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

The authors carried out histochemical determinations of the glycogen level and the activity of some enzymes controlling carbohydrate metabolism (glycogen transferase and phosphorylase, succinate dehydrogenase) in the lumbar segments of the spinal cord of 40 animals (cats) with circulatory ischemia caused by aorta ligation. The examinations were performed at different periods of time after the ischemia induction under conditions of carbohydrate load. In the course of the pathological process development because of the ischemia (within a period ranging from 6 hours to 26 days) considerable variations of the glycogen-synthetizing capacities of the spinal cord nervous elements were revealed. These variations were of a periodic character. The number of glycogen-containing cells was maximal within a period ranging from the 2nd to the 10th day: this correlated with the highest enzymatic activity in this period. The glycogen content in a cell and the degree of the latter's damage were found to be in an inverse relationship. It is shown that different resistance of the nervous elements to hypoxia is determined to a great measure by their capacity to synthetize and deposit glycogen. Thus, the glycogen metabolism, being a specific compensatory-adaptive mechanism of the nervous tissue, is, thereby, a material basis of its vital activity.
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PMID:[Glycogen metabolism of neuronal systems of the spinal cord in experimental ischemia]. 617 33

Effects of regional ischemia on myocardial glycolysis were studied by measuring the levels of glycolytic intermediates in the endo- and epicardial layers of the left ventricle in dogs anesthetized with pentobarbital. Regional ischemia was induced by ligating a small branch of the left anterior descending coronary artery. The myocardial tissue samples were removed before and 1.5, 3, 7, or 30 min after coronary artery ligation. Based on a crossover plot study of the glycolytic intermediates, it is suggested that the activity of glycogen phosphorylase was accelerated, while that of phosphofructokinase was inhibited in ischemic myocardium samples removed 1.5, 3, 7, and 30 min after ligation. When the frozen myocardium was allowed to stand at room temperature for 10 min, the crossover plot study revealed acceleration of phosphofructokinase activity. The metabolic response to regional ischemia of the endocardial layers was more marked than that of the epicardial. During ischemia the levels of adenine nucleotides did not change significantly, but those of citrate and hydrogen ions increased significantly. It appears that inhibition of myocardial phosphofructokinase activity during ischemia is partly due to an increase in the levels of citrate and hydrogen ions in the ischemic tissue.
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PMID:Crossover plot study of glycolytic intermediates in the ischemic canine heart. 621 59

Dosaged restriction of coronary blood flow (by 30, 50, 70 and 90%) was reproduced for 30 minutes in dogs with a closed chest. In all degrees of coronary blood flow restriction the loss of glycogen, accumulation of lactic acid and cAMP (in reduction of blood flow by 50 and 70%) and activation of glycogenolysis, phosphorylase and phosphofructokinase were recorded in the zone of ischemia. The changes advanced with the deepening of ischemia. Similar, though less pronounced changes were found outside the ischemic zone. Marked metabolic shifts were disclosed in the right ventricle. The mechanisms of anaerobic oxidation activation in ischemia are discussed.
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PMID:[Myocardial carbohydrate metabolism in limited coronary blood flow]. 626 47

Following coronary artery ligation (CAL), levels of cAMP and the activity ratio of cAMP-dependent protein kinase, of phosphorylase kinase, and of phosphorylase are significantly elevated in both ischemic and nonischemic areas of the canine left ventricle. The aerobic level of cAMP was found to be 0.4 to 0.6 pmol/mg myocardium only after a precooled clamp or a cryobiopsy device was employed to guarantee tissue freezing in situ. Maximal changes in response to ischemia are observed within 2 min in both parts of the heart. Twenty minutes after the onset of ischemia, different responses have been found in the nonischemic and ischemic tissue. Whereas the levels of cAMP and the activity ratio of protein kinase, of phosphorylase kinase, and of phosphorylase returned to aerobic values in the nonischemic area, these parameters remained elevated in the ischemic area. The changes in the levels of myocardial cAMP and in the cAMP-dependent protein kinase activity ratio following CAL could be prevented by propranolol.
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PMID:Cyclic nucleotides and changes in protein kinase activity ratio in the ischemic and nonischemic myocardium. 630 32

