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

The article deals with oxidation of different substrates, intensity of glycolytic and glycogenolytic processes in mitochondria and homogenates of dog liver with its 2-hour exclusion from circulation under conditions of endotracheal ether-oxygen narcosis. It was established that already 30-60-minute ischemia causes a decrease in intensity of succinate, alpha-ketoglutarate oxidation and acceptor respiration, inhibiton in the activity of the citrate cycle enzymes; succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, isocytrate dehydrogenase. The activity of NAD-dependent malate dehydrogenasedehydrogenase and Mg2+-ATPase as well as intensity of NADN oxidation in mitochondria increase. After 2-hour ischemia the activity of Mg2+-ATPase, cytochrome oxidase and peroxidase lowers. A sharply developed glycogenolysis is accompanied by inhibition of phosphorylase activity and a two-fold stimulation of the glycolytic reactions. Peculiarities in regulation of enzymatic reactions under conditions of ischemia and their role in origin of metabolism disturbances in the liver are under discussion.
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PMID:[Carbohydrate metabolism in the liver in acute ischemia]. 17 60

The excretional patterns of lactate, pyruvate and alpha-ketoglutarate were investigated after renal transplantation in 36 patients. Fourteen patients had received a living-donor kidney with short ischemia time and good initial graft function, 22 had a cadaver transplant with an initial 125iothalamate clearance of more than 6 ml/min. The excretion of lactate and pyruvate did not vary significantly from that seen in normal controls or patients with uremia. In six patients with cadaver transplants, clearance values of alpha-ketoglutarate exceeded that of the glomerular filtration rate, indicating a net tubular secretion of this substance. During acute rejection episodes in 5 patients, no changes were seen in the excretional patterns of lactate, pyruvate and alpha-ketoglutarate.
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PMID:The excretional patterns of lactate, pyruvate and alpha-ketoglutarate in renal transplants. 34 53

Progressive cerebral ischemia was induced by blood pressure (BP) reduction in rats during status epilepticus, and the sequence of cerebral functional (EEG, extracellular K+ activity) and metabolic (levels of high energy phosphates, glucose, glucose-6-phosphate, lactate, pyruvate, alpha-ketoglutarate) changes were determined. Very moderate reductions of BP were accompanied by tissue lactate accumulation and a decrease of the rate of re-uptake of K+ extruded during discharges. These changes were pronounced at BP about 50 mm Hg, when also the energy state showed some deterioration, and the EEG activity changed from one of bursts and suppressions into single spikes. At BP about 30 mm Hg EEG activity was abolished, but not until a slightly lower BP level was there a severe energy depletion and a massive K+ release, indicating generalized membrane depolarization. The results show an increased susceptibility to ischemia during seizures with changes of membrane pump function, and energy metabolism appearing at moderate reductions of BP. Concomitant decrease of seizure activity delayed to some extent the development of massive energy failure and membrane depolarization.
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PMID:Effects of reduced cerebral blood flow upon EEG pattern, cerebral extracellular potassium, and energy metabolism in the rat cortex during bicuculline-induced seizures. 49 17

Electron transport in tissue cubes, isolated mitochondria and submitochondria particles were examined as a function of ischemic time. It was found that electron transport remains active in all systems beyond the 2 hour ischemic time interval. The NADH stimulated respiration, however, declined after 2 hours of ischemia in ASU (Ammonia-Sephadex-Urea) particles followed by respiration with matrix-located dehydrogenases tested by substrates such as glutamate, alpha-ketoglutarate and pyruvate plus malate. Succinate dependent respiration remains active at control levels. In contrast proton gradient reveals changes in two phases: Phase A is characterized by gradually increasing gradient without valinomycin and by a rapidly declining gradient with valinomycin in the medium. Phase B is characterized by a declining proton gradient with or without valinomycin. It is suggested that the alteration of the proton gradient between 1 and 2 hours ischemia is an important factor contributing to irreversible cell injury.
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PMID:Studies on the pathogenesis of ischemic cell injury. VII. Proton gradient and respiration of renal tissue cubes, renal mitochondrial and submitochondrial particles following ischemic cell injury. 60 84

Hypoxia is well known to cause an increase in brain anaerobic glycolysis. Ornithine alpha ketoglutarate (OAKG) given to six dogs was shown to attenuate these metabolic disturbances caused by hypoxia. Brain oxygen utilization was higher after ornithine alpha ketoglutarate during hypoxia than during a period of hypoxia alone. It is suggested that the clinical usefulness of OAKG should be explored in those situations where there is cerebral hypoxia or ischemia.
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PMID:Effect of ornithine alpha ketoglutarate (OAKG) on the response of brain metabolism to hypoxia in the dog. 64 19

