（有奖）【每周一问】NO.49-Kidney Protection(part1)

（有奖）【每周一问】NO.49-Kidney Protection(part1)

（有奖）【每周一问】NO.49-Kidney Protection(part1)-2010-07-28 02:37:55 PM

Today we begin a week of questions on protecting the kidney during the perioperatie period.
Which area of the kidney is most at risk for ischemic necrosis and why?

肾小管为一条细长的单层上皮管道，容易发生缺血性坏死。肾脏内血液分布是不均衡的，肾皮质的血供占肾血流量的90％以上，流速很快。髓质血流量不足肾血流量的10％，流速也慢有血循环旁路。围术期由于麻醉、药物、外科手术、缺氧或二氧化碳过多，以及失血和创伤休克等情况，都将引起肾血管收缩和肾血流量减少，小叶间动脉远端发生痉挛，以致皮质外侧2／3血供急骤减少甚至缺血，大量肾小管上皮细胞坏死、崩解、脱落，最终导致急性肾功能衰竭。当肾脏缺血时间较短时，肾功能不难恢复，但如果缺血过久则造成肾组织损伤严重，带来严重不良后果。因此对于失血和创伤性休克患者，补充血容量(输血或补液)仍是最重要的急救措施，而注射肾上腺素一类缩血管药则必须十分慎重，以免肾及其他内脏血管过度收缩，加剧缺血，而给机体带来严重损害。小剂量多巴胺能扩张肾血管，增加肾血供，可以应用参考答案：
肾脏外侧髓质主要包括高密度的亨利(氏)袢升支小管（mTALs，肾小管髓袢升支粗段）。急性肾功能衰竭病人和动物模型的组织病理学证据表明，肾小管细胞比肾脏其他部位坏死更严重。究其原因为人所具有的产生浓缩尿的能力。mTALs通过Na+/K+泵产生浓缩尿逆流交换机制必须的高渗髓质梯度；这样的梯度需要70~90%的肾脏氧消耗。
不幸的是，肾脏的这些区域也接受最低速度的血流，其中40%达到皮质。这种原因也包括髓质osmolar梯度。达到髓质的血流来自于近髓肾小球的输出小动脉，并且因此产生直小血管，像发卡环一样，其对髓质梯度的保护很重要。直小血管对离子和水具有通透性，因此直小血管内的血流通过间质环境的血流与其保持平衡。在早期的降段，血流渗透压正常（285mOsm/l），髓质深部渗透压升高（1200 mOsm/l），在上升段基本正常（300 mOsm/l）。这种机制允许氧的释放和二氧化碳的清除，而避免了梯度破坏，但是其需要低血流。已经证实高血流将降低或破坏这种梯度。
高氧耗和低输送的结果是组织PO2很低，约为10-20 mmHg，而皮质PO2达50 mmHg。因此，正常肾脏总是处于缺氧边缘，并且形成了保护自身免受缺血损害的复杂的调控机制。
Which area of the kidney is most at risk for ischemic necrosis and why?
The outer medullary region of the kidney is comprised mainly of the tubules of the thick ascending loop of Henle (mTALs). Histopathologic eidence from patients with acute renal failure and from animal models of ARF has shown conincingly that these tubular cells exhibit necrosis far more readily than any other area of the kidney. The reason for this is due to our ability to create a concentrated urine. The mTALs, ia a Na+/K+ ATPase pump, create the hyperosmotic medullary gradient necessary for the countercurrent exhange mechanism of urinary concentration; in so doing they are responsible for 70-90% of renal oxygen consumption. Unfortunately, this area of the kidney also receies the lowest rate of blood flow, about 40% of the rate receied by the cortex. The reason for this again inoles the medullary osmolar gradient. Blood flow to the medulla comes from the efferent arterioles of the juxtamedullary glomeruli, and these gie rise to the asa recta, which resemble hairpin loops and are ital to presering the medullary gradient. The asa recta are permeable to ions and water, so that blood within the asa recta equilibrates with the interstitial enironment through which it flows. Blood has normal osmolarity (285mOsm/l) in the early descending portion, high osmolarity (1200 mOsm/l) deep in the medulla, and near normal (300 mOsm/l) osmolarity at the late ascending portion. This mechanism allows for release of oxygen and romoal of CO2 while aoiding washout of the gradient, but necessitates low blood flow. It has been demonstrated that high rates of blood flow will diminish or eliminate the gradient.
The net result of high oxygen consumption and low deliery is a low baseline tissue PO2 of about 10-20 mmHg. This is in contrast to a cortical PO2 of about 50 mmHg. Thus, the normal kidney is always on the erge of hypoxia, and has deeloped sophisticated regulatory strategies to protect itself against ischemic damage.
Question author: Andrew Friedrich, MD, Department of Anesthesiology, Perioperatie and Pain Medicine, Brigham and Women's Hospital, Harard Medical School
References:
1. Brezis, M, Rosen, S. Hypoxia of the renal medulla: its implications for disease. New Engl J Med 1995;332:647-655.
2. Brezis, M. et al. The role of medullary ischemia in acute renal failure. New Horizons 1995; 3:597-607
3. Zimmerhackl, B. et al. The medullary microcirculation. Kidney Int 1987; 31: 641-647.

发表者QINQIN 时间 2010-07-28 02:37:55 PM

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