Several problems in myocardial ischemia are discussed based on our experimental and clinical studies. Histochemical changes of the myocardium of adult mongrel dogs with a coronary artery ligation were as follows: The most noticeable findings were a decrease of phosphorylase activity in the pericapillary region of the infarcted area and an enlargement of the discoloration area due to fusion according to the prolongation of the ligation period. This may be explained by the fact that ischemic process takes place around the pericapillary zone in the early stage due to an arborescent distribution of the vascular system in the myocardium. This is presumed as one of the factors which induces heterogeneity of the ischemic myocardium. The reversibility of the injured myocardium due to ischemia was investigated electron-microscopically. The time limit of the myocardial reversibility from ischemic damage was 30 to 50 min. Characteristic changes of LDH isoenzymes and the pathohistological changes of the myocardium after ligation and reperfusion of the coronary artery were as follows: a) A decrease of the LD5 (H subunit) fraction degeneration of the myocardial fibers, fibrosis of the connective tissue and scar formation took place. b) The minimum value of LD5 (H subunit) was observed in cases with a 7-day ligation in the ligation group and in cases with a 12-hour ligation which was followed by a 7-day reperfusion in the reperfusion group. c) The time to reach the minimum LD5 value differed between these 2 groups. The most probable cause of this difference is the protection of the myocardium by reperfusion. 4) In 24 dogs 20 mCi 99mTc-PYP was injected intravenously one and a half hours before the reopening of the chest. Then, Tc-PYP images were obtained at frontal and left lateral views. Tc-PYP images of each cross-sectional surface were also obtained. In the ligation group, 99mTc-PYP uptake in the ischemic myocardium was demarcated clearly in cases with a 1-7 day ligation. In the reperfusion group, 99mTc-PYP uptake in the ischemic area was clearly noticed in cases with a 12-hour to 6-day ligation, which was followed by a 1- to 7-day reperfusion. When the period of the reperfusion was prolonged, it became more difficult to obtain a positive image. In 14 patients with acute myocardial infarction Tc-PYP scintigrams were studied with reference to their ECG.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:President lecture. Observations on myocardial ischemia. 663 71

Rhabdomyolysis leading to acute renal failure necessitating hemodialysis is described in three chronic alcoholics. In each case an acute medical or surgical event, but not alcoholic intoxication, was implicated. Renal biopsies demonstrated acute tubular necrosis with intraluminal deposits consisting of Tamm-Horsfall protein and myoglobin. After recovery all three patients were demonstrated to have proximal muscle weakness with similar electromyographic abnormalities but nerve-conduction was impaired in only two. Muscle biopsies showed mixed, but predominantly type II fiber atrophy and reduced muscle phosphorylase levels. In the one patient tested the lactate response to forearm muscle ischemia was abnormal. It is postulated that chronic alcoholics may be predisposed to rhabdomyolysis and acute renal failure following acute medical and surgical stress as well as acute alcohol abuse. The muscle damage in these patients may be due to impaired intra cellular glycogen metabolism.
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PMID:Rhabdomyolysis and acute renal failure in chronic alcoholics with myopathy, unrelated to acute alcohol ingestion. 673 97

Under conditions of acute ischemia spontaneous fibrillation which developed in heart ventricles as well as arrhythmias which were medicamentally provoked both were accompanied by a decrease in activity of glycogen phosphorylase a. At the same time, there was a distinct increase of non-phosphorylated isoenzyme ratio to the total phosphorylase activity of the tissue and the total glycogen pool was decreased. The decrease in activity of glycogen phosphorylase a, after pharmacological correction of metabolism of highly ischemized myocardium using obzidan and digoxin at therapeutic doses, occurred simultaneously with a decrease in the level of phosphorylase b activity in the tissue. A hypothesis, considering an increase in glycogenolysis as a trigger mechanism in development of ventricle fibrillation under conditions of acute coronary occlusion, is criticized.
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PMID:[Role of glycogenolysis inhibition in the etiology of arrhythmias in coronary disease]. 715 22

