 to 197 microM in lymph within the ischemic region, a concentration sufficient to induce electrophysiologic derangements.