Roberts P R, Black K W, Zaloga G P
Department of Anesthesia, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27157-1009, USA.
Am J Respir Crit Care Med. 1997 Oct;156(4 Pt 1):1265-9. doi: 10.1164/ajrccm.156.4.9607003.
Acute renal failure is a common cause of morbidity and mortality in critically ill patients and frequently results from vasoconstrictive ischemic injury to the kidney. Protein and amino acids can vasodilate renal blood vessels. Thus, we tested the hypothesis that enteral feeding could prevent renal ischemic injury using an experimental model in which renal vasoconstriction is believed to cause ischemic renal injury. This study was performed using male Sprague-Dawley rats, and renal injury was induced by glycerol injection into the hind limbs. The resulting muscle necrosis (rhabdomyolysis) causes acute renal injury. In the first part of the study, 35 animals were randomized to a peptide-based enteral diet or water via a duodenal feeding tube and subsequently injected with glycerol. Seventy-eight percent (14 of 18) of the animals receiving the enteral diet survived 3 d compared with 35% (six of 17) of the water-fed animals (p < 0.05). Blood urea nitrogen (47+/-8 versus 137+/-27 mg/dl) and creatinine (0.8+/-0.1 versus 2.0+/-0.3 mg/dl) were significantly lower in the enteral survivors than in the water survivors. In the second part of the study, renal plasma flow (para-aminohippurate clearance) and glomerular filtration rate (insulin clearance) were measured in similarly treated animals (n = 14) 1 d after injury. Renal plasma flow (4.83+/-0.65 versus 2.37+/-0.62 ml/min) and glomerular filtration rate (2.05+/-0.27 versus 0.89+/-0.22 ml/min) were significantly higher in the enteral group than in the water group. These data indicate that enteral feeding can prolong survival and decrease renal injury after glycerol-induced rhabdomyolysis. The mechanism for the protection is partly related to maintenance of renal blood flow.
急性肾衰竭是危重症患者发病和死亡的常见原因，常由肾脏血管收缩性缺血损伤所致。蛋白质和氨基酸可使肾血管扩张。因此，我们利用一种实验模型来检验肠内营养可预防肾缺血损伤这一假说，该模型中肾血管收缩被认为会导致缺血性肾损伤。本研究使用雄性Sprague-Dawley大鼠，通过向后肢注射甘油诱导肾损伤。由此产生的肌肉坏死（横纹肌溶解）会导致急性肾损伤。在研究的第一部分，35只动物通过十二指肠喂养管随机接受基于肽的肠内营养或水，随后注射甘油。接受肠内营养的动物中有78%（18只中的14只）存活3天，而接受水喂养的动物中这一比例为35%（17只中的6只）（p<0.05）。肠内营养组存活者的血尿素氮（47±8对137±27mg/dl）和肌酐（0.8±0.1对2.0±0.3mg/dl）显著低于水喂养组存活者。在研究的第二部分，在损伤1天后对同样处理的动物（n = 14）测量肾血浆流量（对氨基马尿酸清除率）和肾小球滤过率（胰岛素清除率）。肠内营养组的肾血浆流量（4.83±0.65对2.37±0.62ml/min）和肾小球滤过率（2.05±0.27对0.89±0.22ml/min）显著高于水喂养组。这些数据表明，肠内营养可延长甘油诱导的横纹肌溶解后的生存期并减轻肾损伤。这种保护机制部分与肾血流量的维持有关。
