Saroyan R M, Roberts M P, Light J T, Chen I L, Vaccarella M Y, Bang D J, Kvamme P, Singh S, Scalia S V, Kerstein M D
Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana 70112.
Am J Physiol. 1992 May;262(5 Pt 2):H1449-57. doi: 10.1152/ajpheart.1992.262.5.H1449.
Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury. Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H1449-H1457, 1992. The recovery of prostacyclin (prostaglandin I2, PGI2) synthesis and endothelium-derived relaxing factor (EDRF) activity, as demonstrated by acetylcholine (ACh)-induced relaxation, by rabbit aorta was examined up to 8 wk after balloon catheter-induced injury. Following injury, basal 6-keto-PGF1 alpha formation was decreased acutely; however, after 3 wk it was not different from control. Arachidonic acid-stimulated 6-keto-PGF1 alpha formation was decreased, returning to control levels at 3 and 8 wk for thoracic and abdominal aorta, respectively. ACh-induced relaxation did not return to control levels over the 8-wk study. Initiation of reendothelialization with a layer of hyperplastic endothelial cells overlying subendothelial fibrosis and intimal hyperplasia were present at 2-3 wk. Intimal hyperplasia appeared 2 wk after injury and progressed throughout the period of the study. These data indicate that following balloon catheter-induced injury the formation of both PGI2 and EDRF is reduced and that recovery follows a differential time course. In addition, the recovery of PGI2 formation did not coincide with the attenuation of intimal hyperplasia, whereas the relationship between EDRF formation and intimal hyperplasia is uncertain.
血管损伤后前列环素和内皮源性舒张因子的差异性恢复。《美国生理学杂志》262卷(心脏循环生理学31):H1449 - H1457,1992年。通过球囊导管诱导损伤后长达8周,检测兔主动脉中前列环素(前列腺素I2,PGI2)合成及内皮源性舒张因子(EDRF)活性的恢复情况,后者通过乙酰胆碱(ACh)诱导的舒张来证明。损伤后,基础6 - 酮 - PGF1α生成急性减少;然而,3周后与对照组无差异。花生四烯酸刺激的6 - 酮 - PGF1α生成减少,胸主动脉和腹主动脉分别在3周和8周恢复至对照水平。在8周的研究期间,ACh诱导的舒张未恢复至对照水平。在2 - 3周时出现内膜下纤维化和内膜增生之上覆盖一层增生性内皮细胞的再内皮化起始。内膜增生在损伤后2周出现并在整个研究期间进展。这些数据表明,球囊导管诱导损伤后PGI2和EDRF的生成均减少,且恢复遵循不同的时间进程。此外,PGI2生成的恢复与内膜增生的减轻不一致,而EDRF生成与内膜增生之间的关系尚不确定。