Early and Sustained Systemic and Renal Hemodynamic Effects of Intravenous Radiocontrast

Abstract

Background and Aims: To measure the extended renal hemodynamic changes induced by intravenous radiocontrast. Methods: Cross-ewes were studied in a randomized cross-over study. Intravenous saline or radiocontrast were administered, and continuous measurement of cardiac output and renal blood flow (RBF) was performed with flow probes. Results: Radiocontrast induced early but transient increases in cardiac output with vasodilatation, followed by return to baseline values within 2 h. There was an initial decline in RBF (–5.2 ± 4.5 vs. 2.1 ± 5.3%; p < 0.0001) and decreased renal vascular conductance (–4.0 ± 7.2 vs. 3.3 ± 7.1%, p < 0.0001; vasoconstriction). This renal vasoconstriction resolved within 2 h and was followed by sustained (72 h) renal vasodilatation with higher RBF (270 ± 13 vs. 236 ± 11 ml/min; p < 0.0001). Conclusions: Radiocontrast induces short renal vasoconstriction followed by sustained vasodilatation and increased RBF. Short-term studies are not representative of the overall sustained renal hemodynamic effects of radiocontrast.

Sepsis-Associated AKI: Epithelial Cell Dysfunction

“…21 In support of this idea is the knowledge that during situations such as major surgery, renal artery occlusion of up to 80% for 2 hours does not cause long-term renal dysfunction. 22 Furthermore, septic AKI has been shown to manifest in situations of renal vasodilatation and normal or even increased renal blood flow. 20 Finally, unlike ischemic damage in which there is tubular cell necrosis, sepsis-induced AKI has a noticeable absence of tubular necrosis, and rather has only patchy, heterogeneous tubular cell injury with apical vacuolization, and can even be devoid of extensive apoptosis.…”

Systemic and renal hemodynamic effects of intra-arterial radiocontrast

“…The relevance of such findings to a condition which leads to peak GFR losses at 72 h is open to question. 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 - 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 ]. However, such observations may not apply to the most common trigger of CIAKI: intra-arterial boluses of radiocontrast given over a short time during PCI.…”