Protective Role of Furosemide and Saline in Radiocontrast-Induced Acute Renal Failure in the Rat

Heyman, Samuel N.; Brezis, M; Greenfeld, Ziv; Rosen, Seymour

doi:10.1016/s0272-6386(89)80171-4

Cited by 92 publications

(55 citation statements)

References 12 publications

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“…However, more recent studies indicate that hypoxia contributes significantly to the tubular damage induced also by various nephrotoxins, such as radiocontrast agents, myoglo- jpet.aspetjournals.org bin, hemoglobin, amphotericin B, and nonsteroidal antiinflammatory drugs (Rosenberger et al, 2006). Inhibitors of mTAL reabsorption reduce tubular damage, at least in some of these disorders, by improving medullary O 2 balance (Heyman et al, 1989).…”

Section: H 2 S and Renal Ischemia-reperfusion Injurymentioning

confidence: 99%

Hypoxia in the Renal Medulla: Implications for Hydrogen Sulfide Signaling

Bełtowski

2010

J Pharmacol Exp Ther

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Hydrogen sulfide (H 2 S) is enzymatically generated in mammalian tissues from either L-cysteine or L-homocysteine. H 2 S possesses multiple biological activities, including regulation of vascular tone and blood pressure. Hydrogen sulfide produced in endothelial cells, vascular smooth muscle cells, and perivascular adipose tissue dilates blood vessels by activating ATP-sensitive potassium channels. In addition, H 2 S produced locally within the kidney stimulates natriuresis and diuresis by increasing glomerular filtration and inhibiting tubular sodium reabsorption. Because H 2 S is oxidized in mitochondria in pO 2 -dependent manner and ambient pO 2 is physiologically low in the renal medulla, it is expected that the activity of H 2 S is higher in the medullary region than the cortical region. H 2 S, accumulating in increased amounts in the renal medulla under hypoxic conditions, may function as an oxygen sensor that restores O 2 balance by increasing medullary blood flow, reducing energy requirements for tubular transport, and directly inhibiting mitochondrial respiration. Hypoxia is an important pathogenic factor in many renal diseases, such as ischemia/reperfusion-or nephrotoxin-induced acute renal failure, progression of chronic nephropathies, diabetic nephropathy, and arterial hypertension. Deficiency of endogenous H 2 S may contribute to the pathogenesis of these pathologies by compromising medullary oxygenation, and administration of H 2 S donors may be of therapeutic value in these disorders.Studies performed during the last decade indicate that, apart from NO and CO, H 2 S is the third "gasotransmitter" involved in the regulation of various physiological functions, including vascular tone and blood pressure, inflammatory reaction, neurotransmission and gastrointestinal system function. H 2 S is enzymatically synthesized in three metabolic pathways (Fig. 1): 1) desulfhydration of L-cysteine or L-homocysteine by cystathionine ␥-lyase (CSE, EC 4.4.1.1), 2) desulfhydration of L-cysteine by cystathionine ␤-synthase (CBS, EC 4.2.1.22), and 3) transamination of L-cysteine by cysteine aminotransferase (identical with aspartate aminotransferase) to 3-mercaptopyruvate, followed by its desulfhydration to pyruvate by 3-mercaptopyruvate sulfurtransferase (3-MST, EC 2.8.1.2). Hydrogen sulfide activates ATP-sensitive potassium channels (K ATP ) in various cells, although many other signaling mechanisms have also been described. H 2 S is inactivated by binding to hemoglobin to form sulfhemoglobin, excretion in exhaled air, and, first and foremost, oxidation in mitochondria. Many studies addressed the role of H 2 S in the regulation of vascular tone and blood pressure. Indeed, it is suggested that H 2 S deficiency may contribute to the pathogenesis of arterial hypertension both in experimental animal models and in humans. Recently, renal synthesis and activity of H 2 S have been characterized (Xia et al., 2009). Because renal sodium handling has a prominent role in the long-term regulation of blood pressure (apart...

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Section: H 2 S and Renal Ischemia-reperfusion Injurymentioning

confidence: 99%

Hypoxia in the Renal Medulla: Implications for Hydrogen Sulfide Signaling

Bełtowski

2010

J Pharmacol Exp Ther

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“…[29] Several clinical and animal studies have been conducted using a number of active substances that behaved as metal-ion inactivators with the intention of aiding in the recovery of oxidative damage, scavenging free radicals, stimulating physiological enzymatic antioxidant systems, and protecting mitochondrial functions. [17,[30][31][32][33] It was presently understood that a closed, piston-activated compression model most accurately mimicked factors causing crush trauma in earthquakes. [20][21][22] In animal experiments with ischemia-reperfusion models, it was shown that disruption of circulation in the extremities increased muscle damage.…”

Section: Discussionmentioning

confidence: 99%

The effects of acetaminophen and mannitol on crush injuries in rats: Experimental study

Çelikmen

Sarıkaya

Özüçelik

et al. 2015

Ulus Travma Acil Cerrahi Derg

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“…Dehydration is a known risk factor for CMIN 66 . However, most recent studies have found it difficult to consider dehydration as an independent variable due to the strict hydration protocols used 9 .…”

Section: Other Risk Factorsmentioning

confidence: 99%

“…A study review totaling 476 subjects with this condition failed to confirm that 67 . It is possible that high risk is related to an underlying renal failure and/or volume depletion, resulting in increased intratubular deposition of filtered light chains 66,67 .…”

Section: Other Risk Factorsmentioning

confidence: 99%