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K. J. KELLY, NINA E. TOLKOFF-RUBIN, ROBERT H. RUBIN, WINFRED W. WILLIAMS, JR., SHANE M. MEEHAN, CAROL L. MESCHTER, JAMES G. CHRISTENSON, AND JOSEPH V. BONVENTRE Medical and Pathology Services, Massachusetts General Hospital, Departments of Medicine and Pathology, Harvard Medical School, Boston, Massachusetts 02114; Center for Experimental Pharmacology and Therapeutics, Harvard-Massachusetts Institute of Technology, Division of Health Sciences and Technology, Cambridge, Massachusetts 02139; and Roche Research Center, Hoffmann-La Roche, Nutley, New Jersey 07110 Kelly, K. J., Nina E. Tolkoff-Rubin, Robert H. Rubin, Winfred W. Williams, Jr., Shane M. Meehan, Carol L. Meschter, James G. Christenson, and Joseph V. Bonventre. An oral platelet-activating factor antagonist, Ro-244736, the rat kidney from . Am. J. Physiol. 271 (RenaZ FZuid Electrolyte Physiol. 40): F1061F1067, 1996.-The role of platelet-activating factor (PAF) in acute failure was evaluated by administering an oral PAF antagonist (Ro-24-4736) to rats prior to or after interruption of blood flow to both kidneys for 30 min. In animals treated with the PAF antagonist prior to ischemia, function was less impaired and histological abnormalities was less pronounced when compared with post kidneys from vehicle-treated animals. Serum creatinine (mg/ dl) 24 h following ischemia was 1.58 ? 0.17 in the PAF antagonist-treated
AJP - Renal Physiology – The American Physiological Society
Published: Nov 1, 1996
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