“…35 Finally, in severe experimental hypotensive sepsis in sheep in which, after an initial increase, RBF then decreased (presumably owing to profound systemic vasodilation and myocardial depression), renal adenosine triphosphate levels, as measured by magnetic resonance imaging spectroscopy, remained unchanged. 36 In fact, even in ischemia-reperfusion models, the role of ongoing renal ischemia in the progression of AKI is unclear. For instance, in a pig model of aortic cross-clamping, renal reperfusion RBF initially was restored and only then decreased progressively, despite normal systemic hemodynamics, 37 suggesting that intrarenal factors including endothelial injury, microvascular thrombosis, and inflammation were causing microcirculatory hypoperfusion and increasing renal vascular resistance.…”