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Assessment of physiological parameters in the rat following intravenous injection of superparamagnetic iron oxide nanoparticles (SPION’s) (LB730)
Author(s) -
Edge Deirdre,
Shortt Christine,
Markos Farouk,
Barry Elaine
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb730
Subject(s) - renal function , chemistry , natriuresis , excretion , endocrinology , renal blood flow , medicine , mean arterial pressure , free water clearance , fractional excretion of sodium , tubular fluid , urine sodium , kidney , urology , blood pressure , reabsorption , heart rate
With a growing number of applications associated with nanostructures, characterization in‐vivo is imperative. Previous MRI studies have described the accumulation of SPION’s in the rat and pig kidneys following intravenous (i.v) injection. Since intra‐renal accumulation of SPION’s may lead to acute kidney injury, we sought to assess an array of physiological parameters including renal function following injection of SPION’s. Adult male Wistar rats (n=16) were anaesthetised with an i.p. injection of sodium pentobarbital (60mg/kg bw). Mean arterial pressure (MAP) was continually monitored. Plasma and urine samples were collected over 20 minute clearance periods, two prior to and two following injection of 2mg/kg SPION’s (MF66 or OD15). Plasma and urine were analysed for electrolyte measurements and determination of the glomerular filtration rate (GFR). I.v. injection of both SPION’s led to a significant transient drop in MAP. Glomerular filtration rate (GFR) was not significantly affected following SPION injection, however fractional sodium excretion (FENa) and absolute sodium excretion (UVNa) significantly increased in SPION‐treated animals compared to baseline values, (p=0.0313, one‐tailed Wilcoxin signed rank test). The mechanisms of this MAP drop and natriuresis is unclear but may involve vasodilator release, e.g. prostaglandins, which oppose the actions of the Renin Angiotensin System. Grant Funding Source : Framework Project 7