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

With the author's own observations and literature sources as a background the key issues concerned with increasing the viability of the myocardium in acute ischemia are considered. The possibility of a material enlargement of the collateral coronary circulation through administration of mesatonemonoaminoxidase inhibitors, diprazine, preparations of the metabolites type and of other agents is shown. Under consideration are data on the membranes-stabilizing effect in acute ischemia of the myocardium of dimedrol, diprazine and prednisolone, as well as possible ways of increasing the survival of the myocardium by activating the redox-processes and through an adequate supply of energy to ensure the vital functions of the myocardial cell at rest by using pertinent pharmacological agents (cytochrome C, NADP, ubiquinone, hexose-phosphate, monoaminodicarboxylic amino acids).
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PMID:[Problem of increasing the viability of the ischemic myocardium in the light of experimental studies]. 23 63

Neurotrophic factors regulate neuronal survival and neurite growth in development and following injury. Oxidative stress produced in neurons as a consequence of primary injury, or during reperfusion following ischemia, may contribute to cell death. Here, the effects of nerve growth factor (NGF) on the response to H2O2 injury were examined in the PC12 rat pheochromocytoma cell line. Specifically, the effect of NGF on cell viability after H2O2 injury was measured. Pretreatment with NGF enhanced survival after H2O2 treatment, as measured by Trypan blue dye exclusion, radiolabeled amino acid incorporation, tetrazolium salt reduction, or cytoplasmic enzyme release. One early event associated with H2O2 treatment was a rapid decrease in NAD+. Although initial decreases in NAD+ levels were similar in control and NGF-treated cells, the latter recovered more rapidly and extensively. The decline in total NAD observed after NGF treatment was almost equal in magnitude to the measured increase in NADP. Inhibition of poly(ADP-ribose) polymerase also enhanced viability following H2O2 injury. Treatment with both NGF and an inhibitor of this enzyme resulted in a greater reduction of H2O2 toxicity than was observed with either agent alone. These data suggest that NGF protection is multifactorial and that a significant component of the NGF effect is due to its regulatory role in the metabolism of pyridine nucleotides.
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PMID:Nerve growth factor effects on pyridine nucleotides after oxidant injury of rat pheochromocytoma cells. 145 Sep 13

The recovery of both contractile performance and metabolic response of rat heart following 1 h of ischemia after equilibration with glucose + insulin (glucose-ischemia) or with pyruvate (pyruvate-ischemia), was tested in normoxic reperfusion in the presence of glucose + insulin, pyruvate, lactate or acetate. In glucose-ischemia only the reperfusion with pyruvate results in a complete recovery of the contractile force (left ventricular pressure, LVP) (170%) and good recovery of high energy phosphate compounds. Lower LVP and tissue energy charge were found in glucose reperfusion and even less in lactate and acetate reperfusion. Disappearance of the IMP accumulated during ischemia is evident only in the pyruvate reperfusion indicating a higher metabolic recovery. On the contrary in pyruvate-ischemia all types of reperfusion tested were effective in reactivating the contractile force (although acetate to a lesser extent); the contractile activity was accompanied by a good recovery of phosphocreatine, ATP, energy charge and by the decrease of IMP. Large decreases of adenine nucleotides and NADP and lower decreases of NAD are observed during ischemia/reperfusion in both systems. Pyruvate-ischemia is quite similar to, if not worse than glucose-ischemia, for all the metabolic parameters considered, but not worse for the possibility of recovery. Some specific effect of pyruvate should be exerted during the ischemic phase. The mechanism of pyruvate protection is discussed in relationship to: (i) the possible activation of pyruvate dehydrogenase, (ii) the activation of NADPH-dependent peroxide scavenging systems, (iii) the direct scavenging action of pyruvate on H2O2.
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PMID:The protective action of pyruvate on recovery of ischemic rat heart: comparison with other oxidizable substrates. 218 87

