Renal Hemodynamic Effects of Contrast Media

The Pathogenesis, Outcomes, and Prevention of Contrast-Associated Acute Kidney Injury

“…Figure 3 demonstrates the time course and variability of renal vascular responsiveness between intrarenal, intraarterial (thoracic aorta), and intravenous bolus injection of ionic and nonionic RCM in the dog. These observed renal vascular effects of RCM are also supported by other investigators (Caldicott et al, 1970;Morris et al, 1978;Norby and DiBona, 1975;Talner and Davidson, 1968). Similar observations were made in both femoral blood flow and RBF before and after the administration of both high-and low-osmolar RCM ( Figure 5).…”

“…An overall schematic representation integrating these factors and the resulting consequences of RCM administration is summarized in Figure 2. Of these factors, the magnitude of RCM osmolality is central to both the acute hemodynamic and tubular changes following RCM administration (Caldicott et al, 1970;Harvey, 1960;Heyman et al, 1993;Katzberg et al, 1983;Morris et al, 1978;Norby and DiBona, 1975;Talner and Davidson, 1968). Nephrotoxicity from vasoconstriction has been postulated to be responsible for the majority of RCM nephrotoxicity (Bakris and Burnett, 1985;Byrd and Sherman, 1979;Caldicott et al, 1970;Harvey, 1960;Heyman et al, 1993;Katzberg et al, 1983;Larson et al, 1983;Morris et al, 1978;Norby and DiBona, 1975;Talner and Davidson, 1968).…”

“…Medications evaluated to blunt the vasoconstriction that follows these agents include blockers of the renin-angiotensin system, adrenergic antagonists, calcium antagonists and vasodilators like hydralazine. In each case, these agents have failed to attenuate the vasoconstriction associated with RCM (Katzberg et al, 1983;Morris et al, 1978;Norby and DiBona, 1975;Talner and Davidson, 1968). However, in 1984, calcium channel blockers (CCBs) were reported to ameliorate the RCM-induced vasoconstriction (Bakris and Burnett, 1985).…”

N-Acetylcysteine In The Prevention Of Radiocontrast-Induced Nephropathy

“…There is a biphasic vascular response with a brief period of vasodilation, followed by prolonged vasoconstriction (23)(24)(25)(26)(27). Within the kidney, there appears to be a further redistribution, or shunting, of blood flow resulting in reduced flow to the medulla (28).…”

Altered response in renal blood flow and oxygen tension to contrast media in diabetic rats

“…Hemodynamic changes may be involved, since a vasodilation occurs in most regional vascular beds following CM administration. However, in the kidney this phase is transient and followed by a sustained vasoconstriction (26,33). Unique for the kidney is the highly specialized angioarchitecture, with only $10% of renal blood directed through vasa recta, which means that the medulla even during normal conditions functions at the brink of anoxia (4,10,21).…”