PMID: 11322173Apr 27, 2001Paper

Role of humoral mediators in, and influence of a liposomal formulation on, acute amphotericin B nephrotoxicity

Pharmacology & Toxicology
R SabraH Serhal

Abstract

The mechanisms responsible for amphotericin B nephrotoxicity remain incompletely understood, but clearly involve reduction in renal blood flow and glomerular filtration rate. Both direct effects of amphotericin B on contractile vascular cells, and indirect effects, due to humoural mediators, have been proposed. This study examines the role of nitric oxide, endothelin and angiotensin II in the acute nephrotoxic effects of amphotericin B in rats, and compares the anti-fungal and nephrotoxic effects of liposomal amphotericin B and amphotericin B-deoxycholate. Anaesthetized rats were given infusions of amphotericin B-deoxycholate in the presence or absence of N-nitro-L-arginine, PD 145065, a non-specific endothelin receptor antagonist, and L-158809, an angiotensin II type I receptor antagonist, or increasing doses of liposomal amphotericin B. Amphotericin B-deoxycholate (0.03 mg/kg/min intravenously) caused a significant 44% reduction in glomerular filtration rate and 65% maximal fall in renal blood flow. N-Nitro-L-arginine-treated rats had a lower renal blood flow and glomerular filtration rate at baseline, but sustained similar reduction of 53% and 75% in these parameters, respectively. PD145065 and L-158809 did not modify these ...Continue Reading

Citations

Jun 26, 2004·Journal of Pediatric Hematology/oncology·Ran D Goldman, Gideon Koren
Apr 11, 2008·Critical Care Medicine·Neesh Pannu, Mitra K Nadim
Mar 13, 2014·The Pediatric Infectious Disease Journal·David F BesElvira Arrizurieta
Jan 24, 2002·Current Opinion in Critical Care·S Costa, M Nucci
Feb 3, 2011·Critical Care Nurse·Susan Dirkes

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