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

The ability of prostaglandins to protect the kidney against ischemic and toxic renal injury was evaluated by in vivo and in vitro models of renal ischemia. The prostaglandin E1 analogue, misoprostol, was found to provide significant protection against ischemia-induced renal dysfunction in rats subjected to 40 minutes of renal artery occlusion. Misoprostol-treated rats had glomerular filtration rates almost threefold greater than control animals, although renal blood flow and renal vascular resistance were not significantly different. Improved tubular function was reflected in a lower fractional excretion of sodium and a higher urine-to-plasma creatinine ratio. Misoprostol also provided similar protection in a model of toxic renal injury produced by mercuric chloride. In an in vitro model employing primary cultures of proximal tubule epithelial cells subjected to hypoxia and reoxygenation, misoprostol limited cell death. Posthypoxic cells had apical membrane disruption and loss of microvilli when examined by transmission electron microscopy. These changes were not seen in misoprostol-treated cells. The "cytoprotective" effect was also produced by prostaglandin E2 and prostacyclin. The ability of prostaglandin E to protect against toxic and ischemic renal injury did not appear to be due to an antioxidant effect because misoprostol did not limit lipid peroxidation in vivo and did not protect against oxidant injury by tert-butyl hydroperoxide in vitro. Although the exact mechanism of prostaglandin protection was not revealed, these studies demonstrate that prostaglandins protect renal tubule epithelial cells from hypoxic injury at the cellular level independent of hemodynamic factors or inflammatory responses. Such a "cytoprotective" effect of prostaglandins may be a generalized phenomenon since it has also been demonstrated in gastrointestinal epithelium.
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PMID:Prostaglandins protect kidneys against ischemic and toxic injury by a cellular effect. 147 66

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

Renal ammoniagenesis has been studied in 6 dogs before and 48 h after a 60-min period of renal ischemia induced by clamping the renal artery and in 6 sham-operated animals. Two days after temporary renal ischemia, the dogs showed a 25% decrease in glomerular filtration rate and renal plasma flow and a similar decrease in sodium reabsorption. Renal production of ammonium was not significantly different under basal conditions or 2 days after ischemia, but more ammonia was released by the urine in the postischemic dogs. Renal uptake of glutamine was similar in control and in postischemic kidneys. It is concluded that during the recovery phase of the ischemia, renal ammoniagenesis is conserved.
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PMID:Renal ammoniagenesis during the recovery phase of postischemic acute renal failure in the dog. 169 87

The recovery of renal function following renal ischemia was studied using rats fed for 1-, 3-, and 5-week periods with an alcoholic diet (ethanol provided 36% of total calories). Renal ischemia was produced by clamping the renal artery and vein for 20 min. Renal function was determined 24 hr after the ischemia. In the absence of ischemic insult, the renal function of rats fed with an alcoholic diet for 1, 3, and 5 weeks was not significantly different from those of nonalcoholic rats. In nonalcoholic rats, renal function (24 hr postischemia) were: glomerular filtration rate (GFR) 430.4 +/- 29.6 microliters/min/g KW (kidney weight), renal plasma flow rate (RPFR) 1.4 +/- 0.17 ml/min/g KW, and fractional sodium excretion (FENa) 2.0 +/- 0.04% (mean +/- SE). Postischemic renal function of rats on 1- and 3-week alcoholic diets were essentially the same as that of the control rats. However, the 24-hr postischemic renal function of 5-week alcoholic diet rats was significantly depressed. The values were only 117.2 +/- 35.2 microliters/min/g KW (p less than 0.05) for GFR, 0.31 +/- 0.12 ml/min/g KW (p less than 0.05) for RPFR, and 7.46 +/- 3.59% for FENa. The present results demonstrate that the rat kidney subjected to prolonged alcohol ingestion was more susceptible to renal insult than a nonalcoholic kidney.
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PMID:Chronic alcoholism impedes the recovery of renal function following renal ischemia. 175 5

