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

The release of glycogen phosphorylase from isolated, perfused rabbit heart was studied after substrate depletion and after global ischemia. The assayed efflux of the enzyme was found to be not only related to alterations in membrane integrity but also to the amount of glycogen in the injured heart tissue. The differential efflux profile of phosphorylase as a constituent of the sarcoplasmic reticulum-glycogenolysis complex in cardiac cells in comparison to cytosolic creatine kinase was found to be more pronounced employing K+-arrested, hypothermically perfused hearts exposed to imipramine (0.4 to 0.6 mM), known for altering specifically membrane integrity. Under these conditions only a rise in the release of creatine kinase occurs, whereas both glycogen content and the efflux of phosphorylase remains uneffected. It is suggested that the metabolical dependence of phosphorylase efflux from the injured heart muscle is of importance for its high sensitivity being a marker of acute heart infarction.
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PMID:On the release of glycogen phosphorylase from heart muscle: effect of substrate depletion, ischemia and of imipramine. 265 84

Earlier studies from our laboratory have shown that hyperbaric oxygen (HBO) treatment reduces edema, enhances aerobic metabolism and improves the recovery of the phosphorylase activity in postischemic rat skeletal muscle. However, as it has become increasingly apparent that oxygen in excess may have harmful effects, it was of interest to study if HBO caused an increased formation of oxygen free radicals. Toxic peroxides, as a result of oxygen free radicals, were quantitated in the postischemic skeletal muscle of rat and with HBO treatment by measuring the thiobarbituric acid reaction which includes the lipid peroxides and the alkydes including malondialdehyde (MDA), a key intermediate in the formation of peroxides. A tourniquet model of temporary ischemia of the rat hindlimb was used for 3 hours. Muscle biopsies were taken at various intervals before and after tourniquet release with and without hyperbaric oxygen at 2.5 atmospheres absolute (ATA) for 45 min after tourniquet release. Three hours of anesthesia caused a significant rise of thiobarbituric acid reactive material (TBAR) concentration in muscle compared to normal controls without anesthesia. An increase of similar magnitude was seen after 3 hours of ischemia, with or without reperfusion. These values were normalized after 45 min. HBO in the postischemic phase did not cause a further increase in the TBAR concentration in muscle immediately postischemically. However, the levels remained increased at 45 min after the onset of reperfusion, immediately after HBO treatment and had returned to normal values 2 hours postischemically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipid peroxidation products in postischemic skeletal muscle and after treatment with hyperbaric oxygen. 281 89

Pedicled skin flaps in the pig have been used to investigate the effects of 3-h ischemia and reperfusion on the epidermal metabolism of glycogen and glucose. Epidermal glycogen content fell steadily at a rate of about 1.2 mumol of glucose-equivalents per g wet weight per h whereas the rate of glucose consumption declined from 1.8 mumol per g wet weight during the first hour to about 0.25 mumol per g wet weight in the third hour. During ischemia the proportion of glycogen synthase in the I form increased progressively from an initial value of about 8% to about 70%, but the proportion of phosphorylase in the a form decreased only in the third hour of ischemia. The concentration of ATP decreased and ADP and AMP increased but the total pool of epidermal adenine nucleotides was not depleted. On reperfusion, these changes were reversed and normal epidermal concentrations of glucose and adenine nucleotides were restored within 30 min and remained stable thereafter. The resynthesis of glycogen proceeded at a steady rate of about 1 mumol per h per g wet weight and the phosphorylation state of both glycogen synthase and phosphorylase approached normal values after 3 h. It is concluded that epidermal glycogenolysis in ischemia is, at least in part, a consequence of activation of phosphorylase b by AMP, and that glycogen resynthesis on reperfusion is promoted by the ischemic activation of glycogen synthase.
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PMID:Effect of ischemia and reperfusion of pig skin flaps on epidermal glycogen metabolism. 309 2

