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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal metabolism has been studied in eight dogs before and 48 hr after a 60-min period of renal ischemia induced by clamping the left renal artery with the simultaneous removal of the right kidney, and in 12 sham-operated animals. The study involved the measurement of renal uptake and production of lactate, glutamine, glutamate, alanine, ammonium, and oxygen, and the measurement of the tissue concentrations of ATP, glutamine, lactate, alpha-ketoglutarate, aspartate, and alanine in the renal cortex. Two days after a temporary renal ischemia, the remaining kidney showed a 22% decrease in glomerular filtration rate (GFR) and a 25% decrease in renal plasma flow. Fractional sodium and potassium excretions were similar to those of control dogs. Renal production or extraction of glutamine, glutamate, alanine, ammonium, and oxygen (all expressed by 100 ml of GFR) was not significantly different in basal conditions or 2 days after ischemia, but lactate extraction was reduced in postischemic kidneys (-101 +/- 29 vs -204 +/- 38 mumol/100 ml GFR in control dogs). The cortical concentrations of glutamine and glutamate were lower in postischemic than in control kidneys. No differences were found in cortical concentration of alpha-ketoglutarate, aspartate, lactate, pyruvate, or ATP, but total nucleotides and inorganic phosphate were decreased in postischemic kidneys. It is concluded that in the recovery phase of the ischemia, a decreased lactate uptake is the main metabolic change, and total ATP production is adapted to the decrease of GFR and sodium reabsorption.
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PMID:Renal cortical intermediary metabolism in the recovery phase of postischemic acute renal failure in the dog. 153 34

Content of adenine nucleotides, lactic and pyruvic acids, glucose and fructose-6-phosphate was studied in kidney of rats with hemorrhage constituting 3% of body mass after intravenous administration at a dose of 100 mg/kg of agonists of mu-opiate receptors DAGO and delta-opiate receptors DADL and dalargin. Stimulation of both these types of receptors amplifies the kidney ischemia developed after hemorrhage, which was expressed as increased decomposition of ATP, decrease in energetic charge of the adenine nucleotide system (DAGO) and increase in content of AMP (DADL, dalargin).
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PMID:[The negative effect of enkephalins on kidney energetics in rats with hemorrhages]. 165 73

The effect of atrial natriuretic polypeptide (ANP) on hemodynamics and renal function was evaluated after the reconstructive surgery of the left renal artery in a patient with renovascular hypertension secondary to Takayasu's arteritis. The reconstructive surgery was done using the femoral artery, since we were unable to obtain adequate vein segments to fit the renal artery. The femoral artery was reconstructed by her saphenous vein segments. After 30 min of the aortorenal bypass operation, alpha-human ANP (alpha-hANP) was infused intravenously for 10 min at a rate of 0.1 microgram/kg/min. Although total peripheral resistance was decreased by alpha-hANP infusion, blood pressure was not changed because of the increased cardiac output. Glomerular filtration rate was increased markedly with concomitant increase in urine volume and urinary excretions of sodium, potassium and phosphate. Fractional excretions of water and sodium were not changed, but fractional excretion of phosphate and potassium clearance were increased. Thus, the infusion of alpha-hANP markedly improved the renal function of the ischemic kidney by the reconstructive surgery of the renal artery, suggesting that alpha-hANP seems clinically applicable as a protective agent in renal ischemia at renovascular surgery as well as the renal transplantation.
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PMID:Atrial natriuretic polypeptide (ANP) as protective agent of renal ischemia. 253 78

Noninvasive investigation of renal metabolic changes is possible with 31P-MR, which is characterized by the determination of amounts of "free" phosphorus metabolites and intracellular pH and the possibility of measuring enzyme kinetics by the 31P-MR magnetization transfer method. 31P-MR has been extensively used to monitor such alterations in response to kidney ischemia, in which the ratios of anorganic phosphate to ATP and phosphomonoesters change drastically. The stages of ultrastructural ischemic renal damage can already be accurately classified with reference to a scale of 31P-MR-spectrum-derived renal function predictors. The recent application of MR high-resolution imaging may allow further improvement of organ viability assessment. The clinical use of combined MR imaging and spectroscopy is an essential and imminent step.
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PMID:[31-phosphorus magnetic resonance spectroscopy--a new research instrument in urology. Determination of current status and outlook for clinical use]. 266 5

