Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whole excis ed rat hearts were treated with 5, 10, or 15% (v/v) dimethyl sulfoxide/glycerol and then some were frozen in liquid nitrogen while the balance remained unfrozen. Freezing and thawing rates were approximately 30degreesC/min. Ventricular tissue was examined for histological damage, glycogen depletion, and enzyme sites, using histological, histochemical, and electron microscopy techniques. Early signs of cellular degeneration and ischemia were observed in all unfrozen groups; depletion of glycogen reserves, fuchsinophilic staining, vacuolization and granulation of the sarcoplasm were noted. Results from frozen groups were similar, but ultrastructural damage was more severe and extensive. Alkaline phosphatase and succinic dehydrogenase sites were abundant in unfrozen specimens and absent or markedly reduced in frozen specimens which also exhibited widespread nonspecific staining throughout intercellular spaces.
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PMID:Cryoprotectant-treated myocardium evaluation. 6 Nov 4

Ligature and section of the abdominal aorta results in only minor and temporary functional and metabolic changes in the slow soleus muscle of the rat. A very small decrease in maximal tetanic tension corresponds to a few scattered areas of damaged and necrotic muscle fibres, in which decreased succinic dehydrogenase and loss of phosphorylase activity was observed. A new experimental approach, i.e. ligature and section of the abdominal aorta combined with terminal devascularisation, preserving intact tendons and innervation of the muscle causes maximal muscle ischemia, followed by an almost complete loss of tetanic tension output, marked shortening of contraction time and profound morphological and histochemical changes. The decrease in succinic dehydrogenase and ATPase activities and loss of phosphorylase activity occur in the majority of degenerating muscle fibres except for a thin rim of peripheral fibres during the first 4 days. Subsequently, the contractile properties recover gradually and enzyme activities reappear in the regenerating muscle fibres simultaneously with new revascularisation. Thirty days after the operation all the parameters observed returned to control values.
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PMID:Effect of ischemia on contractile and histochemical properties of the rat soleus muscle. 15 45

The histochemical and ultrastructural effects of extracorporeal circulation and aortic cross-clamping during coronary heart surgery have been examined in drill biopsy samples of the left ventricle in 22 patients. The biopsies were obtained before and after bypass with a DeSoutter drill. Histochemical studies indicated definite differences between control and experimental biopsies, with increased succinic dehydrogenase, cytochrome oxidase, and LDH activity, while phosphorylase A and myosin ATPase activities declined. Furthermore, free phospholipid levels increased, as determined by the acid hematein reaction. Ultrastructural examination demonstrated loss of glycogen, intracellular swelling, and mitochondrial damage, which included loss of matrix density, loss of cristae, and eventual disruption in the postbypass biopsy. These results, which closely resemble the effects of ischemia and reperfusion observed in animal experiments, suggest that the initial insult is a change in membrane permeability regulation.
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PMID:Histochemical and structural changes in human myocardial cells after cardiopulmonary bypass. 16 88

Animals develop 'infarct-like' lesions when injected with isoproterenol (ISP), a potent synthetic catecholamine. These lesions are morphologically similar to those of 'coagulative myocytolysis' (COAM) or myofibrillar degeneration, one of the findings described in acute myocardial infarction and sudden death in man. Wistar rats were divided into 8 groups: some were injected with 10 mg/kg ISP i.p. plus 5 muCi of tritiated ISP, while others served as control. Animals were sacrified at 5 and 30 min and 24 and 72 h. The ISP-induced lesions were studied by means of light microscopy, histochemistry, autoradiography and electron microscopy. Myofibrillar degeneration, positive tests for ischemia, increase of succinic dehydrogenase enzymes, hypercontraction and widening of Z bands of sarcomers were correlated with the rapid distribution of ISP. These lesions were minimized by prenylamine, a drug which inhibits catecholamine effects by slowing down Ca transport. It is concluded that myocardial necrosis induced by ISP is probably due to a primary act on the sarcolemmal membrane, followed by stimulation of adenylate cyclase, activation of Ca and Na channels, exaggreated Ca inflow, excess of excitation-contraction coupling mechanism, energy consumption and cellular death. The close resemblance of human COAM to ISP-induced lesions suggests that similar mechanisms may be involved.
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PMID:Pathogenesis of isoproterenol-induced myocardial lesions: its reation to human 'coagulative myocytolysis'. 63 73

