Tissue oxygen and hemodynamics in renal medulla, cortex, and corticomedullary junction during hemorrhage-reperfusion

Previous studies of intrarenal perfusion and tissue oxygenation have produced a wide range of results and have not matched tissue oxygen tension (tPO₂) with concurrent changes in flow in three distinct regions. We thus used an anesthetized rat model of hemorrhage-reperfusion to address this question. Combined tPO₂/laser-Doppler fiber-optic probes were simultaneously sited in cortical, corticomedullary (CMJ), and medullary regions of the left kidney. Total renal blood flow was measured in separate experiments. Recordings were made during exsanguination of 10 and 20% of estimated blood volume at 10-min intervals, followed by shed-blood resuscitation after a further 10 min. The decay in tPO₂ was then recorded following total cessation of blood flow, allowing estimation of local oxygen consumption. During exsanguination, tPO₂ was maintained in all intrarenal regions, despite significant falls in blood pressure and total renal blood flow. However, intrarenal flow was redistributed with reduced cortical, unchanged CMJ, and increased medullary blood flow. After resuscitation, significant rises above baseline were seen in blood pressure and in tPO₂ across all regions. Whereas cortical and medullary flows regained baseline values, CMJ flow fell. The ratio of tPO₂ to microvascular blood flow increased significantly in all regions during resuscitation, suggesting decreased oxygen consumption. On total cessation of blood flow, the cortex and CMJ showed significant increases in the oxygen decay half-life, consistent with decreased consumption. To our knowledge, this is the first quantitative demonstration of a markedly heterogeneous intrarenal cardiorespiratory response to a hemodynamic insult, with effects most marked at the corticomedullary junction.