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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN) reduced the ischemia-reperfusion induced acute renal failure in the rat. Renal ischemia was produced in unilateral nephrectomized rats by complete occlusion of the left renal artery for 60 min. Perfusion of the kidney was then reestablished, and the rats were sacrificed 48 h later. PBN (100 mg/kg i.p.) administered 30 min prior to renal artery occlusion significantly reduced the increase in serum creatinine and urea and renal failure index, as well as the decrease in urine/plasma creatinine ratio and creatinine clearance compared to saline-injected ischemic rats. PBN injected to control rats had no effect on these parameters. These data support the hypothesis of an involvement of reactive free radicals in the pathogenesis of ischemia-reperfusion induced acute renal failure in the rat and suggest that PBN may be a useful agent for the prevention of renal ischemia-reperfusion damage.
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PMID:Ischemia-reperfusion induced acute renal failure in the rat is ameliorated by the spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN). 146 97

During the past several years studies using freshly isolated proximal tubules in suspension have contributed to understanding several of the major cellular processes underlying ischemic and related forms of acute renal failure. Tubules have a large capacity to augment their intracellular ATP content when supplemented with exogenous purines. This process has been shown to be mostly explained by adenosine uptake. Reductions of cell pH such as occur prominently during ischemia strongly protect tubules against a variety of insults. Increases of cytosolic free calcium to micromolar levels are highly damaging to tubules and do occur prior to lethal cell injury induced by ATP-depleting metabolic inhibitors, but do not critically determine the outcome in the latter setting. Given their ubiquitous occurrence and well-documented importance in a variety of systems, reactive oxygen metabolites play a surprisingly small role in oxygen deprivation-induced injury to isolated tubules. Several small neutral amino acids, glycine being the prototype and most potent, have a critical, constitutive effect to maintain tubule cell structural integrity during a variety of acute insults.
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PMID:Relationships between oxidant and non-oxidant mechanisms in the pathogenesis of acute renal failure. 146 46

The hypothesis that dietary fish oil would protect dogs from ischemic acute renal failure was tested. Fish oil (eicosapentaenoic acid, 55 mg/kg per day, and docosahexaenoic acid, 40 mg/kg per day was given to eight instrumented, female, beagle dogs for 6 wk, while seven control dogs received vehicle. After 3 wk, unilateral nephrectomy was performed and a pneumatic cuff with flow probe was placed around the remaining renal artery of each dog. Three weeks thereafter, the cuff was inflated for 120 min. Renal function, RBF, and prostanoid excretion were measured 24 and 72 h after ischemia. In dogs receiving fish oil, blood pressure, GFR, RBF, renal vascular resistance (RVR), cholesterol, triglycerides, and prostanoid excretion were measured weekly for 6 wk. Further, cytosolic calcium was measured before and five times after fish oil. Blood pressure decreased, serum cholesterol and triglycerides decreased, and the cytosolic calcium within platelets decreased. The urinary excretion (expressed as picograms per milligram of creatinine) of the thromboxane (TX) metabolite TXB2 and the excretion of prostaglandin (PG)E2, as well as the excretion of the PGI2 metabolite 6-keto PGF1 alpha were decreased. GFR, RBF (Cl inulin and Cl para-aminohippuric acid), and RVR were not influenced by fish oil. Unilateral nephrectomy decreased GFR and RBF and increased RVR as expected, whereas it further decreased prostanoid excretion. Acute renal ischemia caused a significant, reversible decrease in GFR and urine volume in vehicle-treated animals, whereas no significant effect on renal function or urine volume was observed in animals pretreated with fish oil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration of ischemic acute renal failure by dietary fish oil administration in conscious dogs. 147 27

