Acute effects of hypoxaemia, hyperoxaemia and hypercapnia on renal blood flow in normal and renal transplant subjects

The aim of this investigation was to study noninvasively the effects of hypoxaemia, hyperoxaemia and hypercapnia on renal blood flow in normal subjects and renal allograft recipients, i.e. with denervated kidneys. By comparing these two groups, the influence of renal innervation on any resulting changes in renal blood flow could be ascertained. Nine normal and eight renal allograft recipients were studied. Each subject inhaled the following gas mixtures in order: room air, 10% O2 (hypoxaemia), 10% O2 + baseline CO2 (isocapnic hypoxaemia), 10% O2 + high CO2 (hypercapnic hypoxaemia), 100% O2 (hyperoxaemia), 100% O2 + baseline CO2 (isocapnic hyperoxaemia) and 100% O2 + high CO2 (hypercapnia hyperoxaemia). Using Doppler ultrasonography, the pulsatility index (PI), an index of renovascular resistance, was measured at the various gas inhalation levels. In normal subjects, the renovascular resistance increased in response to hypoxaemia, with a greater increase in response to hypercapnic hypoxaemia. Hyperoxaemia caused a decrease in renovascular resistance but this was abolished with the addition of CO2. There was a similar pattern in the PI response to the different gas inhalations in the renal transplant subjects, but these responses were attenuated in comparison with those of the normals. In conclusion, renal denervation does not completely abolish the renovascular responses to inhaled oxygen and carbon dioxide.

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