Systemic and renal hemodynamic effects of intra-arterial radiocontrast.

Paolo Calzavacca,Michael Bailey,Ken Ishikawa,Clive N May,Rinaldo Bellomo

doi:10.1186/s40635-014-0032-z

Abstract

BackgroundDecreased renal blood flow (RBF) and vasoconstriction are considered major mechanisms of contrast-induced acute kidney injury (CIAKI). To understand the severity and duration of such putative effects, we measured systemic and renal hemodynamics after intra-arterial radiocontrast administration. The subjects were six Merino ewes. The setting was a university-affiliated research institute. This is a randomized cross-over experimental study.MethodsTransit-time flow probes were implanted on the pulmonary and left renal arteries 2 weeks before experimentation. We simulated percutaneous coronary intervention by administering five intra-arterial boluses of 0.5 mL/kg saline (control) or radiocontrast (iodixanol) to a total of 2.5 mL/kg over 1 h. Cardiac output (CO), heart rate, mean arterial pressure (MAP), RBF, renal vascular conductance (RVC), urine output (UO), creatinine clearance (CrCl), and fractional excretion of sodium (FENa) were measured.ResultsIn the first 8 h after intra-arterial administration of radiocontrast, CO, total peripheral conductance (TPC), and heart rate (HR) increased compared with those after normal saline administration. Thereafter, CO and TPC were similar between the two groups, but HR remained higher with radiocontrast (p < 0.001). After a short (30 min) period of renal vasoconstriction with preserved RBF secondary to an associated increase in MAP, RBF and RVC showed an earlier and greater increase (vasodilatation) with radiocontrast (p < 0.001) and remained higher during the first 2 days. Radiocontrast initially increased urine output (p < 0.001) and FENa (p = 0.003). However, the overall daily urine output decreased in the radiocontrast-treated animals at 2 days (p < 0.001) and 3 days (p = 0.006). Creatinine clearance was not affected.ConclusionsIn healthy animals, intra-arterial radiocontrast increased RBF, induced renal vasodilatation, and caused a delayed period of oliguria. Our findings suggest that sustained reduction in RBF and renal vasoconstriction may not occur in normal large mammals after intra-arterial radiocontrast administration.

Highlights

Decreased renal blood flow (RBF) and vasoconstriction are considered major mechanisms of contrast-induced acute kidney injury (CIAKI)
mean arterial pressure (MAP) was higher at baseline in the radiocontrast-treated animals and remained higher with radiocontrast during the following 5 days, with significant differences (p < 0.001) between groups (Table 2)
heart rate (HR) was higher with radiocontrast (Table 2)

Summary

Introduction

Decreased renal blood flow (RBF) and vasoconstriction are considered major mechanisms of contrast-induced acute kidney injury (CIAKI). Dog, and small-animal studies have reported that intravenous infusion of contrast media significantly reduces total renal plasma flow [11,12,13,14] In these studies, investigators administered amounts of contrast that exceed current practice, measured RBF with techniques of limited accuracy, and performed measurements only for a few hours after radiocontrast administration. We recently used a validated methodology to measure systemic and renal hemodynamics directly, accurately, and over several days by implanted transit-time flow probes [15,16,17] and found that, contrary to expectation, intravenous contrast administration induced only short-lived renal vasoconstriction (first hour) followed by sustained (days) renal vasodilatation and increased RBF [18] Such observations may not apply to the most common trigger of CIAKI: intra-arterial boluses of radiocontrast given over a short time during PCI

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