scholarly journals In vitro and in vivo protective effect of atriopeptin III on ischemic acute renal failure.

1987 ◽  
Vol 80 (3) ◽  
pp. 698-705 ◽  
Author(s):  
M Nakamoto ◽  
J I Shapiro ◽  
P F Shanley ◽  
L Chan ◽  
R W Schrier
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Ischemic Acute Renal Failure

In vitro versus in vivo mitochondrial calcium loading in ischemic acute renal failure

1985 ◽  
Vol 248 (6) ◽  
pp. F845-F850
Author(s):  
P. E. Arnold ◽  
D. Lumlertgul ◽  
T. J. Burke ◽  
R. W. Schrier
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Ruthenium Red ◽  
Respiratory Dysfunction ◽  
Calcium Loading ◽  
Ischemic Tissue ◽  
High Concentrations ◽  
Ischemic Acute Renal Failure

Progressive mitochondrial Ca2+ accumulation and respiratory dysfunction have been observed during reperfusion after renal ischemia. The present study demonstrated that normal mitochondria, isolated in the presence of high Ca2+ concentrations, are capable of accumulating large amounts of Ca2+ in vitro and exhibit depressed respiratory rates. Since mitochondria isolated from reperfused ischemic tissue may be exposed to high concentrations of Ca2+ during the isolation procedure, the present study examined the effect of in vitro versus in vivo mitochondrial Ca2+ loading on mitochondrial function during ischemic acute renal failure (ARF) in anesthetized rats. When ruthenium red was added during isolation to prevent mitochondrial Ca2+ exchange with the medium, mitochondrial Ca2+ increased from 10.8 +/- 0.3 to 65.6 +/- 11.6 nmol/mg (P less than 0.001) after 24 h of postischemic reperfusion; this resulted in a 47% reduction in the acceptor-control ratio (ACR) from 4.19 +/- 0.09 to 2.70 +/- 0.13 (P less than 0.001). These data were compared with an increase in mitochondrial Ca2+ from 52.5 +/- 2.9 to 167.6 +/- 25.4 nmol/mg (P less than 0.001) and a 95% fall in ACR (3.84 +/- 0.40 to 1.15 +/- 0.08, P less than 0.001) at 24 h of reperfusion when no ruthenium red was added. However, at each time point examined, in vivo mitochondrial Ca2+ accumulation was shown to account for 50% or more of the mitochondrial respiratory dysfunction observed during ischemic ARF.

Xanthine oxidase: evidence against a causative role in renal reperfusion injury

1990 ◽  
Vol 258 (2) ◽  
pp. F232-F236 ◽  
Author(s):  
M. Joannidis ◽  
G. Gstraunthaler ◽  
W. Pfaller
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Xanthine Oxidase ◽  
Time Course ◽  
Ischemia Reperfusion ◽  
Xanthine Dehydrogenase ◽  
Causative Role ◽  
Conversion Rates ◽  
Ischemic Acute Renal Failure

The conversion rates of xanthine dehydrogenase (XDH) to xanthine oxidase (XO) were compared with the time course of in vivo lipid peroxidation (LPO) in an ischemia-reperfusion model of acute renal failure in the rat. LPO, measured as the renal release of malondialdehyde (MDA), was found to be markedly elevated only during the first 5 min of blood reflow following a 45-min interval of ischemia (arteriovenous MDA difference -277.3 +/- 53.5 vs. 3.7 +/- 5.7 nmol/l in controls, n = 14). After 30 min of reperfusion, arteriovenous MDA differences nearly reached control values (9.7 +/- 31.8 nmol/l, n = 7). In contrast to enhanced LPO, no significant conversion of XDH to XO was found (XO activity in controls: 23 +/- 1% of XO plus XDH activity vs. 26 +/- 3% after 45 min of ischemia, n = 7). Therefore XO-derived superoxide anion radicals cannot be considered causative for LPO in the reperfusion interval of experimental ischemic acute renal failure.

