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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

This case illustrates the difficulty of diagnosing a colonic stenosis of ischemic origin. A 70-year-old lady presents with abdominal pain, fever and melaena. Lc are 15.2, ESR 39 mm, CEA 2.7 ng/ml. A barium enema shows a stenosis of the transverse colon that is suspicious of neoplasia. At time of operation, an induration of the transverse colon is found with edema of the corresponding mesocolon but no tumour is palpated. A resection of this area is performed and an end to end anastomosis performed. Pathology shows an ischemic colitis secondary to a lymphocytic thrombotic venulitis. The patient is discharged home one month postoperatively. 4 weeks later she is readmitted with the same symptoms. A gastrograffin enema shows a similar stenosis in the transverse colon including the anastomosis. The diagnosis is made of a recurrent ischemic stenosis. The patient improves over a 10-day period of conservative treatment (anticoagulation, TPN, steroids). A control barium enema shows a near resolution of the stenosis. The majority of ischemic colitis are of arterial origin nevertheless ischemic colitis of venous origin exists. The factor causing venous ischemia are not known. It is though thought to be associated with hypersensitivity vasculitis of drug origin. Its initial diagnosis versus neoplasia is difficult but once made there is a good response to a conservative treatment.
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PMID:[Segmental ischemic colitis in lymphocytic thrombotic venulitis]. 822 85

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

The therapeutic potential of alpha-lipoic acid (thioctic acid) was evaluated with respect to its influence on cellular reducing equivalent homeostasis. The requirement of NADH and NADPH as cofactors in the cellular reduction of alpha-lipoic acid to dihydrolipoate has been reported in various cells and tissues. However, there is no direct evidence describing the influence of such reduction of alpha-lipoate on the levels of cellular reducing equivalents and homeostasis of the NAD(P)H/NAD(P) ratio. Treatment of the human Wurzburg T-cell line with 0.5 mM alpha-lipoate for 24 hr resulted in a 30% decrease in cellular NADH levels. alpha-Lipoate treatment also decreased cellular NADPH, but this effect was relatively less and slower compared with that of NADH. A concentration-dependent increase in glucose uptake was observed in Wurzburg cells treated with alpha-lipoate. Parallel decreases (30%) in cellular NADH/NAD+ and in lactate/pyruvate ratios were observed in alpha-lipoate-treated cells. Such a decrease in the NADH/NAD+ ratio following treatment with alpha-lipoate may have direct implications in diabetes, ischemia-reperfusion injury, and other pathologies where reductive (high NADH/NAD+ ratio) and oxidant (excess reactive oxygen species) imbalances are considered as major factors contributing to metabolic disorders. Under conditions of reductive stress, alpha-lipoate decreases high NADH levels in the cell by utilizing it as a co-factor for its own reduction process, whereas in oxidative stress both alpha-lipoate and its reduced form, dihydrolipoate, may protect by direct scavenging of free radicals and recycling other antioxidants from their oxidized forms.
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PMID:Modulation of cellular reducing equivalent homeostasis by alpha-lipoic acid. Mechanisms and implications for diabetes and ischemic injury. 906 43


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