Numerous and extremely varied conditions (intense muscular activity, ischemia, metabolic and genetic disorders, infections, immunological diseases and toxic causes) may play a role in the genesis of non-traumatic rhabdomyolysis. Over the past years there has been an increased number of reports of forms due to drug or narcotic intoxication. Seven cases of rhabdomyolysis are reported in patients admitted to emergency wards in a state of coma due to heroin overdose (4 cases), cocaine overdose (1 case), carbamazepin (1 case), and tricyclic anti-depressives (1 case). In all cases it was possible to hypothesise a multifactorial pathogenesis of the disease in which other factors, such as acidosis, hypoxia, hypothermia and compression of the muscle mass during coma, were associated with the direct toxic damage caused by the drug. The most frequent complication was acute renal failure. One case of myocardial involvement with non-Q infarction characteristics was also observed.
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PMID:[Rhabdomyolysis during acute poisoning with drugs and narcotics. Experience with 7 clinical cases]. 149 66

Oxygen free radicals are generated during reperfusion of ischemic organs. Studies employing several species of laboratory animal (rat, dog, pig, rabbit, mouse) have documented protective effects of a variety of free-radical scavengers and antioxidants when administered before or immediately preceding reperfusion of ischemic kidneys. These protective agents include superoxide dismutase, dimethylthiorea, dimethyl sulfoxide, alpha-tocopherol, glutathione, the iron chelator deferoxamine, probucol, allopurinol and oxypurinol, and the spin-trapping agent PBN. Furthermore, deficiency of antioxidants (selenium, alpha-tocopherol, or catalase) exacerbates postischemic renal injury. These findings have been applied to renal transplantation in an attempt to decrease the incidence of posttransplantation acute renal failure. This is important because acute renal failure results in morbidity, increases hospital stay and the cost of transplantation, and complicates the use of cyclosporine. In porcine and in canine kidney transplantation, superoxide dismutase and allopurinol have provided renal protection. Transplantation is complicated because there may be prolonged hypoperfusion before harvesting plus a brief period of total ischemia during harvesting, followed by a prolonged period of cold ischemia and/or reperfusion, then followed by another brief period of ischemia and reperfusion during transplantation. Injury may occur at each of these phases by different mechanisms.
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PMID:Free radical-mediated postischemic injury in renal transplantation. 150 58

Acute renal failure is common in kidney transplantation due to immunologic, nephrotoxic, and ischemic events. In this paper the subject of posttransplant acute renal failure is reviewed in relation to arachidonic acid metabolism. Although experimental abnormalities noted in ischemia, rejection, and cyclosporin nephrotoxicity are discussed separately, it is obvious that in the clinical situation there is great overlap. The effects of altering the substrate arachidonic acid by feeding of dietary omega-3 fatty acids, both experimentally and clinically, are discussed. Finally, the limited clinical trials of prostaglandin analogues in renal transplant patients show conflicting conclusions as regards beneficial effects on rejection and renal function. Careful clinical studies of compounds with proven efficacy in animals are needed if acute renal failure posttransplant is to be modified or prevented.
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PMID:Therapeutic implications of arachidonic acid metabolism in transplant-associated acute renal failure. 150 59

In the acute phase of ischemic renal failure, the severe depression of the glomerular filtration rate (GFR) is due to obstruction of the tubules by cells and cell debris rejected from the proximal tubules, a blockade which can be prevented at least partly, by treatment with osmotic diuretics. The isosthenuria, the second typical sign in ischemic acute renal failure, probably derives from the medullary ischemia that results from an intracapillary trapping of red cells. This, in turn, is suggested to be caused by oxygen-derived free radicals, which via increasing the capillary macromolecular permeability result in a massive extravasation of plasma and hence in hemoconcentration. As expected from this hypothesis, scavengers may ameliorate both the trapping and the consequent medullary ischemia. Unfortunately, however, a therapy using both osmotic diuretics and scavengers fails to improve the long-term outcome. Hemodilution would seem more promising, since it will both prevent the medullary ischemia seen in the acute phase and substantially improve the long-term outcome. At a hematocrit of 0.30, rat kidneys exposed to 45-min ischemia will show a GFR 1 month after the insult of more than 50% of the normal GFR as against 15% in untreated animals.
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PMID:Osmotic diuretics and hemodilution in postischemic renal failure. 150 60

