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Abstract
Previous studies have demonstrated that the sympathomimetic agent clonidine, administered
intravenously immediately prior to injury, provides partial protection against the
acute structural and functional impairments associated with experimental ischemic
and nephrotoxic ARF. To determine the effect of clonidine, administered orally, on
the prolonged course of HgCl2-induced ARF, two groups of rats were studied for a period of 5 days after injury.
For 5 days before HgCl2 administration (2 mg/kg s.c.) and throughout the study group I drank water while
group II had clonidine (5 mg/L) added to water. The fatality rate was 77% in group
I as compared to 11% in group II (p < 0.001). Renal function (CCr and FENa) was better preserved and recovered more rapidly in group II rats protected with
clonidine. Both groups showed varying degrees of proximal tubular cell injury, but
group II had significantly fewer necrotic cells and demonstrated earlier evidence
of regeneration. Whereas none of the injured cells in the clonidine-pretreated group
revealed evidence of calcification, on the second day half the cells of the pars recta
in the outer stripe of the medulla were calcified in group I. In group III animals,
oral clonidine was started 2 hr after the injection of HgCl2 and also resulted in a significant reduction in fatality rate from 40% in control
group to 0% in the clonidine-treated group. In addition, CCr and FENa were better preserved and recovered more rapidly in this group of clonidine-treated
rats. These results indicate that oral clonidine, administered either before or shortly
after HgCl2-induced ARF, exerts a salutory effect on the course and mortality of ARF by providing
protection of renal function and enhancement of the recovery process.
Abbreviations:
(FENa) (fractional excretion of sodium), (ARF) (acute renal failure), (s.c.) (subcutaneously), (CCr) (creatinine clearance), (H&E) (hematoxylin and eosin)To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
June 21,
1983
Received:
November 15,
1982
Footnotes
☆This work was supported in part by National Institutes of Health Grant AM26134 and in part by a grant from Boehringer Ingelheim, Ltd.
Identification
Copyright
© 1983 Published by Elsevier Inc.
