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Iodinated contrast media inhibit oxygen consumption in freshly isolated proximal
tubular cells from elderly humans and diabetic rats: Influence of nitric oxide
#MMPMID26933994
Liss P
; Hansell P
; Fasching A
; Palm F
Ups J Med Sci
2016[]; 121
(1
): 12-6
PMID26933994
show ga
Objectives Mechanisms underlying contrast medium (CM)-induced nephropathy remain
elusive, but recent attention has been directed to oxygen availability. The
purpose of this study was to evaluate the effect of the low-osmolar CM iopromide
and the iso-osmolar CM iodixanol on oxygen consumption (QO2) in freshly isolated
proximal tubular cells (PTC) from kidneys ablated from elderly humans undergoing
nephrectomy for renal carcinomas and from normoglycemic or
streptozotocin-diabetic rats. Materials PTC were isolated from human kidneys, or
kidneys of normoglycemic or streptozotocin-diabetic rats. QO2 was measured with
Clark-type microelectrodes in a gas-tight chamber with and without each CM (10?mg
I/mL medium). L-NAME was used to inhibit nitric oxide (NO) production caused by
nitric oxide synthase. Results Both CM reduced QO2 in human PTC (about -35%)
which was prevented by L-NAME. PTC from normoglycemic rats were unaffected by
iopromide, whereas iodixanol decreased QO2 (-34%). Both CM decreased QO2 in PTC
from diabetic rats (-38% and -36%, respectively). L-NAME only prevented the
effect of iopromide in the diabetic rat PTC. Conclusions These observations
demonstrate that CM can induce NO release from isolated PTC in vitro, which
affects QO2. Our results suggest that the induction of NO release and subsequent
effect on the cellular oxygen metabolism are dependent on several factors,
including CM type and pre-existing risk factors for the development of CM-induced
nephropathy.
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