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

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

Intermediary metabolism has been studied in a viable suspension of renal proximal tubules isolated from dogs before and after 48 h of a 60 min period of renal ischemia by clamping the renal artery. The study consisted in measurements of tubular uptake/production of glucose, lactate, glutamine, glutamate, alpha-ketoglutarate, alanine, ammonium, and oxygen, using as substrates either glutamine 1 or 5 mM (+ glutamate 0.1 or 0.5 mM) or lactate 1 or 5 mM (+ pyruvate 0.1 or 0.5 mM). The combination of glutamine + lactate was also studied. Data revealed that the gluconeogenic ability of the postischemic tubules was maintained, with the exception of glutamine 5 mM as substrate (8.5 +/- 2.1 vs 15.4 +/- 2.1 mumol/min/g in control tubules). The production of NH4 was also decreased only with this substrate (from 214 +/- 15 to 165 +/- 9 mumol/min/g). Lactate extraction was decreased in the postischemic tubules, but the difference was only significant when lactate + glutamine 1 mM was used as substrate (72 +/- 12 vs 44 +/- 6 mumol/g/min). Postischemic tubules showed a greater oxygen consumption when either glutamine or lactate 1 mM were used, but lower ouabain-inhibitable O2 consumption when these substrates were used at 5 mM. These data revealed a modification of the metabolic profile of proximal tubules during the recovery of transient renal ischemia.
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PMID:Intermediary metabolism in renal proximal tubules in the recovery phase of experimental renal ischemia in dogs. 168 89

Water soluble ionic contrast media (CM) and glucose 5% were administered to Sprague-Dawley rats 36 hours after bilateral warm renal ischemia for 45 min. In all animals (n = 28) the renal ischemia caused a decrease of the absolute urinary creatinine output. Intra-arterial injection of glucose 5% or CM did not produce different patterns of absolute urinary creatinine output. The serum creatinine increased after 36 hours of reflow. When compared by means of a Mann-Whitney U-test to a normal median serum creatinine obtained in a separate group of 22 normal rats, the increase was statistically significant (p less than or equal to 0.01). The serum creatinine medians returned to a normal level after 24 hours. It seems therefore that 45 min of warm renal ischemia and 36 hours of reflow is an insufficient challenge to the rat kidney for the detection of the nephrotoxic properties of CM as opposed to when CM are injected during ischemia.
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PMID:Absence of functional renal effects of uro-angiographic contrast media on post-ischemic rat kidneys. 186 6

Intravenous doses of 92.6 and 185.2 mumol S-(1,2-dichlorovinyl)-D-cysteine (D-DCVC)/kg were acutely nephrotoxic in pentobarbital-anesthetized dogs. During the 6-h period following administration of either dose, renal arterial blood flow decreased modestly, urinary excretion rate of protein increased, and in contrast to findings in rabbits, ultrastructural lesions developed only in S1 and S2 cells of proximal tubules. The higher dose also induced significant increases in urine flow rate and urinary excretion rate of glucose. The adverse changes noted following the low dose of D-DCVC were due to its direct renal actions and not to extrarenal actions such as major changes in blood gases, total renal blood flow or mean arterial blood pressure that could have indirectly contributed to renal damage via induction of episodes of renal ischemia or hypoxia. In addition, there was a correlation between the proximal tubular cell types injured by D-DCVC and the location of D-amino acid oxidase (DAAO) in the canine nephron. Overall, the nephrotoxicity of D-DCVC was characterized by the same renal function and ultrastructure changes as noted previously with L-DCVC, but the D-isomer was slightly less potent. Our data suggested that the similarity in the toxicity of D- and L-DCVC might be related to DAAO-catalyzed conversion of D-DCVC to the corresponding alpha-ketoacid (DCV-O-MPA) and subsequent biotransformation of the latter to the same highly reactive fragment as generated from the L-isomer.
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PMID:Acute effects of the D-isomer of S-(1,2-dichlorovinyl)cysteine on renal function and ultrastructure in the pentobarbital-anesthetized dog: site-specific toxicity involving the S1 and S2 cells of the proximal tubule. 194 44

