Improved Renal Function Using Adenosine Triphosphate-Magnesium Chloride in Preservation of Canine Kidneys Subjected to Warm Ischemia

Lytton, Bernard; Vaisbort, Victor R.; Glazier, Wayne B.; Chaudry, Irshad H.; Baue, Arthur E.

doi:10.1097/00007890-198103000-00009

Cited by 20 publications

(7 citation statements)

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“…Recent studies have suggested many potentially determinants of ischemic injury including intracellular Ca 2+ accumulation [1], ATP depletion [2], activation of intrarenal adenosine [3], superoxide-induced membrane changes [4,5], and vasoactive factors. In accordance with these studies, several pharmacological agents including calcium channel blockers [6], ATP [7], theophylline [8], methylxanthines [9], oxygen free radical scavengers and antioxidants [10,11], and vasodilators [12] have been implicated as theoretically protective agents which may reduce the amount of tubular epithelial cell injury associated with renal isch-610 Am J Nephrol 1999;19:609-614 Ogawa/Mimura emia. The release of superoxide radicals in the process of renal I/R plays an important role in tissue damage [4,5].…”

Section: Introductionmentioning

confidence: 85%

Antioxidant Effect of Zinc on Acute Renal Failure Induced by Ischemia-Reperfusion Injury in Rats

Ogawa¹,

Mimura²

1999

Am J Nephrol

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Zinc may have an antioxidant effect mediated by induction of metallothionein. Based on the assumption that metallothionein can scavenge oxygen free radicals, we examined whether zinc administration prior to renal ischemia would improve renal dysfunction caused by ischemia-reperfusion injury in rats. Wistar rats weighing 265 g were treated with an intraperitoneal injection of 20 mg/kg zinc 24 h prior to the renal ischemia-reperfusion procedure, which was achieved by a 30-min clamping of the bilateral renal vessels and subsequent 90-min reperfusion. Thirty-minute renal clearance tests were performed before and after renal ischemia in zinc- (n = 11) and saline-treated (n = 8) rats. Thiobarbituric acid reactive substance, conjugated diene, and metallothionein levels in the renal tissues were also determined. Sham-operated rats (n = 5 in each treatment) served as control for the ischemia-reperfusion rats. Ischemia-reperfusion resulted in significantly lower glomerular filtration rate values and marked increases in tissue concentrations of thiobarbituric acid reactive substance and conjugated diene compared with sham-operation. Zinc administration improved the reduced glomerular filtration rate values seen after the ischemia-reperfusion procedure, but not to the extent of pre-ischemic levels. Zinc pretreatment significantly reduced the increased levels of thiobarbituric acid reactive substance and conjugated diene during ischemia-reperfusion and increased metallothionein levels compared with saline injection. These findings suggest that zinc has an antioxidant effect mediated through the induction of metallothionein, but appears only to have a minor protective effect on renal function induced by renal ischemia-reperfusion injury.

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Section: Introductionmentioning

confidence: 85%

Antioxidant Effect of Zinc on Acute Renal Failure Induced by Ischemia-Reperfusion Injury in Rats

Ogawa¹,

Mimura²

1999

Am J Nephrol

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“…Renal injury can arise as a consequence of ischemia and reperfusion during renal transplant surgery. Kidneys subjected to warm ischemia before transplantation are salvaged by addition of ATP-MgCl 2 to the perfusate (Lytton et al, 1981). The mechanism underlying the beneficial effects of ATP is still not clear, although several mechanisms have been proposed.…”

Section: Ischemiamentioning

confidence: 99%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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“…This result indicates that influx of the exogenous ATP into the cells after death occurs and makes up for the loss of endogenous ATP consumed by Na, K-ATPase. Lytton et al also reported that renal function after ischemia was improved by ATPMgCl2 perfusion (21).…”

Section: Resultsmentioning

confidence: 94%

Postmortem changes in the rat kidney. I. Histopathological, electron microscopical, and enzyme histochemical studies of postmortem changes at room temperature.

Itō

Ando

Mayahara

et al. 1991

Acta Histochem. Cytochem

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To get a better understanding of the factors that are related to the rapidity of the postmortem changes, we studied the postmortem changes in various parts of the nephron in the rat kidney at room temperature histopathologically, electron microscopically, and enzyme histo-and cytochemically. We found that the rapidity of the postmortem changes in the tubular epithelia of the rat kidney, at room temperature, is related to the intensity of cellular K-NPPase activity, that is the partial phosphatase activity of Na, KATPase. The postmortem changes, characterized by cytoplasmic vacuolization and karyopyknosis, in the epithelial cells in the distal tubule and the thick ascending limb of the loop of Henle (TAL) with intense KNPPase activity began earlier and progressed faster than those in the epithelia of the proximal tubules, macula densa and other parts of the nephron with low K-NPPase activity. These postmortem changes were delayed by flushing the kidney with PBS containing ouabain, ATP, verapamil, or EDTA. It is probable that the cells with intense ATPase activity tend to consume intracellular ATP faster than the cells with low ATPase activity after death, and the resulting lack of intracellular ATP and calcium ion influx cause various postmortem changes. On the other hand, the postmortem changes in the proximal tubules, with a large number of lysosomes, are slower and milder than those in the distal tubules and TAL at room temperature. Enzyme cytochemistry revealed hardly any signs of leakage of acid phosphatase, one of the lysosomal hydrolytic enzymes, up to at least 10 hr after death, during which time, the postmortem changes in the proximal tubules are slight and those in the distal tubules and TAL are severe.These results suggest that the rapidity of the postmortem changes in the rat kidney at room temperature depends mainly on the intensity of cellular Na, K-ATPase activity and that lysosomes do not participate in the cellular postmortem changes to a great extent until at least 10 hr after death.In the histopathological examination in toxicity studies using laboratory animals, it is important to differentiate postmortem changes from toxic changes caused by the test compound when animals are found dead during the dosing period. Thus, an attempt was made in our laboratory to obtain data on the postmortem changes in various organs and tissues. We studied histopathologically the postmortem changes in various organs and tissues at room temperature up to 20 hr after death in rats sacrificed by ether anesthesia (15). During the course of that study, we found that the rapidity of the postmortem changes in the rat kidney varies with the part of the nephron: at room temperature, epithelial cells in the distal tubules and the thick ascending limb of the loop of Henle show faster postmortem changes, which were characterized by cytoplasmic vacuolization and karyopyknosis, than do other parts of the nephron (16,23).In the present study, postmortem changes in the various parts of the nephron in the rat kidneys were studied...

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Improved Renal Function Using Adenosine Triphosphate-Magnesium Chloride in Preservation of Canine Kidneys Subjected to Warm Ischemia

Cited by 20 publications

References 0 publications

Antioxidant Effect of Zinc on Acute Renal Failure Induced by Ischemia-Reperfusion Injury in Rats

Antioxidant Effect of Zinc on Acute Renal Failure Induced by Ischemia-Reperfusion Injury in Rats

Purinergic Signaling and Blood Vessels in Health and Disease

Postmortem changes in the rat kidney. I. Histopathological, electron microscopical, and enzyme histochemical studies of postmortem changes at room temperature.

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