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Abstract
Oxygen free radicals have been implicated in postischemic renal injury. However, the
source of these oxygen free radicals has not been well defined. One potential source
is activated neutrophils. Neutrophil depletion was produced in rats by using two different
techniques, and the effect on ischemic injury was examined. Rabbit anti-rat neutrophil
serum was prepared by immunizing a rabbit with a Percoll gradient centrifugation-purified
(approximately 90%) suspension of rat neutrophils. Rats received antineutrophil serum
in one of four protocols and were subsequently subjected to 40 minutes of renal artery
occlusion. Control animals received nonimmune rabbit serum. The serum creatinine levels
24 hours after ischemia were not different between control and immune serum-treated
rats in any of the protocols despite significant reductions in absolute neutrophil
count. In a separate study, nitrogen mustard was administered 40 hours before ischemia.
Nitrogen mustard-treated rats developed moderate neutropenia and 24 hours after ischemia
had lower serum creatinine levels and higher inulin clearance. However, nitrogen mustard-treated
rats lost 31.5 ±5 gm body weight in the 2 days after nitrogen mustard administration,
whereas control animals gained 5.9 ± 5.9 gm during the same interval. Furthermore,
among nitrogen mustard-treated rats there was no correlation between neutrophil count
and postischemic renal function. It is thus possible that the beneficial effects of
nitrogen mustard were caused by a mechanism other than neutrophil depletion. In summary,
in four protocols that used antineutrophil serum, neutropenia did not protect against
ischemic injury. Nitrogen mustard provided protection, but probably by a neutrophll-independent
mechanism. We conclude that there is no clear-cut role of circulating neutrophils
to mediate ischemic renal injury in the rat.
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Article info
Publication history
Accepted:
November 22,
1988
Received in revised form:
November 14,
1988
Received:
August 8,
1988
Footnotes
☆Supported in part by National Institutes of Health Grant HL-17871.
Identification
Copyright
© 1989 Published by Elsevier Inc.
