Yan X, Guo Z
Labortary of Molecular Phamacology, Hunan Medical University, Changsha.
Hunan Yi Ke Da Xue Xue Bao. 1997;22(3):189-91.
In isolated guinea pig papillary muscles, the endocardial endothelium (EE) was selectively damaged by exposing the muscles to a flow of dry air for 30s for removal of function EE. The results showed that LPC induced positive inotropic effect on papillary muscles was observed in a concentration-and time-dependent manner [PT after 15 mins' exposure to 5, 10 and 20 mumol.L-1 lysophosphatidylcholine (LPC) was increased by 104 +/- 7%, 110 +/- 6% and 124 +/- 10%, respectively]. The positive inotropic effect of 10 mmol.L-1 LPC on papillary muscles denuded of EE was significantly enhanced (PT: 163 +/- 23% vs 130 +/- 17% after exposing to LPC for 30 min). Scanning and transmission electronic microscopic studies exhibited signs of EE damage of papillary muscles incubated with LPC 10 mumol.L-1 for 30 minutes, such as disruption of gap junction between overlapping EE cells, retraction of the cell borders, fenestration on the EE, and denudation of the subjacent basal lamina. The present study suggests that the EE may affect the LPC-induced contractibility of papillary muscle via its barrier function signs, in addition, the present data provides further evidence that LPC may be a trigger for some kind of biological active factor release form EE.
在离体豚鼠乳头肌中，通过将肌肉暴露于干燥空气流中30秒以去除功能性心内膜内皮（EE），从而选择性地损伤心内膜内皮。结果表明，溶血磷脂酰胆碱（LPC）对乳头肌产生的正性肌力作用呈浓度和时间依赖性[暴露于5、10和20μmol·L-1溶血磷脂酰胆碱（LPC）15分钟后的乳头肌张力分别增加104±7%、110±6%和124±10%]。10 mmol·L-1 LPC对去除EE的乳头肌的正性肌力作用显著增强（暴露于LPC 30分钟后乳头肌张力：163±23%对130±17%）。扫描电镜和透射电镜研究显示，用10μmol·L-1 LPC孵育30分钟的乳头肌出现EE损伤迹象，如重叠的EE细胞间缝隙连接破坏、细胞边界回缩、EE上出现窗孔以及其下方基膜剥脱。本研究提示，EE可能通过其屏障功能影响LPC诱导的乳头肌收缩性，此外，本研究数据进一步证明LPC可能是触发EE释放某种生物活性因子的因素。
