Lavoie J C, Chessex P
Hôpital Ste-Justine, Department of Pediatrics, University of Montreal, Quebec, Canada.
Free Radic Biol Med. 1994 Jun;16(6):795-9. doi: 10.1016/0891-5849(94)90195-3.
The aim of the study was to verify whether the infusion of a lipid emulsion causes a rise in vascular pressure related to an imbalance in the production of vasoconstricting and vasodilatating eicosanoids. Segments of umbilical veins were perfused with and without 1.5 microM indomethacin (cyclooxygenase inhibitor) in solutions differing only in their lipid content (control vs. lipid). The lipid-induced higher pressure (p < 0.05) was associated with an inhibition (p < 0.05) in the output of the vasodilatator PGI2, and an increase (p < 0.01) in the production of the vasoconstrictor PGF2 alpha. Indomethacin abolished differences in pressure, but produced a rise (p < 0.01) in vascular tone of both the control and lipid-containing solutions by inhibiting PGI2 synthesis. Prostacyclin was the only eicosanoid significantly correlated (p < 0.01) to vascular tone. The lipid emulsion was therefore linked to the inhibition of the conversion of PGH2 to PGI2. The ensuing greater PGH2 availability would result in vivo, in the increased synthesis of vasoconstricting eicosanoids. The lipid-containing solution produced vasoactive responses similar to those reported with tert-butyl hydroperoxide, suggesting that hydroperoxides contaminating commonly used lipid emulsions could be causing a prostanoid-dependent vasoconstriction.
本研究的目的是验证输注脂质乳剂是否会因血管收缩和血管舒张类花生酸生成失衡而导致血管压力升高。在仅脂质含量不同的溶液（对照与脂质）中，对脐静脉段进行有无1.5微摩尔吲哚美辛（环氧化酶抑制剂）的灌注。脂质诱导的较高压力（p<0.05）与血管舒张剂前列环素（PGI2）输出的抑制（p<0.05）以及血管收缩剂前列腺素F2α（PGF2α）生成的增加（p<0.01）相关。吲哚美辛消除了压力差异，但通过抑制PGI2合成使对照溶液和含脂质溶液的血管张力均升高（p<0.01）。前列环素是唯一与血管张力显著相关（p<0.01）的类花生酸。因此，脂质乳剂与PGH2向PGI2转化的抑制有关。由此产生的更多PGH2可用性在体内会导致血管收缩类花生酸合成增加。含脂质溶液产生的血管活性反应与叔丁基过氧化氢报道的相似，表明污染常用脂质乳剂的氢过氧化物可能导致类前列腺素依赖性血管收缩。