Hyperglycemia worsens ischemic injury in several ischemic models. To determine whether renal lactate accumulation was associated with hyperglycemia-exacerbated postischemic renal dysfunction and mortality, halothane-anesthetized rats underwent right nephrectomy and 45 min of left renal artery and vein occlusion. Prior to ischemia, rats received saline (n = 22), glucose (2 g/kg, n = 22), or insulin (4 U/kg, n = 18). Sham-operated glucose-treated rats (2 g/kg, n = 4) underwent right nephrectomy and no vascular occlusion. As anticipated, glucose pretreatment elevated plasma glucose, while insulin pretreatment lowered plasma glucose; both were significantly different from values in saline controls. Creatinine was unchanged in sham-operated rats but was significantly higher in glucose-treated rats at 24 and 48 hr postischemia compared to saline controls. No statistical differences in creatinine were found when comparing saline controls to insulin-treated rats. Eighteen percent of glucose-treated rats survived to 72 hr postocclusion, while 45% of insulin-treated rats, 73% of saline control rats, and 100% of sham-operated rats survived this period. In a separate but identical treatment protocol, renal tissue was serially sampled and lactate content was determined in rats pretreated with saline (n = 7), glucose (n = 6) or insulin (n = 6) or sham-operated (n = 2) and receiving identical operation. Tissue lactate concentration did not change during serial sampling in the sham group. During ischemia, lactate was significantly higher in glucose-treated rats and significantly lower in insulin-treated rats as compared to saline controls. The adverse effects of exogenous glucose and attendant hyperglycemia on renal function during normothermic renal ischemia are demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperglycemia exacerbates and insulin fails to protect in acute renal ischemia in the rat. 265 96

To determine if moderate hyperglycemia produced by dextrose administration was detrimental in normothermic renal ischemia, 15 halothane-anesthetized mongrel dogs underwent right nephrectomy and 60 minutes of left renal artery and vein occlusion. Six dogs received 1 L of lactated Ringer's solution (LR) and six others received 1 L of 5% dextrose in lactated Ringer's solution (D5LR). Three sham-operated dogs received 1 L of D5LR and underwent right nephrectomy but no occlusions. All dogs received 500 mL of fluid before occlusion and 500 mL after occlusion. The blood glucose concentration for the LR group was 7.6 mmol/L (137 mg/dL) after 500 mL and 7.2 mmol/L (130 mg/dL) after 1000 mL. In the D5LR group, the blood glucose concentration was 21.5 mmol/L (387 mg/dL) after 500 mL and 20.2 mmol/L (363 mg/dL) after 1000 mL. In the sham-operated group, the blood glucose concentration was 22.8 mmol/L (410 mg/dL) after 500 mL and 20.7 mmol/L (373 mg/dL) after 1000 mL. At 30 hours, the plasma creatinine concentration rose from 70 to 300 mumol/L (0.8 to 3.4 mg/dL) in the LR group and from 90 to 500 mumol/L (1.0 to 5.8 mg/dL) in the D5LR group; the increase for the D5LR group was significantly greater than that for the LR group. In the sham-operated group, the plasma creatinine concentration was stable throughout the 30-hour period. This study demonstrates a significant detrimental effect of dextrose administration on renal function during normothermic ischemia.
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PMID:Dextrose administration exacerbates acute renal ischemic damage in anesthetized dogs. 359 69

In 12 dogs anesthetized with chloralose, angiotensin (angiotensin II amide) given intravenously increased the glomerular filtration rate (GFR) of an ischemic kidney while simultaneously having little effect on the GFR of the contralateral kidney. In the ischemic kidney, in 14 of 30 observations, increments of GFR greater than 100% of mean control GFR (9 ml/min) occurred in response to angiotensin. The magnitude of the increase in GFR produced by angiotensin was independent of dose (range 0.005-0.050 mug/kg per min), the degree of accompanying pressor response, and alterations in renal blood flow (RBF) (electromagnetic flow-meter). In the ischemic kidney, increments of GFR could be produced by sub-pressor doses of angiotensin. Dissociations between increments of GFR and sodium excretion occurred. Equivalent increments of GFR in the ischemic kidney in dogs receiving either 5% glucose in water or 10% mannitol in 0.3% saline were associated with natriuresis only in the latter group: a) as an initial response of the contralateral kidney to renal arterial constriction (RAC) in spite of a concomitant reduction in RBF and an unchanged GFR; b) in the ischemic kidney on giving angiotensin. The natriuresis produced by angiotensin was independent of the magnitude of elevations in blood pressure, altered filtration fraction, and was associated with a further reduction in RBF. After release of RAC in the dogs receiving mannitol, an antinatriuresis was again observed in response to angiotensin. The presence of unilateral renal ischemia allowed the demonstration of a differential action of angiotensin on the GFR of an ischemic and nonischemic kidney. The natriuresis in response to angiotensin requires, in addition to mannitol, the participation of undefined factors invoked by unilateral renal ischemia.
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PMID:Some determinants of the effects of VAL-5-angiotensin II amide on glomerular filtration rate and sodium excretion in dogs. 430 89

