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

Fructose-1,6-diphosphate has been shown to improve neurologic recovery following resuscitation from cardiac arrest and to restore brain electrical activity during hypoglycemic coma in rabbits. In view of these findings, we determined whether fructose-1,6-diphosphate protects the brain during ischemia-hypoxia. We subjected 16 rabbits to hypotension, hypoxemia, and bilateral common carotid artery occlusion. Five minutes after the onset of isoelectric electroencephalograms, seven randomly selected rabbits received 10% fructose-1,6-diphosphate (350 mg/kg bolus followed by 10 mg/kg/min infusion for 90 minutes) and the remaining nine rabbits (controls) received an equal volume of 1.5% NaCl (3.5 ml/kg bolus followed by 0.1 ml/kg/min infusion for 90 minutes). After isoelectricity lasting 7.86 +/- 0.8 minutes (mean +/- SEM) in the treated group and 6.44 +/- 0.38 minutes in the control group, the rabbits were reinfused with autologous shed blood and reoxygenated and the carotid artery occluders were removed. Treated rabbits recovered electrical activity more rapidly than the controls (p less than 0.005), and all seven treated rabbits survived. Only two controls (22%) survived (p less than 0.001), and they were severely disabled. Histology showed extensive cortical necrosis and focal necrosis in the hippocampi and cerebellum of brains from the two surviving controls. Brains from two treated rabbits exhibited minimal neuronal loss limited to the neocortex, and the brains from the remaining five treated rabbits were normal. This study suggests that fructose-1,6-diphosphate protects the brain from ischemic-hypoxic insults.
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PMID:Prevention of ischemic-hypoxic brain injury and death in rabbits with fructose-1,6-diphosphate. 232 42

The main purpose of our study is to investigate the possible protective effects of Fructose 1-6 diphosphate (FDP) and Danshen (Salvia Miltiozzhiza Bunze) on renal cortical Na-K-ATPase activity after renal ischemia and gentamicin nephrotoxicity. An 18.6% reduction in renal cortical Na-K-ATPase activity was shown after 30 min of renal pedicle clamping and 60 min of reflow, and a 32.5% reduction after 90 min of single injection of 100 mg/kg gentamicin. Light and electronic microscopy revealed no significant morphologic changes in both groups in the experiment. 4g/kg FDP and 18g/kg Danshen were infused 60 min after reflow in the ischemic group, 90 min after injection of gentamicin in the gentamicin-treated group and 90 min in the sham-operated group separately. The enzyme activity in the FDP-treated groups was found to be higher than that in the control kidneys while in the Danshen-treated groups no significant difference could be found. Our study showed that FDP and Danshen could prevent the decline of renal cortical Na-K-ATPase activity induced by ischemia and gentamicin. FDP could increase this enzyme activity while Danshen showed no such direct effect.
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PMID:Effects of FDP and Danshen on renal cortical Na-K-ATPase activity in rats after treatment with renal ischemia and gentamicin. 256 Sep 55

Fructose-1,6-diphosphate (FDP) improves survival in experimental shock. To determine if FDP would protect against single organ damage, rats pretreated with an intravenous infusion of 5% FDP were subjected to 30 minutes of bilateral renal artery occlusion. Controls received an equal volume of a dextrose and sodium chloride solution. Renal function and histology were examined in all groups 24 hours after the insult. Following ischemia, FDP-treated rats had inulin clearances (FDP 897 +/- 129 vs control 349 +/- 59 microliter/min/100 gm BW; P less than 0.01) and solute excretion rates (FDP 6,386 +/- 1,346 vs control 2,602 +/- 396 mOsm/kg/min/100 gm BW; P less than 0.05) greater than control and not different (P-NS) from sham-operated rats. Renal histology was better preserved in the FDP-pretreated group. Thus, pretreatment with FDP provides histologic and functional protection from an ischemic renal insult.
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PMID:Protection from ischemic renal injury by fructose-1,6-diphosphate infusion in the rat. 405 95

