Hypoxic renal tissue damage by endothelin-mediated arterial vasoconstriction during radioangiography in man.

Abstract

In vivo, a high rate of renal blood flow provides a more than sufficient rate of oxygen supply to the kidney. Limitations in tissue oxygenation may occur under systemic circulatory alterations (i.e. cardiovascular failure, arterioscelorosis), respiratory insuffiency (i.e. lung diseases, hypoxia, extreme anemia, acclimation to high altitude), or during perfusion of isolated organs with blood substitutes (Klause, N., and Gronow, G., 1990; Klause, N., et al., 1990). Hypoxic limitation of renal function at a maintained systemic respiration and circulation is less well understood. One example is tissue hypoxia in the kidney due to a vasoconstrictory side effect of radiocontrast media (RCM). Recent animal experiments support evidence that in the pathophysiology of RCM-induced renal vasoconstriction the balance between production of endothelium derived nitric oxide (NO) and endothelin (ET) is disturbed, whereby NO does not seem to play an important role (Bagnis et al., 1997, Morcos et al., 1997).