1. Ischaemia was applied for 30 min to the liver of Wistar rats and of gsd/gsd rats, which have a genetic deficiency of phosphorylase kinase. The rate of glycogenolysis corresponded closely to the concentration of phosphorylase a. The loss of glycogen from Wistar livers was accounted for by the intrahepatic increase in glucose plus lactate. Further, the accumulation of oligosaccharides was negligible in the gsd/gsd liver. 2. Isolated hepatocytes from Wistar and gsd/gsd rats were incubated for 40 min in the presence of either KCN or glucagon. Again, the production of glucose plus lactate was strictly dependent on the presence of phosphorylase a. However, the catalytic efficiency of phosphorylase a was about 2-fold higher in the presence of KCN. 3. We conclude that the hepatic glycogenolysis induced by anoxia and by KCN is solely mediated by phosphorylase a. The higher catalytic activity of phosphorylase a under these circumstances could be due to an increased concentration of the substrate Pi.
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PMID:The hepatic glycogenolysis induced by reversible ischaemia or KCN is exclusively catalysed by phosphorylase a. 322 40

In the post-ischemic muscle, hyperbaric oxygen (HBO) treatments have been shown to reduce post-ischemic edema and enhance aerobic metabolism. In the present paper histological, histochemical and ultrastructural methods were used to study the influences of HBO treatment on the morphology of post-ischemic skeletal muscle. The changes were also quantified using morphometry. The circulation of the rat hindlimb was interrupted for 3 hours and muscle biopsies were taken 5 and 12 hours post-ischemia. Light microscopy showed signs of ischemic changes in the muscle. Morphometrically, the area with activity of the muscle enzyme phosphorylase was greatly reduced post-ischemia. HBO treatment at 2.5 atmospheres of absolute pressure (ATA) for 45 min significantly increased muscle cross sectional area with a positive phosphorylase reaction 5 hours post-ischemia. Three HBO treatments were necessary to maintain this effect, 12 hours post-ischemia. Ultrastructurally, the ischemic changes seen using light microscopy were confirmed. Morphometrically, there was a significant increase of mitochondrial size in the ischemic muscle compared with the control uninjured muscle but HBO did not markedly reduce these ultrastructural changes. It was concluded that the reduction of phosphorylase activity, a sensitive marker for muscle cell damage, is to a great extent prevented by HBO treatment in the post-ischemic phase.
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PMID:Effects of hyperbaric oxygen treatment in post-ischemic muscle. A quantitative morphological study. 338 22

The study of patterns of serum AST, ALT, CPK, LDH, and glycogen phosphorylase (GP) activity following bicycle ergometry in 26 male patients 1 to 1.5 months after myocardial infarction demonstrated no increase in AST, ALT and CPK activity, whereas total LDH activity was increased, with a tendency to elevated LDH-1 and LDH-2 fractions, as compared to the baseline, in those cases where exercise was discontinued because of ST depression. Patients with favorable response to bicycle ergometry that continued until the submaximum heart rate for a given age was achieved showed a tendency to elevated LDH-5 that may be a physiological response to exercise. The demonstrated increase in total GP activity, both in patients with exercise-induced ST depression and in those with elevated ST from the leads corresponding to the site of myocardial infarction, may reflect stress-induced reversible ischemia.
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PMID:[Effect of physical loading on serum enzyme activity in post-myocardial infarct patients]. 370 99

Perfusion of rat hearts according to the Langendorff technique with micromolar concentrations of palmitoylcarnitine or millimolar concentrations of phenylmethylsulfonyl fluoride protect the heart from deterioration by reperfusion after total-ischemia. This is based on the retention of the cytosolic enzymes determined (lactate dehydrogenase, glycogen phosphorylase and glycogen synthase) and of myoglobin, as well as on the resumption of contractile activity. Palmitoylcarnitine, like phenylmethylsulfonyl fluoride, could protect through plasma membrane stabilization, since more hydrophilic compounds had no effect.
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PMID:Protection by acyl-carnitines and phenylmethylsulfonyl fluoride of rat heart subjected to ischemia and reperfusion. 393 96

