ROENTGENOGRAPHIC CONTRAST MEDIUM (RCM)-INDUCED RENAL VASOCONSTRICTION

Abstract

Contrast media, and other hypertonic solutions, have been shown to induce renal vasoconstriction, but their influence on acute changes in FF and GFR have not been assessed. All known vasoactive agents that reduce renal blood flow (RBF), such as norepinephrine (NEPI), reduce GFR and increase FF. We compared intrarenal bolus injections of RCM (4 cc meglumine/sodium diatrizoate 76%, 1650 mOsm/kg) and NEPI, (3–10 μg) on RBF (electromagnetic flowmeter) and GFR (Tc 99m DTPA extraction) in dogs. To assess GFR transients, a pump was used with a rapid, simultaneous renal venous and arterial sampling at 15 second intervals. NEPI induced a fall in renal plasma flow (RPF) (69 ± 14 vs. 16 ± 3 ml/min) and the expected rise in FF (0.36 ± .04 vs. 0.42 ± 0.07). RCM induced a fall in RPF (102 ± 5 vs. 79 ± 10 ml/min) and an unanticipated fall in FF (0.32 ± 0.01 vs. .18 ± 0.02). The fall in FF post RCM reflected a larger and more sustained fall in GFR (33 ± 2 vs. 14 ± 2 ml/min; -Δ 19 ml/min) than post NEPI (20 ± 5 vs. 6 ± 2 ml/min; -Δ 14 ml/min). To examine the role of intrarenal pressures on RBF and FF, acute changes in renal length (L), ureteral pressure (UP) and wedged interlobar venous pressure (VP) were measured following intrarenal bolus injections of RCM and NEPI. Whereas NEPI produced decreases in L, UP, and VP, the RCM-induced vasoconstriction was associated with increases in these parameters. The RCM-induced increases in L, UP, and VP must reflect osmotic forces. The fall in FF probably reflects Starling forces in the glomerular capillaries, with osmotic transients dominating: the same forces may well be responsible for the vascular responses to RCM, and may contribute to RCM-induced acute renal failure.