Abstract

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 mg*kg−1). A deliberate reduction in arterial blood pressure was caused by infusion of propofol (30 mg*kg−1) 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 (RDO2) 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 RDO2 improved to a greater extent in the losartan-treated compared to vehicle-treated (+ 28 ml*min−1, 95%CI 8–50 ml*min−1, p = 0.01 and + 3.1 ml*min−1, 95%CI 0.3–5.8 ml*min−1, p = 0.03, respectively). Sixty minutes after hypotension RBF and RDO2 remained depressed in vehicle-treated, as renal vascular resistance was still increased (p < 0.001). In losartan-treated animals RBF and RDO2 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.

Highlights

  • Hypotensive events are strongly correlated to the occurrence of perioperative acute kidney injury, but the underlying mechanisms for this are not completely elucidated

  • We studied the effects of losartan on Renal blood flow (RBF), R­ DO2 and short-term renal function in pigs subjected to an anaesthesiainduced hypotensive event

  • During the propofol-induced hypotensive event mean arterial pressure (MAP) was reduced by 38 mmHg in vehicle-treated (95%CI 30–45 mmHg, p < 0.001, Fig. 1a) and 42 mmHg in losartan-treated (95%CI 34–50 mmHg, p < 0.001, Fig. 1a) without significant intergroup difference

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Summary

Introduction

Hypotensive events are strongly correlated to the occurrence of perioperative acute kidney injury, but the underlying mechanisms for this are not completely elucidated. Renal blood flow (RBF) and renal oxygen delivery ­(RDO2) decreased significantly regardless of treatment but more so in vehicle-treated compared to losartan-treated (p = 0.001, p = 0.02, respectively). 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. Unloading baroreceptors increase sympathetic nerve activity and release of endogenous vasoactive hormones, such as catecholamines, renin and angiotensin-II (Ang-II), vasopressin and a­ ldosterone[13,14,15] This may aid in restoring MAP it theoretically causes a prolonged renal vasoconstriction, even after blood volume and/or pressure is restored. We hypothesise that Ang-II released by propofol-induced hypotension may cause renal ischemia by reducing ­RDO2 due to prolonged renal vasoconstriction. We studied the effects of losartan (an intravenously administered ARB) on RBF, R­ DO2 and short-term renal function in pigs subjected to an anaesthesiainduced hypotensive event

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