Loss of renal function and microvascular blood flow after suprarenal aortic clamping and reperfusion (SPACR) above the superior mesenteric artery is greatly augmented compared with SPACR above the renal arteries

ObjectiveRenal insufficiency continues to be a complication that can affect patients after treatment for suprarenal aneurysms and renal artery occlusive disease. To our knowledge, no data are available showing that suprarenal aortic clamping and reperfusion (SRACR) above the renal arteries (renal-SRACR) preserves renal function compared with SRACR above the superior mesenteric artery (SMA-SRACR). This study examined the hypothesis that SMA-SRACR–induced downregulation of renal blood flow and function is more severe than renal-SRACR owing to the addition of systemic oxygen-derived free radical (ODFR) release.MethodsMale Sprague-Dawley rats (about 350 g) were anesthetized and microdialysis probes or laser Doppler fibers were inserted into the renal cortex (depth of 2 mm) and into the renal medulla (depth of 4 mm). Laser Doppler blood flow was continuously monitored, and the microdialysis probes were connected to a syringe pump and perfused in vivo at 3 μL/min with lactated Ringer’s solution.ResultsSMA-SRACR and Renal-SRACR decreased medullary and cortical blood flow and nitric oxide (NO) synthesis. SMA-SRACR downregulated cortical inducible NO synthase, whereas renal-SRACR did not. The cortex and medulla responded to the decreased blood flow and NO synthesis by increasing in prostaglandin E2 synthesis, which was due to increased cyclooxygenase-2 content. Superoxide dismutase restored SMA-SRACR (but not renal-SRACR) cortical and medullary NO synthesis, suggesting that ODFRs generated during mesenteric ischemia–reperfusion were one of the systemic mechanisms contributing to decreased renal NO synthesis in the SMA-SRACR model. The 90% decrease in creatinine clearance after SMA-SRACR was greater than the 60% decrease after renal-SRACR.ConclusionsThese data show that NO is important in maintaining renal cortical and medullary blood flow and NO synthesis after renal and SMA-SRACR. These data also suggest that in addition to the renal ischemia–reperfusion caused by both models, SMA SRACR induces mesenteric ischemia–reperfusion, resulting in the generation of ODFRs, which contribute to decreased renal cortical and medullary NO synthesis. Maintaining splanchnic blood flow or attempting to keep SRACR below the SMA level may be helpful in developing strategies to minimize the renal injury after SRACR.

Clinical RelevanceThis study suggests that clinically relevant cortical and medullary vasodilators (nitric oxide and vasodilator prostanoids) are required to maintain microvascular renal cortical and medullary blood flow after superior mesenteric artery suprarenal aortic clamping and reperfusion (SRACR) both above the superior mesenteric artery (SMA) and above the renal arteries (Renal-SRACR). The data strongly suggest that the renal injury after SMA-SRACR is worse than that after renal-SRACR. The more severe injury caused by SMA-SRACR is partly mediated by oxygen-derived free radicals that were not involved with the renal injury after renal-SRACR. Maintaining SMA blood flow and preventing or inhibition of oxygen-derived free radical production during SMA-SRACR should be one treatment strategy that could help maintain renal microvascular blood flow during the treatment of complex aortic pathology that require SRACR.