Alterations in the Renin-Angiotensin System in Experimental Septic Shock.

Q4 Medicine Critical care explorations Pub Date : 2024-10-11 eCollection Date: 2024-10-01 DOI:10.1097/CCE.0000000000001163
Bruno Garcia, Benoit Ter Schiphorst, Fuhong Su, Adrien Picod, Theo Ikenna-Uba, Raphaël Favory, Filippo Annoni, Alexandre Mebazaa, Jean-Louis Vincent, Jacques Creteur, Fabio S Taccone, Antoine Herpain
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Abstract

Objectives: To analyze dynamic changes in the renin-angiotensin system (RAS) during septic shock, focusing on angiotensin-converting enzyme (ACE) activity and the balance between angiotensin peptides, using a mass spectrometry method.

Design: Experimental septic shock model induced by peritonitis in swine.

Setting: Experimental Laboratory, Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles.

Subjects: Forty time points from eight mechanically ventilated pigs.

Interventions: Septic shock was induced using intraperitoneal instillation of autologous feces, followed by standardized fluid resuscitation, norepinephrine infusion, antibiotic administration, and peritoneal lavage.

Measurements and main results: The induction of sepsis resulted in a significant increase in plasma renin activity and levels of angiotensin I and II, with a significant decrease in ACE activity observed from 4 hours post-resuscitation and a notable rise in the angiotensin I/angiotensin II ratio at 12 hours. Additionally, a shift toward the angiotensin-(1-7) axis was observed, evidenced by an increased angiotensin-(1-7)/angiotensin II ratio.

Conclusions: The study highlighted dynamic shifts in the RAS during septic shock, characterized by reduced circulating ACE activity, elevated angiotensin I/II ratio, and a shift toward the angiotensin-(1-7) axis. These findings suggest an adaptive response within the RAS, potentially offering new insights into sepsis management and therapeutic targets.

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实验性脓毒性休克中肾素-血管紧张素系统的变化
目的:分析脓毒性休克期间肾素-血管紧张素系统(RAS)的动态变化:利用质谱法分析脓毒性休克期间肾素-血管紧张素系统(RAS)的动态变化,重点是血管紧张素转换酶(ACE)活性和血管紧张素肽之间的平衡:设计:猪腹膜炎诱发的实验性脓毒性休克模型:地点:布鲁塞尔自由大学 Erasme 医院重症监护部实验实验室:40 个时间点,来自 8 头机械通气的猪:干预措施:通过腹腔灌注自体粪便诱发败血症休克,然后进行标准化液体复苏、去甲肾上腺素输注、抗生素给药和腹腔灌洗:脓毒症诱导导致血浆肾素活性及血管紧张素 I 和 II 水平显著升高,复苏后 4 小时起观察到 ACE 活性显著下降,12 小时时血管紧张素 I/ 血管紧张素 II 比值明显升高。此外,还观察到向血管紧张素-(1-7)轴的转移,表现为血管紧张素-(1-7)/血管紧张素 II 比率的增加:该研究强调了脓毒性休克期间 RAS 的动态变化,其特点是循环 ACE 活性降低、血管紧张素 I/II 比值升高以及向血管紧张素-(1-7)轴转移。这些研究结果表明了 RAS 内的适应性反应,有可能为脓毒症管理和治疗目标提供新的见解。
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