Department of Surgical Sciences, Anaesthesiology and Intensive Care, Uppsala University, Uppsala University Hospital, Entrance 78, 1st floor, 75185, Uppsala, Sweden.
Sci Rep. 2020 Oct 21;10(1):17924. doi: 10.1038/s41598-020-74640-6.
Hypotensive events are strongly correlated to the occurrence of perioperative acute kidney injury, but the underlying mechanisms for this are not completely elucidated. We hypothesised that anaesthesia-induced hypotension causes renal vasoconstriction and decreased oxygen delivery via angiotensin II-mediated renal vasoconstriction. Pigs were anaesthetised, surgically prepared and randomised to vehicle/losartan treatment (0.15 mgkg). A deliberate reduction in arterial blood pressure was caused by infusion of propofol (30 mgkg) for 10 min. Renal function and haemodynamics were recorded 60 min before and after hypotension. Propofol induced hypotension in all animals (p < 0.001). Renal blood flow (RBF) and renal oxygen delivery (RDO) decreased significantly regardless of treatment but more so in vehicle-treated compared to losartan-treated (p = 0.001, p = 0.02, respectively). During recovery RBF and RDO improved to a greater extent in the losartan-treated compared to vehicle-treated (+ 28 mlmin, 95%CI 8-50 mlmin, p = 0.01 and + 3.1 mlmin, 95%CI 0.3-5.8 mlmin, p = 0.03, respectively). Sixty minutes after hypotension RBF and RDO remained depressed in vehicle-treated, as renal vascular resistance was still increased (p < 0.001). In losartan-treated animals RBF and RDO had normalised. Pre-treatment with losartan improved recovery of renal blood flow and renal oxygen delivery after propofol-induced hypotension, suggesting pronounced angiotensin II-mediated renal vasoconstriction during blood pressure reductions caused by anaesthesia.
低血压事件与围手术期急性肾损伤的发生密切相关，但其中的潜在机制尚不完全清楚。我们假设麻醉诱导的低血压通过血管紧张素 II 介导的肾血管收缩导致肾血管收缩和氧输送减少。猪被麻醉、手术准备并随机接受载体/氯沙坦治疗（0.15mgkg）。通过输注异丙酚（30mgkg）10 分钟来故意降低动脉血压。在低血压前后 60 分钟记录肾功能和血液动力学。异丙酚诱导所有动物发生低血压（p<0.001）。肾血流量（RBF）和肾氧输送（RDO）均显著下降，但与氯沙坦治疗相比，载体治疗的下降更为明显（p=0.001，p=0.02）。在恢复期间，与载体治疗相比，氯沙坦治疗的 RBF 和 RDO 恢复到更大程度（+28mlmin，95%CI 8-50mlmin，p=0.01 和+3.1mlmin，95%CI 0.3-5.8mlmin，p=0.03）。低血压后 60 分钟，载体治疗的 RBF 和 RDO 仍处于抑制状态，因为肾血管阻力仍升高（p<0.001）。在氯沙坦治疗的动物中，RBF 和 RDO 已经正常化。氯沙坦预处理可改善异丙酚诱导的低血压后肾血流量和肾氧输送的恢复，表明麻醉引起的血压降低期间存在明显的血管紧张素 II 介导的肾血管收缩。
