Affiliation:
1. Departments of Medicine, Pathology, Physiology and Biophysics, University of South Florida Health Sciences Center, and James A. Haley Veterans Hospital, Tampa, Florida 33612
Abstract
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 ± 1 and 0.56 ± 0.05 mg/dl to increase to 162 ± 4 and 8.17 ± 0.5 mg/dl, P < 0.001, respectively, at day 4 of postischemia. Vessel dilator, a 37-amino-acid cardiac peptide hormone (0.3 μg ⋅ kg− 1 ⋅ min− 1ip), decreased the BUN and creatinine levels to 53 ± 17 mg/dl and 0.98 ± 0.12 mg/dl ( P < 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 <5% in the vessel dilator-treated rats compared with 25% to >75% in the placebo-treated ARF animals. We conclude that vessel dilator improves acute tubular necrosis and renal function in established ARF.
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Cited by
20 articles.
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