Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The effects of two different H2-receptor antagonists, cimetidine and famotidine, on the acute renal failure induced by 20 min of renal artery occlusion and gentamicin (240mg/kg BW, s. c., for 3 days) were investigated in Sprague-Dawley rats. The animals were treated with either cimetidine (80 or 160 mg/kg BW) or famotidine (4 or 8 mg/kg BW) mixed in the drinking water for 7 days. The low dose of cimetidine and famotidine did not alter the renal function in the absence of renal trauma. However, the high dose of cimetidine or famotidine decreased the GFR by 32% and 22%, whereas RPFR increased by 46% and 62%, and % FENa by 92% and 558%, respectively. The data for the renal function obtained 24 hrs after 20 min of renal ischemia demonstrated a decrease of 54% in GFR, a decrease of 47% in RPFR and an increase of 370% in %FENa over the non-ischemic control values (p less than 0.05). Cimetidine (80 mg/kg BW) or famotidine (4 mg/kg BW) did not modify the recovery of renal function following the ischemic insult, showing 55% and 539% decreases in GFR, 74% and 101% increases in RPFR, and 393% and 461% increases in %FENa over the non-ischemic control rats, respectively. Famotidine reduced the decrease in RPFR significantly during the recovery period following ischemia. In the gentamicin study, gentamicin treatment was found to lower the renal function significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Do the H2-receptor antagonists, cimetidine and famotidine, modify the degree of renal recovery following renal insult? 225 Apr 7

A series of 62 femorofemoral bypass grafts (FFBG) is reported. The indication for this operation was unilateral iliofemoral occlusion with severe ischemia of the lower limb in poor-risk patients. Severe ischemia presented as rest pain and/or minor necrotic lesions to the foot fingers, while patients were defined poor-risk for aging and concomitant diseases advising major surgical procedures and general anaesthesia. Claudication was not considered as an indication for this operation, and this statement is discussed in detail reviewing the literature. Operative death rate was approximately 6.4% (4 subjects), due to acute renal failure, revascularization syndrome, cardiac arrest and pulmonary oedema. Twenty subjects had had a total of 33 previous vascular reconstructive procedures; this occurrence did not reveal any statistically significant consequences on long-term patency rate, although a difference was seen in favour of the patients who had not undergone previous vascular reconstructive procedures. In the group of patients who underwent FFBG as the first vascular procedure, five early occlusions occurred: three Fogarty catheter thrombectomies were successful. Cumulative patency rate was then 77% at 36 months in the series of 58 survivors. Rest pain was relieved in any instances and a satisfactory improvement of claudication was obtained.
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PMID:The femorofemoral bypass graft. Report of a 11-year experience. 225 Sep 77

The conversion rates of xanthine dehydrogenase (XDH) to xanthine oxidase (XO) were compared with the time course of in vivo lipid peroxidation (LPO) in an ischemia-reperfusion model of acute renal failure in the rat. LPO, measured as the renal release of malondialdehyde (MDA), was found to be markedly elevated only during the first 5 min of blood reflow following a 45-min interval of ischemia (arteriovenous MDA difference -277.3 +/- 53.5 vs. 3.7 +/- 5.7 nmol/l in controls, n = 14). After 30 min of reperfusion, arteriovenous MDA differences nearly reached control values (9.7 +/- 31.8 nmol/l, n = 7). In contrast to enhanced LPO, no significant conversion of XDH to XO was found (XO activity in controls: 23 +/- 1% of XO plus XDH activity vs. 26 +/- 3% after 45 min of ischemia, n = 7). Therefore XO-derived superoxide anion radicals cannot be considered causative for LPO in the reperfusion interval of experimental ischemic acute renal failure.
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PMID:Xanthine oxidase: evidence against a causative role in renal reperfusion injury. 230 86