To clarify the reversibility of ischemically induced mitochondrial dysfunction, a murine model of hepatic ischemia was used. Following 60 minutes ischemia to one hepatic lobe, significant alterations in mitochondrial, energy-linked metabolism were apparent. After the ischemic episode, 30 minutes of reperfusion resulted in partial restoration of mitochondrial function with succinate but not alpha-ketoglutarate as substrate. Lactate accumulation was also partially reversed with reperfusion. Histologic examination subsequent to the ischemic episode revealed development of partial necrosis in nine of ten ischemic lobes. alpha-Ketoglutarate oxidation is more sensitive to injury than succinate oxidation. With proper choice of substrate, measurement of mitochondrial function just after an ischemic insult may predict subsequent hepatic failure due to cellular necrosis.
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PMID:Reversibility of ischemically induced mitochondrial dysfunction with reperfusion. 91 Feb 15

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

Intracellular pH (pHi) and cytoplasmic and mitochondrial oxidation-reduction (redox) states of cerebral tissue were examined in relation to perturbations of glycolytic and tricarboxylic acid cycle intermediates and of high-energy phosphate reserves during hypoxia-ischemia and the early recovery period in the immature rat. Seven-day postnatal rats underwent unilateral common carotid artery ligation and exposure to 8% O2 for 3 h, after which they were quick frozen in liquid N2 at the terminus of hypoxia-ischemia and at 10, 30, 60, and 240 min of recovery for enzymatic fluorometric analysis of cerebral metabolites. During hypoxia-ischemia, concentrations of glucose and alpha-ketoglutarate in the cerebral hemisphere ipsilateral to the carotid artery occlusion were depleted to 10 and 70% of control, respectively; pyruvate was unchanged. During recovery, glucose, pyruvate, and alpha-ketoglutarate increased above their respective control values. Calculated pHi decreased from 7.0 (control) to 6.6 during hypoxia-ischemia and normalized by 10 min of recovery. The cytoplasmic NAD+/NADH ratio decreased (increased reduction) to 50% of control during hypoxia-ischemia and remained in the reduced state throughout 4 h of recovery. Paradoxically, mitochondrial NAD+/NADH was oxidized at the terminus of hypoxia-ischemia. The mitochondrial oxidation which developed during hypoxia-ischemia presumably results from a limitation of cellular substrate (glucose) supply, which in turn leads to a depletion of high-energy phosphate reserves, culminating in brain damage.
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PMID:Cerebral oxidative metabolism and redox state during hypoxia-ischemia and early recovery in immature rats. 192 92

In order to evaluate the importance of glycogen for the hepatic tolerance to ischemia, livers of swine fed a glucose-potassium solution for premedication were perfused with either Bretschneider's HTK-solution (histidine-tryptophan-ketoglutarate) or with Euro-Collins-solution (EC) prior to subsequent ischemia at 25 and 5 degrees C. During ischemia, in regular intervals or continuously, energy rich phosphates, lactate, intrahepatic pH and the electrical impedance of liver tissue were determined. The results were compared with corresponding data from swine which had starved for 48 h. Corresponding to the higher glycogen content, energy supply during ischemia was markedly improved by the premedication. Despite high amounts of glucose in the EC-solution, energy supply after glucose-potassium premedication was no better with EC-solution than with HTK-solution. Moreover, glucose uptake led to concomitant cellular water uptake. Electrical impedance measurements during ischemia mirrored improved energetical protection by the glucose-potassium premedication.
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PMID:Glycogen effects on energy state and passive electric properties of liver during protection. 211 13

Amino acids are known to increase glomerular filtration rate (GFR). There is also an early resumption of filtration following 2-h renal ischemic stress under protection by histidine-buffered histidine-tryptophan-ketoglutarate solution (HTK), possibly due in part to an amino acid effect. Hence, we have examined the possibility of further enhancing the postischemic GFR by adding 32 (ASP I; 4 mM Mg2+) or 36 (ASP II; 6 mM Mg2+) mM L-aspartate (asp) or 32 mM DL-aspartate (ASP III) to the HTK solution in place of chloride. After infusion of 500 ml 5% glucose, canine kidneys were protected by an 8-min perfusion with HTK (n = 5), ASP I (n = 4), ASP II (n = 5) or ASP III-solution (n = 3). The subsequent ischemia lasted for 2 h at 27-31 degrees C. During reperfusion, both GFR and filtration fraction (FF) were higher in kidneys protected by L-aspartate-containing solutions. ASP III showed no improvement against HTK. An additional preischemic intra-aortal application of HTK or ASP I solution just above the exit of the renal arteries prior to the intrinsic protective perfusion further raised the postischemic GFR. The present results suggest that L-aspartate but also histidine may have favorable amino acid effects in renal protective solutions in addition to known positive effects of histidine.
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PMID:Contribution of amino acids in protective solutions to postischemic functional recovery of canine kidneys. 251 51


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