Atrial natriuretic factor (ANF) has been demonstrated to be effective in the treatment of acute renal failure (ARF) in both rat and humans. The biological effects of ANF are presumed to be mediated by the generation of intracellular 3',5'-cyclic guanosine monophosphate (cGMP). Therefore, the current investigation examined whether zaprinast (M&B 22948), a guanosine 3',5'-cyclic monophosphate (cGMP)-specific phosphodiesterase inhibitor, would be effective in the treatment of established acute renal failure in the rat. Acute renal failure was induced by 60 minutes of bilateral renal artery clamping. Twenty-four hours after the ischemic insult, rats received either vehicle (5% Dextrose), zaprinast (0.03 or 0.3 mg/kg/min) or ANF24 (0.2 micrograms/kg/min) intravenously for four hours. Renal function, as measured by daily serum creatinine (days 1 to 7) and day 2 inulin clearances, was dramatically improved by zaprinast but not ANF treatment. Forty-eight hours post-renal ischemia, glomerular filtration rate (GFR) was 0.14 +/- 0.04 (ml/min/100 g body wt) in the vehicle and 0.94 +/- 0.29 in the zaprinast treated animals. To evaluate the mechanism by which zaprinast accelerated renal recovery, we measured regional blood flow in the postischemic rat kidneys during drug treatment with a laser doppler flowmeter. Both high and low dose zaprinast significantly increased cortical (17%) and outer medullary blood flow (40% and 60%), an effect not seen with ANF. In summary, zaprinast is effective in the treatment of established ischemic ARF. The mechanism by which zaprinast accelerates renal recovery is due to its unique ability to stimulate regional renal blood flow and increase intracellular cGMP in the setting of tissue ischemia.
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PMID:Zaprinast accelerates recovery from established acute renal failure in the rat. 764 25

Endocytosis in the renal tubular cell is a permanent process serving the role of saving nitrogen from plasma peptides that are continuously cleared away by kidney glomerulus. Since small proteins appear in urine after strenuous exercise, it was hypothesized that renal ischemia impairs the tubular endocytic reabsorption of proteins. The aim of this paper is to describe a simple in vitro model of renal endocytosis and to use it in studies of endocytic metabolic requirements. The results show that rabbit renal proximal tubules in suspension are able to take up 125I-lysozyme, as well as RITC-lactalbumin. The fluorescent protein was taken up only by the ends of the everted tubule fragments, and accumulated into intracellular vesicles, demonstrating the luminal pathway of endocytosis. The amount of 125I-lysozyme taken up was equivalent to that taken up by isolated perfused tubules (Nielsen et al. (1986) Am. J. Physiol. 251, F822-F830). Anoxia decreased 12-fold the intracellular accumulation of 125I-lysozyme; however, the time-course of inhibition shows that only the late steps of endocytic accumulation are energy-dependent. Substrate deprivation studies suggest a specific role of glucose to sustain endocytosis. Lastly, renal uptake of 125I-lysozyme was shown to be strongly depressed by chloroquine, an alkalinizing agent of endosomes and lysosomes. We conclude that (1) renal tubules in suspension are a satisfactory model for endocytic studies in kidney; (2) suppressing oxygen and substrate supplies to kidney impairs endocytic tubular reabsorption of proteins.
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PMID:Protein endocytosis by a kidney tubule suspension: metabolic requirements. 829 19

The 72-kDa heat stress protein (HSP-72) is an inducible cytoprotectant protein. Although transient renal ischemia in vivo induces HSP-72, it is not known whether prior heat stress protects renal epithelial cells from injury mediated by ATP depletion. To evaluate this hypothesis, opossum kidney (OK) cells were exposed to sodium cyanide and 2-deoxy-D-glucose in the absence of medium glucose, a maneuver that reduced cell ATP content to < 10% of the control value within 10 min and decreased cell survival. One day after 2 h of ATP depletion, OK cells previously exposed to heat stress (to induce accumulation of HSP-72) exhibited marked improvement in survival (a > 4-fold increase in total DNA), less uptake of vital dye, and less release of lactate dehydrogenase (LDH) than cells subjected to ATP depletion alone (23.0 +/- 1.6 vs. 34.1 +/- 1.2% of total LDH, respectively). Enhanced clonogenicity post-heat stress was completely prevented by cycloheximide and positively correlated with the steady-state content of HSP-72. In the recovery period after ATP depletion, cell ATP content, maximum mitochondrial ATP production rate, and total LDH activity were all significantly higher in cells with abundant HSP-72. Although the protective effects associated with heat stress are likely to be multifactoral, preserved cell metabolism and higher ATP content could enhance cellular repair processes after ATP depletion.
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PMID:Prior heat stress enhances survival of renal epithelial cells after ATP depletion. 876 25


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