Protective effect of heme oxygenase induction in ischemic acute renal failure

2000 ◽  
Vol 28 (3) ◽  
pp. 809-817 ◽  
Author(s):  
Hiroko Shimizu ◽  
Toru Takahashi ◽  
Tsutomu Suzuki ◽  
Akira Yamasaki ◽  
Tadao Fujiwara ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Heme Oxygenase ◽  
Ischemic Acute Renal Failure

scholarly journals Protective effect of KB-R7943, a novel Na+/Ca2+ exchange inhibitor, on ischemic acute renal failure in rats

2000 ◽  
Vol 82 ◽  
pp. 70
Author(s):  
Junji Yamashita ◽  
Tosihiko Kuro ◽  
Makoto Itoh ◽  
Yutaka Kobayashi ◽  
Masanori Takaoka ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Exchange Inhibitor ◽  
Ischemic Acute Renal Failure

Enhanced skeletal muscle arteriolar reactivity to ANG II after recovery from ischemic acute renal failure

2005 ◽  
Vol 289 (6) ◽  
pp. R1770-R1776 ◽  
Author(s):  
David P. Basile ◽  
Deborah L. Donohoe ◽  
Shane A. Phillips ◽  
Jefferson C. Frisbee
Keyword(s):  
Skeletal Muscle ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Pressor Response ◽  
Gracilis Muscle ◽  
Ang Ii ◽  
Sprague Dawley

In addition to the long-term renal complications, previous studies suggested that after acute renal failure (ARF), rats manifest an increased pressor response to an overnight infusion of ANG II. The present study tested whether recovery from ARF results in alterations in sensitivity to the peripheral vasculature. ARF was induced in Sprague-Dawley rats by 45 min of bilateral renal ischemia and reperfusion. Animals were allowed to recover renal structure and function for 5–8 wk, after which the acute pressor responses to ANG II were evaluated either in vivo in in situ skeletal muscle arterioles or in isolated gracilis muscle arteries in vitro. Baseline arterial pressure was not different in ARF rats vs. sham-operated controls, although ARF rats exhibited an enhanced pressor response to bolus ANG II infusion compared with control rats. Steady-state plasma ANG II concentration and plasma renin activity were similar between ARF and control rats. Constrictor reactivity of in situ cremasteric arterioles from ARF rats was enhanced in response to increasing concentrations of ANG II; however, no difference was observed in arteriolar responses to elevated Po2, norepinephrine, acetylcholine, or sodium nitroprusside. Isolated gracilis muscle arteries from ARF rats also showed increased vasoconstriction in response to ANG II but not norepinephrine. In conclusion, recovery from ischemic ARF is not associated with hypertension but is associated with increased arteriolar constrictor reactivity to ANG II. Although the mechanisms of this altered responsiveness are unclear, such changes may relate, in part, to cardiovascular complications in patients with ARF and/or after renal transplant.

scholarly journals Protective effect of 17β-estradiol on ischemic acute renal failure through the PI3K/Akt/eNOS pathway

2008 ◽  
Vol 73 (3) ◽  
pp. 308-317 ◽  
Author(s):  
A. Satake ◽  
M. Takaoka ◽  
M. Nishikawa ◽  
M. Yuba ◽  
Y. Shibata ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
17Β Estradiol ◽  
Ischemic Acute Renal Failure

scholarly journals The protective effect of erythropoietin pretreatment on ischemic acute renal failure in rats

2016 ◽  
Vol 5 (5) ◽  
pp. 408-412 ◽  
Author(s):  
Jing-Guang Liao ◽  
Min-Yan Li ◽  
Xiao-Hua Wang ◽  
Qiang Xie
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Ischemic Acute Renal Failure

Effects of chitosan oligosaccharide (COS) on the glycerol-induced acute renal failure in vitro and in vivo

2008 ◽  
Vol 46 (2) ◽  
pp. 710-716 ◽  
Author(s):  
Hyun Joong Yoon ◽  
Myoung E. Moon ◽  
Haeng Soon Park ◽  
Hyun Woo Kim ◽  
Shun Young Im ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Chitosan Oligosaccharide
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