A number of methods have been used to protect organ systems and cells from the ravages of ischemia and hypoxia. Some have attempted to reduce the metabolic needs, such as by hypothermia, cardioplegia, and slow calcium channel blockers. Others have attempted to provide the metabolic needs, such as by cold blood cardioplegia and solutions of readily metabolized substrates. Our work has centered on the use of fructose 1-6-diphosphate, which can be used anaerobically after glycolysis has been stopped by the effects of anoxia and acidosis. Fructose diphosphate has proved effective experimentally in ameliorating the effects of local and global ischemia of the heart. It has also been found to be of value in many hypoxic or ischemic states including traumatic, septic, endotoxic, and hypovolemic shock. The rationale and a survey of preliminary results are presented.
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PMID:Metabolic effects of fructose diphosphate in hypoxic and ischemic states. 623 13

Hepatic metabolism in intact livers has been studied by 31P nuclear magnetic resonance (NMR) spectroscopy. 31P NMR spectroscopy of normal liver detects little ADP and much lower amounts of inorganic phosphate than are found by enzymatic or chemical analysis. Ischaemia of 30 min duration provokes a rapid fall in ATP to undetectable levels; reflow restores the ATP concentration to 70% of its former level. Intracellular pH changes are qualitatively similar. Fructose and glycerol both cause rapid falls in ATP and inorganic phosphate; these original concentrations are almost restored after 30 min in the case of fructose but not with glycerol where they remain depressed.
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PMID:Hepatic metabolism by 31P NMR. 713 82

We evaluated the effects on cerebral ischemia of a treatment with fructose-1,6-bisphosphate, a compound known to possess protective effects on acute ischemic injury in a variety of different tissues. We investigated the ability of the compound, administered either 15 minutes before or 15 minutes after the ischemic insult, in reducing the ischemia-induced changes in polyamine brain levels. The experiments were performed in adult, chloral hydrate-anesthetized Mongolian gerbils that underwent a 15 minutes ligation of the common carotid arteries followed by recirculation. Animals were sacrificed 1, 8 and 24 hours and immediately after the release of the occlusion. Polyamine brain levels were not modified during ischemia. Putrescine began to increase after eight hours from the release of the occlusion and we found it significantly increased after 24 hours in the hippocampus and striatum. We did not detect any significant changes in spermidine brain levels either during ischemia or during recirculation. Conversely, spermine appeared to decrease in the hippocampus while it did not show changes in striatum and medulla-pons. The activity of ornithine decarboxylase, a key enzyme in the biosynthesis of polyamines, resulted enhanced at the end of the ischemic period in all the brain regions tested and showed a peak at eight hours of recirculation in striatum and hippocampus whereas returned to control values in the medulla-pons. Fructose-1,6-bisphosphate significantly reduced the ischemia induced changes in polyamine brain content when administered before the ischemic insult while did not show protective properties when administered post-ischemically.
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PMID:Effects of fructose-1,6-bisphosphate on brain polyamine biosynthesis in a model of transient cerebral ischemia. 815 42

Fructose-1,6-bisphosphate (FBP), an intermediate of glucose metabolism, is neuroprotective in brain hypoxia or ischemia. Because the mechanisms for this protection are not clear, we examined the effects of FBP on two important events in brain ischemia, i.e., loss of ATP and release of the excitatory neurotransmitter glutamate. Glutamate release from cortical brain slices was measured fluorometrically (glutamate dehydrogenase-catalyzed conversion of glutamate to alpha-ketoglutarate) during hypoxia (PO2 15 mm Hg) or hypoxia plus 100 microM cyanide. FBP (3.5 mM, with glucose 20 mM) reduced glutamate release during hypoxia by 55% and during hypoxia/cyanide by 46% (p < 0.005), and prevented a significant fall in [ATP]. [ATP] was maintained in oxygenated glucose-free conditions with 20 but not 3.5 mM FBP, and fell to < 20% of normal with hypoxia. Despite the drop in [ATP], 3.5 or 20 mM FBP without glucose decreased hypoxia-evoked glutamate release. We conclude (1) FBP present without glucose preserves normal [ATP] only when oxygen is available, suggesting limited uptake and metabolism; and (2) FBP decreases hypoxia-evoked glutamate release by processes independent of [ATP]. These results suggest protective actions of FBP that are separate from augmentation of anaerobic energy production, as previously proposed.
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PMID:Effects of fructose-1,6-bisphosphate on glutamate release and ATP loss from rat brain slices during hypoxia. 885 28

