Amelioration with vessel dilator of acute tubular necrosis and renal failure established for 2 days
American Journal of Physiology. Heart and Circulatory Physiology
Amelioration with vessel dilator of acute tubular necrosis and renal failure established for 2 days. Am J Physiol Heart Circ Physiol 278: H1555-H1564, 2000.-Seventeen Sprague-Dawley rats had ischemic nonoliguric acute renal failure (ARF) induced by vascular clamping resulting in their preischemic blood urea nitrogen (BUN) and creatinine levels of 16 Ϯ 1 and 0.56 Ϯ 0.05 mg/dl to increase to 162 Ϯ 4 and 8.17 Ϯ 0.5 mg/dl, P Ͻ 0.001, respectively, at day 4 of postischemia. Vessel dilator, a
... dilator, a 37-amino-acid cardiac peptide hormone (0.3 µg · kg Ϫ1 · min Ϫ1 ip), decreased the BUN and creatinine levels to 53 Ϯ 17 mg/dl and 0.98 Ϯ 0.12 mg/dl (P Ͻ 0.001) in another seven animals where ARF had been established for 2 days. Water excretion doubled with ARF and was further augmented by vessel dilator. Transthoracic echocardiography revealed left ventricular dilation as a probable cause of the increase in vessel dilator in the circulation with ARF, and vessel dilator infusion reversed this dilation. At day 6 of ARF, mortality decreased to 14% with vessel dilator from 88% without vessel dilator. Acute tubular necrosis was Ͻ5% in the vessel dilator-treated rats compared with 25% to Ͼ75% in the placebo-treated ARF animals. We conclude that vessel dilator improves acute tubular necrosis and renal function in established ARF. atrial natriuretic peptides; blood urea nitrogen; serum creatinine; diuresis; transthoracic echocardiography The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.