Reduced depression of renal function by iotrolan in the isolated rat kidney

Oldroyd, S.; Haylor, J.; Morcos, Sameh K.; Nahas, A. Meguid El

doi:10.1016/0720-048x(94)90370-0

Cited by 18 publications

(7 citation statements)

References 25 publications

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“…Both parameters were expressed per g wet weight of the nonperfused kidney, as well as a percentage of the value obtained in the 5 min before addition of CM. GFR and RPF were both stable in this preparation for a period of 150 min in experiments carried out in the absence of any CM or antagonist (GFR, 0.62p0.05 to 0.63p0.06 ml:min −" :g −" ; RPF, 29.5p0.7 to 30.8p0.9 ml:min −" :g −" ; n l 6), as observed previously [9,13,23].…”

Section: Iprk Modelmentioning

confidence: 50%

“…Patients with pre-existing renal inthe primary factors in the effects on renal function [4][5][6][7][8]. CM can induce both a decrease in renal blood flow and a reduction in glomerular filtration rate (GFR) [4][5][6][7][8][9]. These effects could be due to modulation of the intrarenal synthesis and release of vasoactive mediators [10], such as nitric oxide (NO) [11], prostaglandins [12], endothelin [13] and adenosine [14].…”

Section: Introductionmentioning

confidence: 98%

“…This ex vivo system allows the study of the direct local effects of exogenous substances on the kidney without any interference by systemic and nervous influences. This model has been utilized successfully by our group to study the pathophysiology of the renal effects of CM [8,9,13,23], amino acids [24,25] and vasoactive mediators [26].…”

Section: Introductionmentioning

confidence: 99%

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Effects of adenosine receptor antagonists on the responses to contrast media in the isolated rat kidney

et al. 2000

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Contrast media can induce both a decrease in renal blood flow and a reduction in glomerular filtration rate (GFR) when administered to both experimental animals and humans. In the present study we have examined the role of adenosine in mediating these effects using the isolated perfused rat kidney. Kidneys were perfused with a 6. 7%-(w/v)-albumin-based perfusate supplemented with glucose and amino acids (n=6 per group). They were exposed to diatrizoate [20 mg of iodine (mgI)/ml; osmolality 1650 mOsm/kg of water] or iotrolan (20 mgI/ml; osmolality 320 mOsm/kg of water) in the presence or absence of theophylline (10.8 microg/ml), or to diatrizoate in the presence or absence of a specific adenosine A(1) receptor antagonist (KW-3902; 2 microg/ml) or a specific A(2) receptor antagonist (KF17837; 6 microg/ml). Diatrizoate (n=6) produced a fall in GFR from 0.65+/-0.04 to 0.42+/-0.03 ml.min(-1).g(-1) (P<0.05); renal perfusate flow (RPF) also declined, from 36.5+/-3.8 to 22.0+/-3.2 ml. min(-1).g(-1) (P<0.05). Iotrolan (n=6) produced a fall in GFR from 0. 64+/-0.02 to 0.48+/-0.04 ml.min(-1).g(-1) (P<0.05) and in RPF from 33.3+/-3.8 to 24.0+/-3.0 ml.min(-1).g(-1) (P<0.05). Theophylline (10.8 microg/ml) prevented the fall in GFR caused by either diatrizoate (baseline, 0.63+/-0.05 ml.min(-1).g(-1); diatrizoate+theophylline, 0. 60+/-0.04 ml.min(-1).g(-1)) or iotrolan (baseline, 0.64+/-0.04 ml. min(-1).g(-1); iotrolan+theophylline, 0.67+/-0.05 ml.min(-1).g(-1)), but did not affect the decreases in RPF caused by either agent. KW-3902 (2 microg/ml) also prevented the fall in GFR produced by diatrizoate (baseline, 0.66+/-0.05 ml.min(-1).g(-1); diatrizoate+KW-3902, 0.61+/-0.05 ml.min(-1).g(-1)), while the fall in RPF remained unaffected. KF17837 (6 microg/ml) had no effect on the decreases in either GFR or RPF induced by diatrizoate (n=6 per group). The results suggest a role for adenosine acting at the A(1) receptor in mediating the decrease in GFR induced by contrast media. This effect is independent of a change in renal vascular resistance, and possibly secondary to mesangial cell contraction causing a decrease in the ultrafiltration coefficient.