The effect of the reperfusion on myocardial infarction has been studied in the rat in order to assess the possible reversibility of myocardial damage. The present study deals with reperfusion of experimental myocardial infarction in the rat. Two groups of animals were compared: one was subjected to permanent ischemia and the other was subjected to ischemia of variable duration 1) hour to 24 hours). The differences between infarction caused by permanent ischemia and the evolution of infarction following reperfusion were studied by means of histologic (121 specimens) histoenzymatic (56 specimens), ECG (100 specimens), techniques and study of the mcirocirculation (70 specimens). The size of the infarctions caused by temporary ischemia was found to be significantly smaller in 60% of the cases as compared to the infarctions caused by permanent ischemia. Histoenzymatic study (phosphorylase activity and succinodehydrogenase activity) confirmed the existance of a marginal zone extending over one third of the surface of the ischemic myocardium: reperfusion permitted the salvage of this zone and thereby diminished the extent of necrosis. The latter findings were further confirmed by the ECG study showing earlier regression of ischemic ST changes following early reperfusion. Microcirculatory changes secondary to anoxia may account for the fact that, in a certain percentage of the cases, early reperfusion does not prevent extension of infarction.
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PMID:The effect of coronary artery reperfusion on the extent of myocardial infarction. 84 30

The hippocampus provides a suitable area in the brain for the analysis of neuronal plasticity after application of a selective lesioning technique. Using histochemistry and autoradiography, we studied synaptic reorganization in the rat hippocampus with selective CA1 pyramidal cell lesioning caused by transient forebrain ischemia after long-term survival. An autoradiographic study was performed on second messenger systems ([3H]inositol 1,4,5-trisphosphate, [3H]forskolin and [3H]phorbol 12,13-dibutyrate binding). One-hundred days after ischemia, depletion of CA1 pyramidal cells and marked shrinkage of the CA1 subfield was noted in spite of unaltered thickness of the CA3 band and of the dentate molecular layers. Although neuronal density in the CA3 region of animals killed seven days after ischemia was not different from the normal group, 78% of animals showed neuronal loss of 30-50% in the stratum pyramidale of the CA3b 100 days after recirculation. Sixty-seven per cent of animals exhibited supragranular mossy fiber sprouting in the dentate gyrus. However, CA3 neuronal loss did not correlate with mossy fiber sprouting. Succinic dehydrogenase was depleted in the CA1 100 days after ischemia, and animals with CA3 damage showed a reduction of succinic dehydrogenase activity in the CA3. In contrast to the unaltered acetylcholinesterase in the animals killed seven days after ischemia, high density bands of acetylcholinesterase activity in the stratum pyramidale of the CA1 were found to be broadened 100 days after ischemia. In the CA1 subfield, subnormal activity of [3H]phorbol 12,13-dibutyrate and [3H]forskolin binding were observed in spite of the depleted [3H]inositol 1,4,5-triphosphate binding. [3H]Forskolin binding in the hilus had increased by 62% 100 days after ischemia, although binding in the stratum lucidum of the CA3 and in the stratum moleculare of the dentate gyrus was unaltered. However, no visible supragranular increase in [3H]forskolin binding was observed. These results indicate that long-term survival after CA1 pyramidal cell depletion caused by transient forebrain ischemia induced the modulation of neuronal activity and synaptic rearrangements in the whole hippocampal formation.
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PMID:Post-ischemic synaptic plasticity in the rat hippocampus after long-term survival: histochemical and autoradiographic study. 170 23

A homogeneous group of six patients, who underwent coronary artery bypass surgery, was studied to determine the presence of oxidative stress caused by oxygen-derived free radicals and its relationship with reperfusion cell damage. Biopsies were performed before ischemia and 10 minutes after reperfusion. The samples were assayed for hydroperoxide-initiated chemiluminescence and histochemical succinic dehydrogenase activity; the specimens were also studied by electron microscopy. The preischemic biopsy specimens showed chemiluminescence of 40 +/- 2 (cpm/mg protein) x 10(3), normal succinic dehydrogenase activity (grade 4), and generally preserved ultrastructure (necrotic/normal cells 5/100). However, the reperfusion biopsy specimens showed an increase in chemiluminescence to 91 +/- 19 (cpm/mg protein) x 10(3) (p less than 0.025), a partial loss of enzymatic activity (grade 2.6), and ultrastructural changes characterized by mitochondrial swelling and focal myofibrillar disorganization (necrotic/normal cells: 15/100; p less than 0.001). These observations seem to indicate the presence of oxidative stress during reoxygenation, a situation that may play a major role in the genesis of reperfusion injury. It appears to be the first observation relating free radical-induced oxidative stress to reperfusion injury in humans.
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PMID:Assessment of myocardial oxidative stress in patients after myocardial revascularization. 334 Nov 66