Thirty-eight recipients of nineteen pairs of cadaveric kidneys were entered into a double-blind randomized study in which one recipient received a 12-hour intravenous infusion of Atriopeptin III (AP-3), a synthetic analogue of atrial natriuretic factor, commencing at release of the vascular clamps, and the other received a placebo infusion. In an initial dose ranging study, successive groups of six kidneys (3 pairs) were randomized to receive each of 0.0125, 0.025, 0.05 micrograms/kg/min AP-3 or placebo. Thereafter 20 kidneys (10 pairs) received 0.1 micrograms/kg/min or placebo. There was no discernable effect of AP-3 on allograft creatinine clearance or sodium excretion either when the highest dose of AP-3 was considered alone or when all doses were considered together. Averaged creatinine clearance over the period 0 to 24 hours after transplantation was 20.1 +/- 14.7 ml/min in patients receiving active treatment and 18.2 +/- 13.7 ml/min in those receiving placebo. Thus, despite the documentation of a protective effect of atrial natriuretic factor in animal models of renal ischemia, it is unlikely that intravenous infusion of AP-3 in this dose range will be of benefit in improving immediate renal allograft graft function.
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PMID:Effect of intravenous infusion of atriopeptin 3 on immediate renal allograft function. 182 57

The following study was performed to determine whether calcium channel blockers, delivered before or after an ischemic insult, were effective at reducing cyclosporine-induced exacerbation of renal ischemic injury. When cyclosporine (5 mg/kg) was administered intravenously to rats after 30 min of renal ischemia, GFR fell by 60% compared with values observed in rats subjected to ischemia alone (190 +/- 30 vs. 330 +/- 40 microliters/min/100 g; P less than 0.05). Pretreatment with verapamil (10 micrograms/kg/min delivered intravenously) prevented the fall in GFR (320 +/- 70 microliters/min 100 g), as did pretreatment with nitrendipine, 1 micrograms/kg/min (460 +/- 90 microliters/min/100 g). Verapamil was less effective if given after the ischemia-cyclosporine insult (GFR 260 +/- 90 microliters/min/100 g), and nitrendipine given at this time had no beneficial effect at all (GFR 180 +/- 10 microliters/min/100 g). The doses of calcium channel blockers used had no protective effect on renal ischemic injury alone. Blood pressure during study ranged between 105 and 119 mm Hg with minor differences between groups. Sodium and potassium excretion and urinary flow rates were similar in all groups, except for a slight increase in sodium excretion in verapamil-treated rats. These values demonstrate that calcium channel blockers ameliorate the exacerbation or renal ischemic injury induced by cyclosporine if given before but not after the ischemia-cyclosporine insult. The protective effect of these agents, used preischemia in cyclosporine-treated rats, is observed with intravenous use of the drugs at doses that have no protective effect on renal ischemic injury alone.
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PMID:Evidence that calcium channel blockade prevents cyclosporine-induced exacerbation of renal ischemic injury. 184 48

The effects of stimulation of renal mechano- and chemoreceptors on the afferent renal nerve activity (ARNA) were observed in 44 anesthetized rabbits. The results obtained were as follows: (1) Elevation of ureteral pressure (UP) could induce an increase in integral value of ARNA by 175.13 +/- 22.41% (P less than 0.001). (2) KCl (0.15 mol/L) and NaCl (1 mol/L) perfused retrogradely into pelvis via ureter route resulted in increase of integral value of ARNA by 253.79 +/- 21.64% and 172.17 +/- 15.19% (P less than 0.001), respectively. (3) Four patterns of afferent unit discharge were found: no spontaneous activity, regular spontaneous activity, regular spontaneous activity with burst and irregular spontaneous activity. (4) The units of afferent renal nerve with no spontaneous activity were activated markedly by elevation of UP, while the units with spontaneous activity showed no change. (5) In response to the retrograde perfusion of KCl (0.15 mol/L) and NaCl (1 mol/L) into pelvis, the activity in units with spontaneous discharge increased markedly by 210.70 +/- 23.40% and 140.07 +/- 15.72% (P less than 0.001), respectively, and the other units may be recruited concomitantly. (6) The units with no spontaneous discharge were activated by renal artery occlusion. The results implied that there are mechanoreceptor, R1 and R2 chemoreceptors in the kidney of the rabbit, and they may sense the change in UP, renal ischemia and ionic (K+, Na+) concentration of the solute within pelvis.
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PMID:[Observation on the afferent nerve activity induced by stimulation of renal receptors in the rabbits]. 208 72

