Myers Stuart I, Wang Li, Myers Daniel J
McGuire Research Institute/McGuire VA Medical Center, Richmond, VA, USA.
J Vasc Surg. 2007 Feb;45(2):357-66. doi: 10.1016/j.jvs.2006.10.045.
Renal 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.
Male 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 microL/min with lactated Ringer's solution.
SMA-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.
These 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.
肾功能不全仍是肾上腺动脉瘤和肾动脉闭塞性疾病治疗后可能影响患者的一种并发症。据我们所知，尚无数据表明肾动脉上方的肾上腺主动脉钳夹和再灌注（SRACR，即肾-SRACR）与肠系膜上动脉上方的SRACR（即SMA-SRACR）相比能保留肾功能。本研究检验了以下假设：由于全身氧衍生自由基（ODFR）释放增加，SMA-SRACR引起的肾血流和功能下调比肾-SRACR更严重。
将雄性Sprague-Dawley大鼠（约350 g）麻醉，将微透析探针或激光多普勒光纤插入肾皮质（深度2 mm）和肾髓质（深度4 mm）。持续监测激光多普勒血流，微透析探针连接到注射泵，在体内以3 μL/分钟的速度用乳酸林格液灌注。
SMA-SRACR和肾-SRACR均降低了髓质和皮质血流以及一氧化氮（NO）合成。SMA-SRACR下调了皮质诱导型NO合酶，而肾-SRACR未下调。皮质和髓质通过增加前列腺素E2合成来应对血流和NO合成的减少，这是由于环氧化酶-2含量增加所致。超氧化物歧化酶恢复了SMA-SRACR（而非肾-SRACR）的皮质和髓质NO合成，表明肠系膜缺血再灌注期间产生的ODFR是SMA-SRACR模型中导致肾NO合成减少的全身机制之一。SMA-SRACR后肌酐清除率降低90%大于肾-SRACR后降低60%。
这些数据表明，NO在肾和SMA-SRACR后维持肾皮质和髓质血流及NO合成中起重要作用。这些数据还表明，除了两种模型引起的肾缺血再灌注外，SMA SRACR还诱导肠系膜缺血再灌注，导致ODFR生成，这有助于降低肾皮质和髓质NO合成。维持内脏血流或试图使SRACR低于SMA水平可能有助于制定策略，将SRACR后肾损伤降至最低。