Poly- and monoclonal antibodies to neoantigens of the human C5b-9 complement complex, as well as polyclonal antibodies to C5, C8, and C9, were used to detect and identify C5b-9 deposits in human myocardial tissue. Immunocytochemical studies were performed on fresh-frozen autopsy material derived from patients with myocardial infarctions; in addition, in 17 of these patients, paraffin sections of formalin-fixed tissue were investigated. Sixteen autopsies from patients with noncardiac diseases were analyzed as controls. Without exception, C5b-9 positivity was registered selectively and exclusively on and in myocardial cells located within the zones of infarction. The selectivity of staining was confirmed by control reactions for succinic dehydrogenase activity performed in adjacent, respective double-stained sections. Most intensive staining with anti-neoantigen antibodies was observed in the peripheral areas of the infarctions. Weak staining for C3d, rather strong staining for C5 and C9, and intermediate staining with anti-C8 antibodies were observed in the same localizations. Stainings for C4 and IgA were negative, whereas immunocytochemical reactions for IgG and IgM revealed an irregular and very weak staining. Only very weak staining was also observed with a monoclonal antibody to complement S-protein, indicating that the terminal complement components were deposited mainly in the form of membrane-damaging C5b-9 complexes. Immunocytochemical staining for C5b-9 was found to represent a most sensitive tool for detection of ischemic myocardial lesions, permitting easy detection even of single cell necroses. As a working hypothesis, we suggest that initial ischemia may cause loss of the ability of the heart muscle cells to regulate complement turnover at the membrane level. The resulting deposition of C5b-9 on the cell membranes may contribute to functional disturbance and irreversible damage of myocardial cells during the infarction process.
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PMID:Deposition of the terminal C5b-9 complement complex in infarcted areas of human myocardium. 352 91

We describe two brothers, 25 and 19 years-old, with muscle pain and decreased strength after prolonged exercise; these symptoms are worsened by cold whether of fasting. One of the patients developed recurrent myoglobinuria and had one episode of renal failure. Laboratory investigations were normal between the crises, but during myoglobinuria, serum creatine kinase activity increased 100 times. Electromyography was suggestive of denervation. Muscle biopsy showed increased lipid droplets by the "oil red O" stain and increased activity of succinic dehydrogenase histochemical reaction. Lactate production during ischemia was normal. Biochemical analysis showed decreased carnitine-palmityl-transferase activity in muscle (7.23 and 10.58 nmoles/min/gr; normal range 66.7 +/- 17.3), with normal values for carnitine-octanoyl-transferase and carnitine-acetyl-transferase. The metabolic pathway of fatty acid utilization as an energy source for muscle during exercise in normal and in pathological conditions is discussed.
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PMID:[Myopathy due to carnitine palmitoyltransferase deficiency. Report of 2 cases with enzymatic analyses on muscle tissue]. 666 Nov 2

The identification of metabolic and drug interventions able to reduce myocardial injury after coronary artery occlusion requires experimental models. The rat model of ischemic injury is technically simple, unexpensive, informative and accessible to quantitative studies. In this present study, 41 rats underwent temporary myocardial ischemia of variable duration using left coronary artery ligation. They were sacrificed at 48 hours, and the heart was immediately frozen in liquid nitrogen. Serial 8 micrometer sections of known intervals were tested for succinodehydrogenase (NBT stain). Gross sectional areas measured planimetrically were utilized to calculate total myocardial volume (Vmyocardium) and infarcted myocardial volume (Vinfarct) with the aid of a programmable calculator. The data showed a linear regression for Vinfarct/Vmyocardium according to the time of ischemia (p 0,001). We suggest to test the efficiency of metabolic and drug interventions on the regression curve of the necrotic tissue using a multiple linear analysis. Since ischemic changes evolve more rapidly in this model, the intervention under study should be set up at the time of coronary artery occlusion.
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PMID:Experimental myocardial infarction in the rat as a quantitative model for the study of anti-ischemic interventions. 731 11


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