Recently, it has been reported that atrial natriuretic peptide (ANP) reverses or prevents acute renal failure induced by norepinephrine in rats. Therefore, we tested the hypothesis that vasoconstrictor doses of arginine vasopressin (VP) can induce renal ischemia and that consequent renal dysfunction is reversed by ANP infusion or bolus injections in rats. Intrarenally infused VP produced a significant decrease of glomerular filtration rate (GFR) and an increase of urinary volume and sodium excretion rate. Systemic blood pressure increased significantly during VP administration. In a second experimental period, ANP was also given intrarenally, control rats received isotonic saline solution. ANP infusion revealed a highly significant increment of GFR, urinary volume and sodium excretion. Blood pressure fell down below values of the preperiod. After cessation of ANP infusion, renal function was reduced again. These results indicate that VP induces a nonoliguric acute renal failure which is reversed by ANP infusion but only at the time of its administration.
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PMID:Atrial natriuretic peptide reverses experimental acute renal failure induced by arginine vasopressin. 213 64

The effect of the calcium blocker S-(+)-methyl 4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitro-phenyl)thieno[2,3-b]pyridine- 5-carboxylate (S-312-d) on ischemic acute renal failure (ARF) was studied in rats. Ischemic ARF was induced by temporary (30-60 min) clamping of the left kidney 2 weeks after contralateral right nephrectomy. Plasma creatinine, creatinine clearance, urinary osmolality and fractional excretion of sodium were used to test the effectiveness of the drug. S-312-d (0.01-0.1 mg/kg b.wt. i.v.) administration before ischemia offered dose-dependent protection against the functional impairment induced by ischemia. This effect was accompanied by an increase in the survival rate of ischemic rats. S-312-d given after ischemia was not effective. The renal cortical edema induced by ischemia was significantly reduced by pretreatment with S-312-d. The increase in renal tissue calcium content observed after ischemia was also suppressed by S-312-d. Comparison with other established calcium blockers indicated S-312-d to be a good candidate for protection against ischemic ARF. These findings indicate that S-312-d may be clinically useful against renal ischemia.
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PMID:Protective effect of a novel calcium blocker, S-312-d, on ischemic acute renal failure in rat. 224 38

Renal effects of 1,4-dihydropyridine (DHP)-type calcium antagonists (nitrendipine and nisoldipine) were analyzed in diverse conditions, such as long-term antihypertensive treatment, acute saline-loading, and acute renal failure in rats. In spontaneously hypertensive rats (SHR), 60-week treatment with nitrendipine resulted in normotensive blood pressure values without increasing body weight, an indicator of salt-water retention, or increasing plasma renin activity and plasma aldosterone concentration compared with the untreated rats. After acute saline-loading of normotensive or hypertensive rats, administration of calcium antagonists nitrendipine and nisoldipine increased urinary volume and sodium excretion. This was in contrast to the effects observed with the vasodilator minoxidil, with which salt-water retention was shown. In acute renal failure induced by 60-min renal ischemia in uninephrectomized rats, administration of nisoldipine decreased mortality rate and improved kidney function. The increase in renal tissue calcium content and the decrease in ATP content associated with the renal failure was abolished by nisoldipine treatment. In conclusion, renal protective effects are present with DHP-type calcium antagonists; however, mechanisms in situations such as hypertension or acute renal failure might be different and deserve further analysis.
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PMID:Renal effects of 1,4-dihydropyridines in animal models of hypertension and renal failure. 244 Nov 91


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