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首页> 外文期刊>Pharmacological research: The official journal of The Italian Pharmacological Society >Inhibition of poly(ADP-ribose) polymerase prevents vascular hyporesponsiveness induced by lipopolysaccharide in isolated rat aorta.
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Inhibition of poly(ADP-ribose) polymerase prevents vascular hyporesponsiveness induced by lipopolysaccharide in isolated rat aorta.

机译：聚（ADP-核糖）聚合酶的抑制作用可防止脂多糖在离体大鼠主动脉中诱导的血管低反应性。

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Recent studies clearly show that there is a relationship between endotoxemia and impaired vascular responsiveness. The aim of this study was to investigate whether treatment with the new potent PARP inhibitor PJ34 could prevent the vascular hyporesponsiveness induced by lipopolysaccharide (LPS). Endotoxemia was induced in rats by LPS injection (20mgkg(-1), i.p.). Administration of LPS caused a decrease in mean blood pressure and an increase in heart rate. In endothelium-denuded rings of thoracic aorta from untreated rats, contractile responses to KCl and phenylephrine decreased after LPS injection. Furthermore, there was a significant loss of endothelium-dependent vasodilatation in response to acetylcholine in LPS-treated rats. The animals pretreated with PJ34 (10mgkg(-1), i.p., 30min before LPS injection), the effect of LPS on vascular responsiveness was lower than the untreated ones. Pretreating the animals with PJ34 before the LPS challenge prevented the decline in mean blood pressure. However, thisdid not result in significant changes to the heart rate. The inhibitory effect of LPS treatment on both KCl- and phenylephrine-induced contraction responses was significantly antagonized by PJ34. Additionally, pretreatment of the rats with PJ34 attenuated the LPS-induced endothelial dysfunction in endothelium-intact aorta rings. This study demonstrates that PARP activation in the vascular system is an important contributory factor to the impaired vascular responsiveness associated with endotoxic shock. Hence, the pharmacological inhibition of PARP pathway might be an effective intervention to prevent endotoxin-induced vascular hyporesponsiveness.
机译：最近的研究清楚地表明内毒素血症与血管反应性受损之间存在关联。这项研究的目的是调查用新型强效PARP抑制剂PJ34的治疗是否可以预防脂多糖（LPS）诱导的血管低反应性。通过注射LPS（20mgkg（-1），i.p.）诱发大鼠内毒素血症。 LPS的使用导致平均血压下降和心率增加。在未经治疗的大鼠的胸主动脉内皮剥脱环中，LPS注射后对KCl和去氧肾上腺素的收缩反应降低。此外，在LPS处理的大鼠中，对乙酰胆碱的响应，内皮依赖性血管舒张功能明显丧失。用PJ34预处理的动物（LPS注射前30分钟，腹腔注射10mgkg（-1）），LPS对血管反应性的影响低于未处理的动物。在LPS攻击之前用PJ34对动物进行预处理可防止平均血压下降。但是，这不会导致心率发生明显变化。 PJ34显着拮抗了LPS治疗对KCl和苯肾上腺素诱导的收缩反应的抑制作用。此外，用PJ34预处理大鼠可减轻LPS诱导的内皮完整主动脉环中的内皮功能障碍。这项研究表明，血管系统中的PARP激活是与内毒素休克相关的血管反应性受损的重要促成因素。因此，PARP途径的药理抑制作用可能是预防内毒素诱导的血管低反应性的有效干预措施。

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