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首页> 外文期刊>Critical care : >Early propranolol treatment induces lung heme-oxygenase-1, attenuates metabolic dysfunction, and improves survival following experimental sepsis
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Early propranolol treatment induces lung heme-oxygenase-1, attenuates metabolic dysfunction, and improves survival following experimental sepsis

机译：早期普萘洛尔治疗可诱发肺血红素加氧酶-1，减轻代谢功能障碍，并改善实验性败血症后的存活率

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IntroductionPharmacological agents that block beta-adrenergic receptors have been associated with improved outcome in burn injury. It has been hypothesized that injuries leading to a hypermetabolic state, such as septic shock, may also benefit from beta-blockade; however, outcome data in experimental models have been contradictory. Thus, we investigated the effect of beta-blockade with propranolol on survival, hemodynamics, lung heat shock protein (HSP) expression, metabolism and inflammatory markers in a rat cecal ligation and puncture (CLP) model of sepsis.MethodsSprague-Dawley rats receiving either repeated doses (30 minutes pre-CLP and every 8 hours for 24 hours postoperatively) of propranolol or control (normal saline), underwent CLP and were monitored for survival. Additionally, lung and blood samples were collected at 6 and 24 hours for analysis. Animals also underwent monitoring to evaluate global hemodynamics.ResultsSeven days following CLP, propranolol improved survival versus control (P < 0.01). Heart rates in the propranolol-treated rats were approximately 23% lower than control rats (P < 0.05) over the first 24 hours, but the mean arterial blood pressure was not different between groups. Metabolic analysis of lung tissue demonstrated an increase in lung ATP/ADP ratio and NAD+ content and a decreased ratio of polyunsaturated fatty acids to monounsaturated fatty acids (PUFA/MUFA). Cytokine analysis of the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) demonstrated decreased expression of TNF-alpha in both lung and plasma at 24 hours post CLP induced sepsis. Finally, propranolol led to a significant increase in lung hemeoxygenase-1 expression, a key cellular protective heat shock protein (HSP) in the lung. Other lung HSP expression was unchanged.ConclusionsThese results suggest that propranolol treatment may decrease mortality during sepsis potentially via a combination of improving metabolism, suppressing aspects of the inflammatory response and enhancing tissue protection.
机译：引言阻断β-肾上腺素能受体的药物与烧伤的预后改善有关。据推测，导致代谢亢进状态的损伤（如败血性休克）也可能受益于β受体阻滞剂。然而，实验模型中的结果数据是矛盾的。因此，我们在败血症的大鼠盲肠结扎穿刺（CLP）模型中研究了普萘洛尔β受体阻滞剂对存活，血液动力学，肺热休克蛋白（HSP）表达，代谢和炎性标志物的影响。重复剂量（CLP前30分钟，术后8小时，术后24小时每8小时）对心得安或对照组（生理盐水）进行CLP，并监测其存活率。此外，在第6和24小时收集肺和血液样本进行分析。结果还进行了监测，以评估整体的血流动力学。结果CLP后7天，普萘洛尔相对于对照组改善了生存期（P <0.01）。在最初的24小时内，经心得安治疗的大鼠的心率比对照组低约23％（P <0.05），但是两组之间的平均动脉血压没有差异。肺组织的代谢分析表明，肺ATP / ADP比例和NAD +含量增加，多不饱和脂肪酸与单不饱和脂肪酸（PUFA / MUFA）的比例降低。炎症细胞因子肿瘤坏死因子α（TNF-alpha）的细胞因子分析表明，CLP诱发败血症后24小时，肺和血浆中TNF-α的表达降低。最后，普萘洛尔可导致肺血红素加氧酶-1（肺血中重要的细胞保护性热休克蛋白（HSP））表达显着增加。其他肺HSP表达未改变。结论这些结果表明，普萘洛尔治疗可通过改善代谢，抑制炎症反应和增强组织保护相结合来降低败血症死亡率。

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