Fructose-1,6-bisphosphate (FBP) has been shown to attenuate central nervous system injury in adult animals. We evaluated whether FBP given after an ischemic-hypoxic insult is protective to the developing brain in a neonatal rat model of hypoxia-ischemia. Postnatal day 7 rat pups were subjected to focal ischemia followed by global hypoxia and then administered either FBP or saline intraperitoneally. A dose of 500 mg/kg or greater of FBP significantly reduced the amount of injury such that 55% of FBP- vs. 17% of saline-treated rats had no injury; 6% of FBP- and 47% of saline-treated rats had severe damage (P = 0.004). There was less infarcted brain in FBP-treated rats (12 +/- 11% vs. 37 +/- 32%; P = 0.005); and fewer FBP-treated rats had > 30% ipsilateral cortical injury (12% of FBP- vs. 50% of saline-treated rats; P = 0.002). FBP lowered serum calcium levels during the first 24 h after the insult without significant changes in ionized calcium or osmolarity. These results indicate that FBP treatment administered systemically after hypoxia-ischemia reduces CNS injury in neonatal rats.
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PMID:Fructose-1,6-bisphosphate after hypoxic ischemic injury is protective to the neonatal rat brain. 900 35

Fructose-1,6-bisphosphate has been shown to exert beneficial effects in different experimental models of cerebral ischemia. In view of this evidence, we have determined whether the compound protects the brain during microsphere-induced ischemia. One thousand two hundred microspheres were injected into female rats through a catheter inserted into the right common carotid artery and, 15 minutes and again 24 hours later, we intravenously treated the animals with 333 mg Kg(-1) of fructose-1,6-bisphosphate. The injection of microspheres produced significant changes in the rats' gross behavior, in their performance in the beam walking test, and in their brain lactate concentrations. The treatment with fructose-1,6-bisphosphate significantly attenuated the behavioral alterations induced by microsphere ischemia, but not in reducing brain accumulation of lactate. Moreover, the compound was shown to ameliorate the blood-brain barrier dysfunction, produced 2 and 4 hours after microsphere injection, evaluated by the Evans blue method. These results suggest that fructose-1,6-bisphosphate possesses salutary properties against the damages induced by microsphere ischemia.
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PMID:Effects of fructose-1,6-biphosphate on microsphere-induced cerebral ischemia in the rat. 925 Jul 17

Fructose-induced hypertriglyceridemic Sprague-Dawley (SD) rats become resistant to hepatotoxicity and susceptible to nephrotoxicity of acetaminophen (APAP) as compared with normal SD rats. Fischer-344 rats, which are susceptible to APAP nephrotoxicity, have two toxic metabolic pathways involving cytochrome P450-dependent oxidation of APAP to N-acetyl-p-benzoquinone imine (NAPQI) and P450-independent deacetylation of APAP to p-aminophenol (PAP). SD rats, however, have only the former pathway. This study was undertaken to investigate whether alterations in the metabolic pathways of APAP and in the intrinsic susceptibility to toxic metabolites are responsible for an enhancement of APAP nephrotoxicity in the fructose-pretreated SD-rats. In the non-pretreated rats, the inhibition of APAP oxidation by the MFO inhibitor, piperonyl butoxide, and deacetylation by carboxyesterase inhibitor, bis(p-nitrophenyl)phosphate, did not alter APAP-induced renal lesions. In contrast, these inhibitors protected the fructose-pretreated rats from APAP-induced renal lesions. Since there were no differences in the severity of gentamicin-, chloroform, and 45 min-ischemia/reperfusion-induced renal lesions between the non-pretreated and the fructose-pretreated rats, it is unlikely that the increased intrinsic susceptibility to chemicals and their metabolites in the fructose-pretreated rats is a major factor in the enhancement of APAP nephrotoxicity. These results indicate that the enhancement of APAP nephrotoxicity in the fructose-pretreated rats is due, at least in part, to an alteration in metabolic pathways of APAP.
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PMID:Enhanced nephrotoxicity of acetaminophen in fructose-induced hypertriglyceridemic rats: contribution of oxidation and deacetylation of acetaminophen to an enhancement of nephrotoxicity. 945 75


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