We used high-resolution phosphate 31(31P)--nuclear magnetic resonance spectroscopy to study the effects of ischemia and reperfusion on intracellular adenosine triphosphate (ATP) and pH changes in isolated perfused rat kidneys. With renal ischemia, ATP levels fell rapidly and the inorganic phosphate (Pi) peak shifted, indicating acidosis. On reperfusion after 45 minutes of warm ischemia, there was a 56% rise in tissue ATP levels within ten minutes that then slowly declined; by 75 minutes the levels were only 33% of normal. Perfusate flow decreased from 21.2 +/- 0.9 mL/min (mean +/- SE) to 16.5 +/- 1.1 mL/min and the Pi peak did not shift during reperfusion. When 0.3mM ATP complexed to magnesium chloride (ATP-MgCl2) was added to the perfusate after ischemia, renal ATP levels increased to 69% of normal within ten minutes of reperfusion and by 75 minutes they were normal. Perfusate flow was also normal during reperfusion. The Pi peak shifted back to the normal frequency, indicating correction of the intracellular acidosis. Thus, intracellular acidosis, ATP depletion, and decreased flow during reperfusion injury were rapidly reversed and sustained by the postischemic administration of ATP-MgCl2.
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PMID:Adenosine triphosphate--magnesium chloride ameliorates reperfusion injury following ischemia as determined by phosphorus nuclear magnetic resonance. 387 13

The postischemic infusion of ATP-MgCl2 will enhance the recovery of both glomerular and tubular function. To assess the effect of ATP-MgCl2 on tissue nucleotides, 31P nuclear magnetic resonance (31P-NMR) spectra were obtained continuously in vivo from the left kidney of rats that had been subjected to 45 min of renal ischemia and then infused with either normal saline or ATP-MgCl2. 31P-NMR spectra with distinct peaks for alpha-, beta-, and gamma-phosphate of ATP, sugar phosphate, and inorganic phosphate were collected every 7 min before, during, and after renal artery occlusion. During ischemia, the ATP beta-peak (the only peak unique to ATP) fell rapidly to 10% of control values in both groups of animals. By 120 min after the ischemic insult, the animals treated with ATP-MgCl2 had recovery of renal ATP to 89 +/- 2.6%, which is significantly greater (P less than 0.001) than 65.2 +/- 1.8% found in rats given normal saline. These data indicate that 1) 31P-NMR can be used to assess renal ATP levels continuously in vivo; 2) during renal ischemia ATP levels fall quickly to less than 10% of control values; 3) tissue ATP returns relatively slowly to control values in rats given normal saline, whereas postischemic treatment with ATP-MgCl2 results in an accelerated recovery of tissue ATP levels. These findings provide a biochemical correlate to the improvement in renal function previously described.
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PMID:Enhanced recovery of renal ATP with postischemic infusion of ATP-MgCl2 determined by 31P-NMR. 660 93

Experiments on albino rats have shown that kidney ischemia and its simulation by the anaerobic incubation of postmitochondrial kidney homogenate fraction without a substrate induce a considerable damage of the glycolytic system at the stage of the glucoso-6-phosphate transformation into fructoso-1.6-diphosphate and a less pronounced damage in the fructoso-1.6-diphosphate transformation into lactate. Administration of adenosine diphosphate (ADP) and nicotinamide adenine dinucleotide (NAD) to rats before kidney vessel occlusion or their addition to the postmitochondrial fraction before the anaerobic incubation without a substrate decreased a degree of the glycolytic system damage. The damage of the glycolytic system and protective action of NAD are also detected under simulation of liver ischemia. Possible mechanisms of the ischemic damage in the glycolytic liver and kidney tissue system are discussed.
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PMID:[Effect of NAD and ADP on glycolysis in the kidneys and liver of rats during ischemia]. 671 Jun 14

Postischemic thyroxin (T4) enhances restitution of cellular ATP and accelerates recovery of renal function. This effect is not related to global improvement in cell integrity. To determine the mechanism by which recovery of cellular ATP is enhanced, the effect of T4 on mitochondrial ATP production was evaluated using specific inhibitor stop assays for mitochondrial phosphate transport and ADP translocator activity. Rats were subjected to 45-min renal ischemia and given normal saline (NS, 0.5 ml) or T4 (20 micrograms/kg) during the reflow period. By 30-min reflow; the values for apparent endpoint of phosphate transport (PiTm, nmol Pi/mg mitochondrial protein) had recovered to rates seen in nonischemic animals (10.3 +/- 0.9) and remained stable at 120 min. T4 treatment did not affect PiTm. In contrast, the apparent endpoint of ADP transport (ADPTm, nmol ADP/mg mitochondrial protein) was dramatically decreased in NS rats at 30-min (6.7 +/- 0.5) and 120-min (13.7 +/- 1.0) reflow compared with nonischemic control rats (24.7 +/- 2.4). T4 significantly improved ADPTm by 30 min (10.1 +/- 0.6, P < 0.05). By 120 min T4 stimulated ADPTm (37.7 +/- 5.2, P < 0.05) to exceed nonischemic control values. These data suggest the following: 1) postischemic mitochondrial PiTm recovers to control values by 30 min of reflow; 2) T4 does not augment PiTm; 3) renal ischemia causes a dramatic decrease in mitochondrial ADPTm; 4) postischemic T4 significantly enhances mitochondrial nucleotide transport at 30-min reflow; 5) by 120-min reflow, T4 rats have ADPTm which exceeds control values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postischemic thyroxin stimulates renal mitochondrial adenine nucleotide translocator activity. 773 9