The purpose of this study was to assess how brief periods of intermittent reperfusion (IR) imposed during a renal ischemic insult affect adenine nucleotide/catabolite concentrations, oxidant stress, and the severity of ischemic acute renal failure (IARF). Rats were subjected to 35 minutes of renal pedicle occlusion with or without brief IR periods (total less than or equal to 3 minutes). Adenine nucleotides and their catabolites were measured at the end of ischemia and at 30 minutes of the recovery period. Oxidant stress in the recovery phase was assessed by non-protein-bound sulfhydryl and malondialdehyde (MDA) concentrations. The severity of IARF was quantified at 24 hours by degrees of azotemia and histologic damage. Although IR had no significant impact on end-ischemic ATP concentrations, it did induce profound adenine nucleotide catabolite depletion; the sum of adenosine, inosine, inosine monophosphate, hypoxanthine, and xanthine fell by 78%, compared with control ischemia values (p less than 0.001). The pattern of IR affected the degree of catabolite depletion: dividing a single 3-minute IR period into two 1 1/2-minute segments increased catabolite loss by 45% without affecting adenine nucleotide content. Although adenine nucleotide catabolites can be resynthesized to ATP, IR did not worsen postischemic adenine nucleotide recovery. IR augmented postischemic sulfhydryl depletion by 8% (p less than 0.02). However, lipid peroxidation (as assessed by MDA) did not result and the severity of IARF was not adversely affected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brief intermittent reperfusion during renal ischemia: effects on adenine nucleotides, oxidant stress, and the severity of renal failure. 234 58

To determine the selective effect of microfilament disruption on both cellular structure and function, microfilament-specific doses of cytochalasin D (10 microM) were used in an isolated perfused kidney system. Structurally, cytochalasin D resulted in extensive disruption of the apical surface with blebbing, vacuolization, and patchy loss and fusion of microvilli. Functionally, cytochalasin D resulted in an initial decrease in glomerular filtration rate (300.8 +/- 29.9 vs. 541.6 +/- 51 microliters.min-1.g-1, P less than 0.05) with subsequent stabilization throughout the duration of the perfusion. In contrast, the tubular reabsorption of sodium decreased significantly in a linear fashion from 97.1 +/- 0.7 to 64.3 +/- 7.0% over the duration of the perfusion. Similarly, the tubular reabsorption of lithium decreased linearly from 74.8 +/- 2.6%, before the addition of cytochalasin, to 33.6 +/- 6.8% by the end of the perfusion. Correlation of the decrements in percent tubular reabsorption of sodium and lithium for individual kidneys was 0.87 (P less than 0.01), suggesting the effect of microfilament disruption on tubular reabsorption of sodium was localized primarily to the proximal tubule. Because ischemic injury is characterized by time-dependent structural alterations in the apical membrane of proximal tubule cells, we set out to determine whether microfilament disruption occurs during ischemic acute renal failure. Utilizing indirect immunofluorescence with an anti-actin antibody, control kidneys demonstrated intact circumferential apical immunofluorescence representing brush-border and terminal web actin staining. Fifteen minutes of ischemia resulted in multiple large gaps in the terminal web, and 50 min of ischemia caused diffuse redistribution of actin immunofluorescence throughout the cytoplasm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of microfilaments in maintenance of proximal tubule structural and functional integrity. 238 6

The potential therapeutic value of the chemically stable carbacyclin analogue iloprost on the course of postischemic acute renal failure was studied in six conscious chronically instrumented dogs and compared with five controls. Immediately after temporary ischemia (180-min cessation of blood flow by inflation of a pneumatic cuff), the investigational group PC received a continuous intraaortal infusion of iloprost (50 ng X min-1 X kg-1) over a period of seven days, whereas the control group C received 0.9% saline. The glomerular filtration rate [( 51Cr]EDTA clearance, endogenous creatinine clearance) was less decreased in the prostacyclin analogue group than in the control group [3rd day, 18 +/- 2.5 vs. 12 +/- 1 ml X min-1 (p less than 0.05); 7th day, 23 +/- 3 vs. 12 +/- 2 ml X min-1 (p less than 0.05)]. On day 1, renal blood flow (electromagnetic flow probe) was markedly lower in the control group (129 +/- 29 ml X min-1) than in the PC group (212 +/- 29 ml X min-1; p less than 0.05), even exceeding baseline levels in the latter group. Accordingly, the excessive rise in renal vascular resistance in the control group (+136%) was abolished in the PC group (-32%; p less than 0.01). Nitrogen retention was also markedly improved. Osmolar clearance was markedly lower in the control group (0.58 +/- 0.2 ml X min-1) than in the PC group (1.41 +/- 0.17 ml X min-1; p less than 0.05). It is suggested that the beneficial effect of iloprost is mediated by preservation of renal perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration of postischemic acute renal failure by prostacyclin analogue (iloprost): long-term studies with chronically instrumented conscious dogs. 242 19