Purine nucleotides, nucleosides, nucleobases, dinucleotides and nucleosides derivatives from acid-extracted rat liver and diaphragm were separated and quantitated by reversed-phase ion-pair high-performance liquid chromatography with a mobile phase composed of 90 mM potassium phosphate, 15 mM tetrabutylammonium hydroxide and a 1-30% methanol gradient. During 5 min of ischemia, adenine and guanine nucleotides decreased along with significant declines in NAD and increases in adenosine, inosine, hypoxanthine, xanthine, NADP and adenylosuccinate. Nitrobenzylthioinosine by gavage (5 mg/kg per day for five days) increased adenosine levels but without any alteration in nucleobase levels. Adenosine was shuttled to every available intracellular reservoir which included in declining order of magnitude GDP greater than adenosylhomocysteine greater than adenosine greater than ADP greater than AMP greater than IMP = XMP = GMP.
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PMID:Demonstration of the adenosine reservoirs with nitrobenzylthioinosine in liver and diaphragm by high-performance liquid chromatography. 339 39

One-hour ischemia followed by rat liver reoxygenation brings about the accumulation of endogenous products of lipid peroxidation (LPO) and deterioration of the monooxygenase system (the drop of cytochrome P-450 content, amidopyrine N-demethylase and NADP X H cytochrome reductase activity). Application of the antioxidant ionol inhibited LPO and protected the monooxygenase system from reoxygenation but not from ischemic injuries. Phenobarbital alone and combined with ionol did not protect the monooxygenase system from ischemic and reoxygenation injuries but provided the retention of high absolute indicators of the system. Ionol and its combination with phenobarbital also increased the survival of rats with ischemized liver.
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PMID:[Protective action of antioxidants and microsomal monooxygenase inducers in ischemic and reoxygenation damage to the liver]. 683 Oct 14

Local disturbance of liver circulation for 40 minutes did not lead to any substantial changes in the hydroxylation system of microsomes of the ischemized area. 60-, 120- and 180-minute circulation distress causes a progressing decrease in amidopyrine and aniline metabolism, diminution of the content of cytochrome P-450 in the microsomes, and of the activity of NADP.H-ferricytochrome-c-reductase, NADP.H-neotetrazolium-reductase and NADP.H-oxidase. After 120-minute ischemia hydrophobic properties of the microsomal membranes were found to be decreased.
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PMID:[Changes in the enzyme activity of the hydroxylating system of the rat liver endoplasmic reticulum in ischemia]. 705 83

Tissue contents of NADPH and NADP+ were measured in freeze-clamped samples of normal rat liver and in four transplantable rat hepatomas covering a wide range of growth rates. Lowry cycling procedures were employed for analysis, using alkaline extracts for NADPH and acid extracts for NADP+. The mean NADPH content in 33 normal livers was 515 nmol/g wet weight, and mean NADP+ content was 311 nmol/g wet weight. In the four hepatomas, the amounts of both NADPH and NADP+ were low, and the extent of decrease correlated with tumor growth rate. In the slowly growing hepatoma 9618A, total NADP was slightly decreased (63% control) and more extensive decreases were observed in the medium growth rate tumors 47C and 8999 (38% and 19%, respectively, of control). In the rapidly growing hepatoma 3924A, total NADP was drastically decreased to 3% of the control liver value. Measurement of NADPH and NADP+ recovery from extracts of hepatoma 3924A showed that there were no inhibitors that might have blocked the activity of the assay enzymes. The NADPH/NADP+ ratio was close to the normal liver value in all four hepatomas. A 30-sec period of ischemia did not cause significant change in NADPH, but gave 33% decrease in liver NADP+. A 5-min period of ischemia decreased NADP+ to 50% of the zero-time value in liver, and to 71% in hepatoma 3924A, but was without effect on NADPH.
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PMID:Decreased content of reduced and oxidized nicotinamide-adenine dinucleotide phosphate in rat hepatomas. 715 Oct 32

Warm ischemia of the intestine is a medical emergency which results from mesenteric vascular occlusion. In addition, intestinal transplantation techniques will also inevitably result in intestinal ischemia. The recovery of organ function following ischemia depends on the extent of irreversible damage produced by the ischemia and the extent of reflow upon reperfusion. In some organs energy homeostasis has been found to correlate with organ recovery and graft survival following ischemia-reperfusion. Investigating the usefulness of the determination of adenine and pyridine nucleotides as indicators of the extent of ischemic injury in intestinal segments, we found that after an initial 40% decrease in ATP following 30 min of ischemia there was no further decrease despite increasing the ischemia period to 120 min. Similarly, the decrease in NAD+ and NADP which occurred after 30 min of ischemia did not decrease further after 60, 90, or 120 min of ischemia. Xanthine was the only biochemical where an increase appeared to correlate with ischemia duration while energy charge was of no value in indicating injury extent. Additionally, after reperfusion there was at best a poor correlation between recovery of ATP content and the duration of ischemia. Microcirculation reflow after reperfusion indicated ischemia time-related endothelial cell injury. Thus, the measurement of high-energy phosphates in intestinal segments is not of value as an indicator of the extent of intestinal ischemic injury.
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PMID:Adenine nucleotides of ischemic intestine do not reflect injury. 841 29

