2007 Abstracts: Ionic and Non-ionic Contrast Media Decreases Renal Microcirculation and Renal Function By Different Mechanisms

Background: The expectation that non-ionic contrast agents (NICA) would prevent the renal dysfunction found following the use of ionic contrast agents (ICA) for endovascular procedures has not been fulfilled. The mechanism(s) underlying the loss of renal function following use of NICA and ICA is not known. This study examines the hypothesis that NICA and ICA induced renal injury is due to loss of different intra-renal vasodilators leading to decreased microcirculatory blood flow and decreased function.
Methods: Anesthetized male Sprague Dawley rats (350g) had Transonic blood flow probes placed around the superior mesenteric artery (SMA) and renal artery and then either had micro-dialysis probes or Laser Doppler fibers inserted into the renal cortex (Co, 2mm) and into the renal medulla (Me, 4mm). SMA, Renal and Laser Doppler blood flow (BF) was continuously monitored and the microdialysis probes were connected to a syringe pump and perfused in vivo at 3 μl/min with lactated ringer's solution. Dialysate fluid was collected following at time zero (Basal) and 60 minutes following infusion of either saline, Conray 400 (ICA, 6 mls/kg) or Optiray 350 (NICA, 6mls/kg). The Conray and Optiray groups were treated with either saline carrier or Superoxide dismutase (SOD, 10,000 u/kg, ODFR scavenger) Dialysate was analyzed for total NO (reported as uM) and PGE₂ and reported as pg/ml. The SMA and total Renal BF is reported as perfusion units and the Laser Doppler BF is reported as percent of Basal. All data expressed as Mean ± SEM, N≥6, p< 0.05 by ANOVA compared to the Saline group (a), Conray group (b) and Optiray group (c).
Results: Conray caused a marked decrease in medullary and cortical BF and NO synthesis but did not alter PGE₂ synthesis. SOD further worsened medullary blood flow suggesting that oxygen radicals were not involved in this injury. Optiray decreased medullary and cortical BF and cortical NO synthesis. Unlike Conray, Optiray did not decrease medullary NO synthesis but profoundly decreased medullary and cortical PGE₂ synthesis.
Conclusions: These data suggest: 1) Conray (ICA) and and Optiray (NICA) both decreased cortical and medullary BF and renal function, although the intra-renal mechanisms differed; 2) Oxygen radicals did not contribute to the renal injury following either Conray or Optiray; 4) Conray-induced fall in SMA blood flow may contribute mesenteric ischemia/reperfusion which was in part oxygen radical-mediated; 5) Preservation of normal levels of renal cortical and medullary NO and vasodilator PG synthesis as well as preserving SMA blood flow may be required to prevent or lessen both NICA and ICA contrast-induced renal injury.