The left anterior descending coronary artery (LAD) of the dog was ligated completely for 1.5 min, and immediately after LAD ligation the heart was taken for determination of the glycogen phosphorylase and glycogen. Trimetazidine was injected intravenously 20 min before LAD ligation. LAD ligation increased the activity of glycogen phosphorylase and decreased the level of glycogen in both ischemic (LAD) and nonischemic (circumflex) areas. Trimetazidine at the dose of 0.3 or 1.0 mg/kg, being the dose that did not affect blood pressure and heart rate markedly, inhibited the ischemia-induced changes in glycogen phosphorylase and glycogen level. It is concluded that trimetazidine inhibits the ischemia-induced increase in the utilization of glycogen in the dog myocardium.
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PMID:Inhibitory effect of trimetazidine on utilization of myocardial glycogen during coronary ligation in dogs. 395 33

Histochemical study of enzymatic activity in the myocardium was performed in sudden cardiac death. Human hearts in which there were no macroscopic and histological focal or diffuse changes served as material. The following enzymes were studied in the anterior or posterior walls of the left ventricle or in the interventricular septum: succinate dehydrogenase, lactate dehydrogenase (LDH), beta-hydroxybutyrate dehydrogenase (OHBDH), alpha-glycerophosphate- and glucose-6-phosphate dehydrogenase, NAD-diaphorase and phosphorylase. Increased activity of OHBDH and LDH was found: 36,0 and 22,6% higher than in trauma and brain hemorrhage that served as control. These alterations seem to be connected with the increase of blood content of fatty acids, and lactate as a response to the catecholamine excess. Foci of an acute ischemia were found in the interventricular septum in 80% of cases in which phosphorylase was revealed. The appearance of the ischemic foci was obviously due to the coronary arteries contraction.
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PMID:[Histoenzymological characteristics of the myocardium in sudden cardiac death]. 405 12

The regulation of glycogen phosphorylase and glycogen breakdown in human skeletal muscle has been investigated using the needle biopsy technique. Preliminary studies showed that the activity of phosphorylase in vitro was dependent upon the concentration of inorganic phosphate (Pi) used in the assay system. The Km of phosphorylase a for Pi was found to be 26.2 mmol/l, and that of (a+b) (assayed in the presence of saturating AMP) was 6.8 mmol/l. Because of the difference in Km the apparent percentage of a to (a+b) activity varies with the Pi concentration used in the assay system. Phosphorylase a and (a+b) activities were therefore adjusted to saturating Pi concentrations. The ratio of the activities in this case is independent of the Pi concentration and constitutes a minimal estimate of the fraction of phosphorylase molecules in the a form. The fraction of phosphorylase in the a form in resting muscle was as a mean 22%. Despite nearly a quarter of the phosphorylase being in the a form glycogenolytic activity is extremely low. It is proposed that the concentration of Pi at the active site of the enzyme is low compared to the Km for this of either form of the enzyme, and is limiting to activity. A Pi concentration in resting muscle of 1-3 mmol/l was calculated. During epinephrine infusion at rest 90% of the phosphorylase was transformed to the a form but only a moderate increase in the glycogenolytic rate occurred. This rate approximated to 5-10% of the maximum rate of the enzyme (Vmaxa). During prolonged epinephrine infusion the glycogenolytic rate decreased despite the continuance of 90% or more of the phosphorylase in the a form. In contrast to epinephrine infusion prolonged ischemia resulted in a decrease in the mole fraction of phosphorylase a and simultaneously in an increase of the glycogenolytic rate. During isometric and dynamic exercise there was a rapid transformation of phosphorylase b to a paralleled by pronounced increase in the rate of glycogen breakdown. The increased rate of glycogenolysis during isometric exercise was close to the Vmax of phosphorylase a in vivo. When either form of exercise was continued to fatigue/exhaustion, a re-transformation of phosphorylase a to b was observed. During dynamic exercise cAMP in the muscle increased two fold. This increase was blocked by the prior administration of propranolol.+
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PMID:The regulation of glycogen phosphorylase and glycogen breakdown in human skeletal muscle. 613 34


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