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Section: Iprk Modelmentioning

confidence: 50%

Section: Introductionmentioning

confidence: 98%

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Effects of adenosine receptor antagonists on the responses to contrast media in the isolated rat kidney

et al. 2000

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“…1 Several experimental studies have been conducted to compare the nephrotoxic effects of newly developed nonionic CM with those of conventional ionic CM. Some in vivo experiments in which renal blood flow, 7,8 glomerular filtration rate, [9][10][11] enzymuria, 9 and histopathological findings 9,10 were evaluated as the indicators of nephrotoxicity demonstrated that nonionic CM were less gluconeogenesis and PAH accumulation. The difference in gluconeogenesis inhibition between ionic and nonionic CM at a concentration of 60 mg I/ml was about 10%.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of gluconeogenesis and p -aminohipuric acid accumulation in rat renal cortical slices by ionic and nonionic contrast media

Nakamura

Uozumi²,

Soejima³

et al. 2003

Clinical and Experimental Nephrology

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“…Experimental studies in animals have demonstrated that, compared with ionic CM, nonionic CM results in diminished reductions in renal blood flow, 12,13 enzymuria, 14 glomerular filtration rate, [14][15][16] and histopathological damage, 14,15 thus implying that nonionic CM is less nephrotoxic than ionic CM. The CM nephrotoxicity demonstrated in these in-vivo experiments reflects both hypoxic damage through hemodynamic change and the direct toxicity of CM in renal epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Nephrotoxic effects of ionic and nonionic contrast media on rat and human renal cortical slices

Uozumi¹,

Nakamura

Soejima³

et al. 2001

Clin Exp Nephrol

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Background. Nephrotoxicity is a well-known adverse effect of radiographic contrast medium (CM). Recently, several kinds of low-osmolality nonionic CM have been developed. However, the nephrotoxic effects of nonionic CM compared with those of ionic CM have not been well evaluated. Methods. To compare the direct nephrotoxic effects of ionic and nonionic CM on renal epithelial cells, rat and human renal cortical slices were incubated with CM at 37°C for 120 min. Diatrizoate and iothalamate were employed as ionic CM. Iopamidol, iohexol, iomeprol, ioversol, iopromide, and ioxilan were employed as nonionic CM. Direct toxicity of CM was evaluated by the activities of N-acetyl--D-glucosaminidase (NAG) and γ-glutamyltransferase (GGT) released from the renal slices into the incubation buffer. Results. In the experiment with rat renal slices, NAG and GGT activities in buffer solutions were increased dosedependently by 30, 60, and 90 mg I/ml of CM. There was no significant difference in NAG or GGT release between ionic and nonionic CM at the concentration of 60 mg I/ml. In the experiment with human renal slices, incubation with 60 mg I/ml of diatrizoate, iothalamate, iomeprol, and iopromide did not affect NAG levels. Significantly greater increases in NAG levels, compared with the control, were observed after incubation with iopamidol, iohexol, ioxilan and ioversol. Nevertheless, the increases in NAG caused by some of the nonionic CM were very slight. GGT release from human renal slices was significantly greater than that of the control in all experimental groups. Again, there was no significant difference in renal toxicity between ionic and nonionic CM.Conclusions. Newly developed nonionic CM had almost the same degree of nephrotoxicity against rat and human renal epithelial cells as conventional ionic CM, when direct renal toxicity was evaluated by enzyme release in an in-vitro experimental system using renal cortical slices.

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Reduced depression of renal function by iotrolan in the isolated rat kidney

Cited by 18 publications

References 25 publications

Effects of adenosine receptor antagonists on the responses to contrast media in the isolated rat kidney

Effects of adenosine receptor antagonists on the responses to contrast media in the isolated rat kidney

Inhibition of gluconeogenesis and p -aminohipuric acid accumulation in rat renal cortical slices by ionic and nonionic contrast media

Nephrotoxic effects of ionic and nonionic contrast media on rat and human renal cortical slices

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