Functionally similar ischemic acute renal failure (ARF), as estimated by glomerular filtration rates (GFR), was induced by renal artery clamping (RAC) or intrarenal norepinephrine (NE) in rats and renovascular reactivity was examined at 1 week. With RAC-ARF induction there was total renal ischemia followed by abrupt return of renal blood flow (RBF). With NE-ARF induction there was subtotal ischemia (10-15% of basal RBF) with RBF recovery over several hours. Renovascular resistance (RVR) did not change to renal perfusion pressure (RPP) reduction in the autoregulatory range in RAC-ARF but paradoxically increased in NE-ARF. There was an exaggerated response to renal nerve stimulation in NE-ARF but no response in RAC-ARF. There was a vasoconstrictor response to intrarenal norepinephrine in the former but a negligible response in the latter. There was no vasodilation to acetylcholine in either group, but there was a normal response to prostacyclin in NE-ARF. Smooth muscle necrosis was found in 46% of resistance arterial vessels in RAC- but in only 8% of NE-ARF (p less than .001). When mean arterial pressure was reduced to 90 mm Hg for 4 h at 1 week, recurrent azotemia and fresh ischemic injury were noted in NE- but not RAC-ARF. It is concluded that different models of ischemic ARF induction result in different patterns of abnormal postischemic vascular reactivity. Differences in vascular smooth muscle and endothelial injury are due to differences in initial ischemia or rates of postischemic reperfusion.
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PMID:Renal vasculature and ischemic injury. 150 62

Two patients with carbon monoxide poisoning are presented, both of whom suffered rhabdomyolysis complicated by acute renal failure. One patient, an attempted suicide, developed a compartment syndrome of the right thigh that required fasciotomy and recovered after a period of hemofiltration and hemodialysis. Muscle biopsy appearances were consistent with partial muscle infarction. The other patient, rescued from a smoke filled room, exhibited raised creatine kinase but no evidence of muscle swelling. He developed anuric renal failure and adult respiratory distress syndrome and died despite maximum intensive care. Muscle biopsy showed early evidence of muscle necrosis. In both cases there was a marked reduction of enzyme activities in the muscle biopsy consistent with metabolic derangement. Although there was a clinical compartment syndrome in the first case, there was no muscle swelling at the time of biopsy or subsequently in the second case. A direct toxic effect of carbon monoxide may thus have been an important mechanism contributing to the muscle necrosis in the second case, although local ischemia may have been an exacerbating factor in the first case.
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PMID:Rhabdomyolysis and acute renal failure following carbon monoxide poisoning: two case reports with muscle histopathology and enzyme activities. 151 16

We studied the pre operative status and the 1st, 4th, 12th and 24th hours of the post operative period after open heart surgery with cardiopulmonary bypass with a crystalloid solution containing 10 gr of mannitol. We considered acute renal failure (ARF) as being any increase in plasma creatinine values of 0.25 mg/dl for the first 24 hours and 0.5 mg/dl for periods longer than 24 hours. Six patients had transitory ARF (28.5%). The maximum value of plasma creatinine was 2.3 mg/dl and no patients required renal function substitution. There were no deaths. We used as ischemia ARF indicators the urinary flow rate, urine/plasma creatinine ratio, urine/plasma osmolality ratio, sodium fractional excretion and free water reabsorption. We also measured the urinary N-A-Glucosaminidase (NAG). We found that creatinine clearance reached its lowest in the first and fourth hours. Beyond the fourth hour we observed, the urinary flow rate reduce significantly, the urine/plasma creatinine and osmolality ratios reach values traditionally associated prerenal ARF, an increase main free water reabsorption and a decrease in sodium fractional excretion with a close relationship between the less than 1 value and the increase in plasma creatinine. There was a significant NAG increase in the 24 th hour. The evidence of a vulnerability period for renal ischemic lesions between the 4 th and 12 th hour suggests a second mannitol administration during the first four hours of the post operative period.
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PMID:[Identification of a period of renal ischemic vulnerability studying the changes in the indicators of acute renal insufficiency after heart surgery with extracorporeal circulation]. 160 64


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