We evaluated, in renal epithelial cells with a proximal tubule phenotype, the effect of nitric oxide (NO) on ecto-5 -nucleotidase (5'-N U), the underlying mechanism and its functional consequence. Sodium nitroprusside (SNP, 1-1000 microM), a NO donor, inhibited 5'-NU activity in a time- and concentration-dependent manner. Consequently, NO blunted the inhibition by extracellular cyclic AMP (cAMP, 10-1000 microM) of sodium-phosphate cotransport, a pathway which involves degradation of adenosine monophosphate (AMP) by 5'-NU. SNP-induced inhibition of 5'-NU was not mediated by cyclic GMP, since it was not mimicked by atrial natriuretic peptide, and was reproduced by isosorbide dinitrate and sodium nitrate, two NO donors. SNP and genuine NO decreased the activity of 5'-NU in renal homogenates, and the effect of SNP was potentiated by dithiothreitol and glutathione, but not by nicotinamide adenine dinucleotide. In vivo in rats, kidney ischemia/reperfusion, which activates inducible NO-synthase, inhibited renal 5'-NU. This inhibition was prevented by Nomega-nitro-L-arginine methyl ester, a NO-synthase inhibitor. These results indicate that: (i) NO-related activity inhibited the activity of an ecto-enzyme, 5'-NU, most likely through S-nitrosylation of the enzyme; (ii) inhibition of 5'-NU activity by NOx, which can occur in vivo under pathophysiological conditions, affected the extent to which extracellular cAMP inhibited sodium-Pi cotransport.
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PMID:Inhibition of ecto-5'-nucleotidase by nitric oxide donors. Implications in renal epithelial cells. 861 29

In vivo administration of low doses of lipopolysaccharide (LPS) to rodents can protect these animals from subsequently administrated, usually lethal doses of endotoxin or LPS. In this study we tested the effects of LPS pretreatment on ischemia/reperfusion injury in the kidney. Male C57/B1 mice were pretreated with different doses of LPS or phosphate-buffered saline on days -4 and -3. The right kidney was removed, and the vessels of the left kidney were clamped for 30 or 45 minutes on day 0. Creatinine levels and survival of animals were monitored. To test the involvement of cytokines, additional animals were harvested before ("time 0") and 15 minutes, 1, 2, 8, and 16 hours after reperfusion for histology, immunohistochemistry, terminal deoxynucleotidyltransferase-mediated UTP end-labeling assay, and reverse transcriptase-polymerase chain reaction analysis (including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, IL-6, inducible nitric oxide synthase (iNOS), and interferon (IFN)-gamma messenger RNA (mRNA)). In controls, renal ischemia of 30 minutes was nonlethal, whereas 73% of the animals died within 48 +/- 18 hours, after 45 minutes of ischemia. All different doses of LPS protected the animals from lethal renal ischemia/reperfusion injury. Starting at similar levels, serum creatinine increased significantly in controls but not in LPS-pretreated animals over time. As early as 2 hours after reperfusion, tubular cell damage was significantly more pronounced in controls than in LPS-treated mice. In controls, tubules deteriorated progressively until 8 hours of reperfusion. At this time, more than 50% of tubular cells were destroyed. This destruction was accompanied by a pronounced leukocytic infiltration, predominantly by macrophages. In contrast, LPS pretreatment prevented the destruction of kidney tissue and infiltration by leukocytes. The terminal deoxynucleotidyltransferase-mediated UTP end-labeling assay revealed significantly more apoptotic cells in controls compared with LPS-pretreated animals. IL-1, IFN-gamma, and iNOS mRNA expression did not differ between the groups throughout the time points examined. However, the expression of TNF-alpha mRNA was significantly increased at 2 hours and IL-6 mRNA was significantly down-regulated before ischemia and shortly after reperfusion in the LPS-pretreated kidneys. Therefore, we found that sublethal doses of LPS induced cross-tolerance to renal ischemia/reperfusion injury. Our data suggest that increased TNF-alpha and reduced IL-6 mRNA expression might be responsible. However, more studies are needed to decipher the exact mechanism.
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PMID:Lipopolysaccharide pretreatment protects from renal ischemia/reperfusion injury : possible connection to an interleukin-6-dependent pathway. 1062 77


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