Hearts of 38 men dying suddenly of acute coronary insufficiency and autopsied within 3 hours after death were examined. Foci of acute ischemic injuries in different parts of the myocardium were studied by histochemical methods for which the activity of succinate dehydrogenase and phosphorylase were determined. Early ischemic lesions in the myocardium were found in 22 fatalities, of them 5 had acute myocardial infarction, in 9 foci of ischemia were combined with the presence of postinfarction scars and fine focal cardiosclerosis, in 8 cases foci of early ischemia were the only changes in the myocardium. The majority of the decreased had stenosing atherosclerosis of the coronary arteries. Localization of ischemia foci in the myocardium did not always correspond to the severity of stenosing or the presence of thrombosis of the artery supplying the corresponding parts of the heart muscle. No foci of ischemia in the myocardium were found in 16 decreased who also had quite marked coronary atherosclerosis.
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PMID:[Early ischemic injuries of the myocardium in sudden cardiac death]. 742 69

The effect of silymarin on liver cell damage induced by ischemia was studied in rats fasted for 24 h. In the first series of experiments in vitro ischemia was induced by storing tissue blocks in closed vials at 37 degrees C for 15, 30, 45 and 60 min. Cell injury was detected by the cytophotometrical measurement of glycogen phosphorylase activity in unfixed cryostat sections demonstrated by a modified histochemical procedure. In the second series of experiments in vivo ischemia was provoked by clamping the afferent vessels to the median and left lateral lobes of the liver for 60 min, followed by removal of the clamp and reperfusion. The extent of cell damage was determined by measuring the ALAT and ASAT activities in serum at 1, 3, 6 and 24 h after ischemia and by quantifying the extent of necrosis in the liver after 24 h reperfusion by measuring the unstained areas in cryostat sections incubated for lactate dehydrogenase activity. Silymarin (100 mg/kg b.w.) was administered intravenously at 5 min before both the induction of ischemia and the restoration of blood flow (in vivo ischemia) and at 1 h and at 5 min before sacrifice (in vitro ischemia). Controls received an equal amount of saline. The serum amino-transferase activities after 24 h reperfusion were significantly reduced in the silymarin-treated group (n = 10); ALAT 293 +/- 193 U/L, ASAT 343 +/- 229 U/L compared with the control group (n = 7): ALAT 1238 +/- 743 U/L, ASAT 948 +/- 541 U/L (p < 0.03), and the extent of necrosis decreased from 25.6 +/- 16.0% ( n = 7) to 7.8 +/- 8.3% (n = 10) (p < 0.01) after treatment with silymarin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of silymarin on rat liver injury induced by ischemia. 828 22

In the present study we have investigated whether enzyme histochemical parameters can be applied to detect early ischemic damage in rat heart after ischemia without restoration of the blood flow. Ischemia was induced by incubating heart fragments for 0, 10, 20, 30, 60, 120 and 240 min at 37 degrees C. The activity and localization of the following enzymes was studied in unfixed cryostat sections using quantitative histochemical methods: lactate dehydrogenase, creatine kinase, succinate dehydrogenase, phosphofructokinase, acid phosphatase, 5'-nucleotidase and glycogen phosphorylase. Moreover, the ultrastructure of the tissue was studied with special attention to the appearance of flocculent densities in mitochondria, which can be seen as a sign of irreversible cell damage. It was shown that glycogen phosphorylase activity in rat heart decreased after short periods (30 min) of in vitro ischemia, whereas all other enzymes studied were not decreased up to 240 min, with the exception of lactate dehydrogenase and phosphofructokinase activities which were diminished only at 240 and 120 min of ischemia, respectively. Some reaction product was found after incubating for 5'-nucleotidase activity in the absence of substrate, indicating the presence of endogenous substrate(s). This endogenous substrate disappeared from the myocytes after 20 min of ischemia. It is assumed that AMP and/or other phosphate-containing compounds play an essential role in the activation of glycogen phosphorylase. Significant reduction of glycogen phosphorylase activity is correlated with the irreversible stage of damage of myocytes as judged from the ultrastructure.
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PMID:Histochemical detection of glycogen phosphorylase activity as parameter for early ischemic damage in rat heart. 850 31


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