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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


FUNCTIONAL IMPAIRMENT OF OUTER MEDULLARY DESCENDING VASA RECTA AND ENDOTHELIAL DAMAGE BY IODINATED CONTRAST MEDIA
Abstract number: P121

*Sendeski1 M., Bondke1 A., Persson1 P.B., Patzak1 A.

Introduction: 

Contrast induced nephropathy (CIN) is a complication of procedures using iodinated contrast media (CM). Outer medullary descending vasa recta (DVR) supply blood flow to the renal medulla, the area at risk of hypoxia in CIN. We investigated the effect of CM on the vasoactivity and NO production of isolated perfused DVR, and on the endothelium of interlobar arteries.

Methods: 

DVR and interlobar arteries from Sprague-Dawley rats were isolated and perfused alternatively with iodixanol, iopromide, amidotrizoate; and ioxaglate. Control group was perfused with vehicle solution. The iodine concentration for all CM was 23 mg iodine/ml. Videomicroscopy was used for measuring serial luminal diameter. Angiotensin II dose response curves were performed after 20 minutes of CM perfusion. Fluorescent techniques were used to measure changes in the bioavailability of nitric oxide (NO) over time. Scan electron microscopy was used to investigate endothelial damage in interlobar arteries.

Results: 

All CM tested led to a comparable reduction of DVR diameter (45±7% to 63±11% of initial diameter). Vasoconstriction by angiotensin II was increased for three of the CM tested. NO bioavailability in DVR was reduced, and endothelial cells from interlobar arteries sustained anatomical damage due to CM. Tempol (a superoxide dismutase mimetic) prevented DVR constriction.

Conclusion: 

Different CM led to comparable constriction of DVR and intensification of the constriction to angiotensin II. This may be caused by reduced bioavailability of NO, due to oxidative stress and endothelial damage. Such findings explain the renal medullary damage in CIN.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P121

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