Different times of incomplete cerebral ischemia (2, 4, 6, 8, 10 and 30 min) were induced by bilateral common carotid artery occlusion in anesthetized rats to evaluate the time course of changes in lipid peroxidation and energy metabolism. Analysis of malondialdehyde (used to assess the levels of lipid peroxidation), ascorbic acid, oxypurines, nucleosides, nicotinic coenzymes and high-energy phosphates, was carried out by high-performance liquid chromatography on neutralized perchloric acid extract of brain tissue. Under the present experimental conditions, malondialdehyde, nicotinic coenzymes and ATP catabolites (oxypurines and nucleosides) were affected by increasing times of ischemia, with respect to control sham-operated rats. In particular, the concentration of malondialdehyde, undetectable in control brains, increased from 1.26 nmol/g wet weight after 2 min of carotid clamping to 13.42 nmol/g wet weight at the end of 30 min of incomplete cerebral ischemia. The presence of oxidative stress was further supported by ascorbic acid depletion, which was particularly significant after 10 and 30 min of incomplete ischemia. Carotid clamping provoked an imbalance between energy production and consumption that was evidenced by a reduction in ATP and GTP concentrations and an increase in ATP degradation products such as AMP, oxypurines and nucleosides. A decrement in the sum of adenine nucleotides and the energy charge potential indicated a progressive malfunctioning of energy-producing metabolic cycles. A possible contribution to such a severe change in energy state might be related to depletion of NAD and NADP, particularly noticeable after the longest incomplete brain ischemia times, that should have provoked a consequent lessening of oxido-reductive reactions. Bilateral carotid clamping causes a significant reduction in brain oxygen and substrate supply that results in inhibition of energy metabolism and triggering of oxygen-radical-induced lipid peroxidation.
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PMID:Effects of increasing times of incomplete cerebral ischemia upon the energy state and lipid peroxidation in the rat. 943 8

The intensity of free radical processes and the regulation of NADP-isocitrate dehydrogenase (EC 1.1.1.42; NADP-IDH) activity have been studied in the cytoplasmic fraction of normal and ischemized rat myocardium. Chemiluminescence parameters, such as the light sum (S) of slow flash and the tangent of the kinetic curve slope angle (tanalpha1), which characterize the intensity of free radical processes, were increased in ischemia 2.1- and 20.0-fold, respectively. The slow flash intensity (Imax) was increased 22-fold. The contents of lipid peroxidation products--diene conjugates and malonic dialdehyde--were increased 11.9- and 4.7-fold, respectively, suggesting pronounced oxidative stress. Using homogenous enzyme preparations of NADP-IDH isolated from the normal and experimentally ischemized rat myocardium, a number of catalytic properties of the enzyme were characterized for normal and pathologic conditions. NADP-IDH from the normal and ischemized myocardium had the same electrophoretic mobility and was regulated similarly by Fe2+, Cu2+, Zn2+, and also with succinate and fumarate. However, under normal and pathologic conditions NADP-IDH was different in the affinity for substrates and in the sensitivity to inhibitory effects of hydrogen peroxide, reduced glutathione, and of Ca2+. The degree of synergy in the enzyme inhibition with Fe2+ and H2O2 was less pronounced in ischemia. The inhibitory effect of the reaction product 2-oxoglutarate was higher under normal conditions than in ischemia (the Ki values were 0.22 and 0.75 mM, respectively). The specific features of the NADP-IDH regulation in ischemia are suggested to promote the stimulation of the enzyme functioning during increased level of free radical processes, and this seems to be important for NADPH supplying for the glutathione reductase/glutathione peroxidase antioxidant system of cardiomyocytes.
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PMID:Intensity of free radical processes and regulation of cytoplasmic NADP-isocitrate dehydrogenase in rat cardiomyocytes under normal and ischemic conditions. 1212 79


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