Renal vasoactive mediator generation in portal hypertensive and bile duct ligated rats

Ackerman, Zvi; Karmeli, Fanny; Amir, Gail; Rachmilewitz, Daniel

doi:10.1016/s0168-8278(96)80169-3

Cited by 19 publications

(14 citation statements)

References 40 publications

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“…Exacerbation of gentamicin nephrotoxicity by inhibition of PGE 2 generation (by aspirin) has also been described (25). On the other hand, it is also possible to speculate that gentamicin itself exacerbated the renal derangement already caused by the effects of chronic bile duct ligation (17,28).…”

Section: Discussionmentioning

confidence: 93%

“…Renal PGE 2 may play an important role in maintaining renal blood flow in patients with advanced liver disease, when the renin-angiotensin and sympathetic nervous systems are activated and there is increased intrarenal production and activity of vasospastic agents, like platelet activating factor, thromboxane B 2 and endothelin (17). Thus, it is possible to speculate that the derangement in PGE 2 generation already present in the BDL rats exposed them to increased gentamicin nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Bile duct ligation was induced as previously described (17). Briefly, under ketamine anesthesia (90 mg/kg intramuscularly (i.m.])…”

Section: Methodsmentioning

confidence: 99%

“…The tissue's capability to generate PGE 2 is expressed as ng/g wet tissue weight. PGE 2 was determined by a modification of the RIA previously reported (17). Briefly, 0.1 mL of the specific monoclonal anti-PGE 2 was added to either 0.1 mL of standard or tested solutions, followed by the addition of 0.1 mL of [ 3 H]-PGE 2 (4500-5500 cpm).…”

Section: Methodsmentioning

confidence: 99%

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Renal Effects of Gentamicin in Chronic Bile Duct Ligated Rats

et al. 2006

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Patients with advanced cirrhosis and rats with short-term bile duct ligation (BDL) are prone to develop nephrotoxicity from aminoglycosides. In this study, we characterized the renal response to gentamicin in rats with chronic BDL. BDL and sham-operated (SO) rats were given gentamicin (20 and 40 mg/kg/d) for 7 consecutive days, starting on the 18th postoperative day. Administration of gentamicin to SO group caused a decrease in cortical and medullary prostaglandin E(2)(PGE(2)) generation. However, mild reduction in creatinine clearance and an increase in fractional excretion of sodium occurred only in the BDL rats given the high gentamicin dose. This was accompanied by a reduction in cortical and medullary PGE(2) generation and a reduction in plasma nitric oxide production. In conclusion, gentamicin administration to rats with chronic BDL causes impairment of renal function. This happens only after the occurrence of simultaneous multiple insults to the renal protective mechanisms.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

“…Bile duct ligation was induced as previously described (17). Briefly, under ketamine anesthesia (90 mg/kg intramuscularly (i.m.])…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Renal Effects of Gentamicin in Chronic Bile Duct Ligated Rats

et al. 2006

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“…PGE 2 levels were determined in renal homogenates and in the gastric mucosa as previously reported [34, 35]. Animals were subjected to the nonsteroidal agents nabumetone (orally), 6-MNA, and indomethacin (intravenously) or their vehicles at the same dose and fashion used in the isolated kidney and hemodynamic studies.…”

Section: Methodsmentioning

confidence: 99%

Renal Effects of Nabumetone, a COX-2 Antagonist: Impairment of Function in Isolated Perfused Rat Kidneys Contrasts with Preserved Renal Function in vivo

Reichman¹,

Cohen²,

Goldfarb

et al. 2001

Nephron Exp Nephrol

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The constitutive cyclooxygenase (COX)-1 enzyme has been considered the physiologically important isoform for prostaglandin synthesis in the normal kidney. It has, therefore, been suggested that selective inhibitors of the ‘inducible’ isoform (COX-2) may be free from renal adverse effects. We studied the renal effects of the predominantly COX-2 antagonist nabumetone in isolated perfused kidneys. As compared with controls, kidneys removed after in vivo administration of oral nabumetone (15 mg/kg) disclosed altered renal function with reduced glomerular filtration rate, filtration fraction, and urine volume and enhanced hypoxic outer medullary tubular damage. By contrast, renal function and morphology were not affected in vivo by nabumetone or its active metabolite 6-methoxy-2-naphthylacetic acid. The latter agent (10–20 mg/kg i.v.) did not significantly alter renal microcirculation, as opposed to a selective substantial reduction in medullary blood flow noted with the nonselective COX inhibitor indomethacin (5 mg/kg i.v.). In a rat model of acute renal failure, induced by concomitant administration of radiocontrast, nitric oxide synthase, and COX inhibitors, the decline in kidney function and the extent of hypoxic medullary damage with oral nabumetone (80 mg/kg) were comparable to a control group, and significantly less than those induced by indomethacin. In rats subjected to daily oral nabumetone for 3 consecutive weeks, renal function and morphology were preserved as well. Both nabumetone and 6-methoxy-2-naphthylacetic acid reduced renal parenchymal prostaglandin E₂ to the same extent as indomethacin. It is concluded that while nabumetone adversely affects renal function and may intensify hypoxic medullary damage ex vivo, rat kidneys are not affected by this agent in vivo, both in acute and chronic studies. COX selectivity may not explain the renal safety of nabumetone.

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Increased expression of cystic fibrosis transmembrane conductance regulator in rat liver after common bile duct ligation

Shen

Fan

Yang

et al. 2004

Journal Cellular Physiology

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Liver disease associated with cystic fibrosis (CF) has been increasingly diagnosed and recognized as one of the major causes of death in CF during recent years. The autosomal-recessive disorder of CF results from mutation of the cystic fibrosis transmembrane conductance regulator (CFTR) that encodes the CFTR protein. Due to its existence and multifunction in biliary epithelial, over- or less-expression of CFTR in the liver may play an important role in the development of CF liver disease (CFLD). The aim of current study is to investigate the expression of CFTR in the liver of common bile duct ligated (BDL) rats. After BDL, there was an increase in the abundance of CFTR mRNA and protein. Immunohistochemical staining also demonstrated an increased intensity of CFTR staining in the liver tissue section. In conclusion, there is an increased expression of CFTR in the liver after common BDL.

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Renal vasoactive mediator generation in portal hypertensive and bile duct ligated rats

Cited by 19 publications

References 40 publications

Renal Effects of Gentamicin in Chronic Bile Duct Ligated Rats

Renal Effects of Gentamicin in Chronic Bile Duct Ligated Rats

Renal Effects of Nabumetone, a COX-2 Antagonist: Impairment of Function in Isolated Perfused Rat Kidneys Contrasts with Preserved Renal Function in vivo

Increased expression of cystic fibrosis transmembrane conductance regulator in rat liver after common bile duct ligation

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