The effect of 45-min clamping of the renal artery was studied in the conscious uninephrectomized rat to reproduce the syndrome of hemodynamically mediated acute renal failure in humans after a single ischemic insult. Twenty-four hours after ischemia, creatinine clearance was reduced by 90%, whereas fractional excretion of sodium was markedly increased; over the subsequent 5 days, both values returned to normal. The animals were nonoliguric. Fractional clearances of graded sizes of neutral dextrans (radii 20-44 A), employed to detect transtubular backleak of inulin, were not significantly different 24 or 48 h postischemia from those in normal animals. The implication that the normal fractional dextran clearances excluded tubular backleak was tested directly by microinjecting [methoxy-3H]inulin into the proximal tubule. In most tubules injected, the recovery of radioactivity in the urine was markedly lower 24 and 48 h postischemia than that in normal rats; in a few injected tubules of postischemic kidneys, recovery was not different from that in normal animals. The low recovery of radioactive inulin was accounted for, at least in part, by transtubular backleak, as shown in experiments in which rats subjected to renal ischemia were cross-transfused with normal animals. These studies indicate that, despite the normal fractional dextran clearances, most tubules were severely injured as shown by tubule backleak of inulin.
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PMID:Course and pathogenesis of postischemic acute renal failure in the rat. 245 26

Calcium channel blockers have been reported to preserve renal function when given prophylactically in animal models of acute renal failure (ARF), but the mechanism by which this effect occurs is unknown. We report that nitrendipine (NTR) ameliorates the decline in endogenous creatinine clearance when administered before to clamp-induced ischemia in rats (NTR + clamp, 0.21 +/- 0.06 ml/min; clamp alone, 0.13 +/- 0.04 ml/min, p less than 0.05). To determine whether this protective effect involves the proximal tubule, we compared the uptake of phosphate by brush border membrane (BBM) vesicles in NTR-pretreated ARF rats and in ARF rats pretreated with vehicle alone. A comparison of vehicle-pretreated/sham-operated and vehicle-pretreated/ARF rats served as a control. The initial uphill phase of Na+ gradient-dependent phosphate transport was significantly greater in NTR/ARF rats as compared with vehicle/ARF rats. Pretreatment with NTR did not affect BBM transport of D-glucose or proline. We conclude that NTR has a modest protective effect on overall renal function, and that preservation of proximal tubular function is probably part of this effect.
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PMID:Modifications in proximal tubular function induced by nitrendipine in a rat model of acute ischemic renal failure. 248 64

In previous studies in humans, mannitol (20%, 250 ml) has been shown to reduce the incidence of acute renal failure (ARF) after transplantation from 54% to 19%. In rats, atrial natriuretic peptide appears to prevent ischemia-induced ARF. We therefore decided to evaluate the effects of alpha-human atrial natriuretic peptide (alpha-h-ANP) both alone and combined with mannitol during transplantation in humans. First, we demonstrated that systemic alpha-h-ANP infusion during kidney transplantation was safe in dosages up to 0.08 micrograms/kg per minute. In these patients the calculated metabolic clearance rate of alpha-h-ANP was relatively low ranging from 0.68 to 1.80 l/min. In a second study of 11 renal graft recipients, no mannitol was used and alpha-h-ANP (0.05 micrograms/kg per minute) was infused into the donor kidney artery during transplantation for 46 +/- 2 min, followed by IV administration for 71 +/- 2 min. Our aim was to reduce the incidence of ARF. Nevertheless, ARF occurred immediately after surgery in four of the patients (36%) in this group and, as a result, mannitol was reintroduced. A third group of nine renal graft recipients received alpha-h-ANP (total dose 400 micrograms) as five IV injections within 90 min after transplantation. ARF occurred in four of these patients (44%). We conclude that alpha-h-ANP, administered according to the aforementioned protocols in such small groups of patients, does not seem to be of value in the prevention of ARF after transplantation.
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PMID:The effect of alpha-human atrial natriuretic peptide on the incidence of acute renal failure in cadaveric kidney transplantation. 214 26


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