Oxygen and renal hemodynamics in the conscious rat

Previous studies have suggested a link between renal metabolism and local k idney hemodynamics to prevent potential hypoxic injury of particularly vuln erable nephron segments, such as the outer medullary region. The present st udy used three different inspiratory oxygen concentrations to modify renal metabolic state in the conscious rat (hypoxia 10% O-2, normoxia 20% O-2, an d hyperoxia 100% O-2). Renal blood flow (RBF) was assessed by ultrasound tr ansit time; renal perfusion pressure (RPP) was controlled by a hydroelectri c servo-control device. Local RBF was estimated by laser-Doppler flux for t he cortical and outer medullary region (2 and 4 mm below renal surface, res pectively). Hypoxia led to a generalized significant increase in RBF, where as hyperoxia-induced changes did not (hypoxia 6.6 +/- 0.6 ml/min versus nor moxia 5.7 +/- 0.7 ml/min, P < 0.05). Moreover, regional and total RBF autor egulation was markedly attenuated by hypoxia. Conversely, hyperoxia enhance d RBF autoregulation. Under normoxic and hyperoxic conditions, medullary RB F was very well maintained even at low RPP (medullary RBF: approximately 70 % of control at 50 mmHg). The hypoxic challenge, however, significantly dim inished the capacity to maintain medullary blood flow at low RPP (medullary RBF: approximately 30% of control at 50 mmHg, P < 0.05). These data sugges t that renal metabolism and renal hemodynamics are closely intertwined In r esponse to acute hypoperfusion, the kidney succeeds in maintaining remarkab ly high medullary blood flow. This is not accomplished, however, when a con comitant hypoxic challenge is superimposed on RPP reduction.