Saldeen K, Nichols W, Lawson D, Andersson R, Saldeen T, Mehta J
Department of Medicine, University of Florida, Gainesville.
Acta Physiol Scand. 1991 Jul;142(3):339-44. doi: 10.1111/j.1748-1716.1991.tb09166.x.
To determine the effects of peptide 6A (a fibrinogen-degradation product) on femoral blood flow, anaesthetized dogs were given saline or peptide 6A intravenously in random order. Bolus injection of peptide 6A (10, 20 or 50 mumoles) caused a short-lasting dose-dependent decrease in femoral bed resistance and an increase in femoral blood flow. Continuous infusion of peptide 6A (50 mumoles min-1) resulted in a sustained decrease in resistance and an increase in femoral artery blood flow (54 +/- 33%), with a small, insignificant decrease in femoral artery mean pressure. Indomethacin pretreatment caused only slight attenuation of the peptide 6A-induced increase in femoral blood flow. In in vitro experiments, peptide 6A relaxed rings of femoral artery, and this effect was associated with an increase in 6-keto-PGF1 alpha in the vascular ring supernatants and in the tissue cyclic GMP concentrations. Peptide 6A-induced relaxation was abolished by de-endothelialization, but not by treatment with indomethacin. These observations suggest that peptide 6A induces vasorelaxation largely by stimulating release of endothelium-derived relaxing factor. PGI2 release appears to play only a minor role in the vasodilator effects of peptide 6A in the femoral bed.
为了确定肽6A（一种纤维蛋白原降解产物）对股血流量的影响，对麻醉的狗随机静脉注射生理盐水或肽6A。静脉推注肽6A（10、20或50微摩尔）导致股床阻力出现短暂的剂量依赖性降低，股血流量增加。持续输注肽6A（50微摩尔/分钟）导致阻力持续降低，股动脉血流量增加（54±33%），股动脉平均压有小幅、不显著的降低。吲哚美辛预处理仅轻微减弱了肽6A诱导的股血流量增加。在体外实验中，肽6A使股动脉环舒张，这种作用与血管环上清液中6-酮-前列环素F1α以及组织中环鸟苷酸浓度的增加有关。肽6A诱导的舒张作用在内皮剥脱后被消除，但吲哚美辛处理不能消除。这些观察结果表明，肽6A主要通过刺激内皮源性舒张因子的释放来诱导血管舒张。前列环素2的释放似乎在肽6A对股床的血管舒张作用中仅起次要作用。
