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)

Regional cerebral protein synthesis following brief ischemia was investigated in the Mongolian gerbil, utilizing L-[methyl-14C]methionine autoradiography. Transient ischemia was induced for 1, 2 or 3 min. At various recirculation periods up to 48 h, animals received a single dose of L-[methyl-14C]methionine and then were terminated 35 min later. Sham-operated animals showed a normal pattern of amino acid incorporation into the proteins of the brain. Following 1-min ischemia, the pattern of protein synthesis was similar to that in the sham-operated gerbils. Ischemia for 2 min, however, caused marked inhibition of protein synthesis in the neocortex, striatum, hippocampal CA1 sector and the thalamus at 1 h of recirculation. Extensive recovery of protein synthesis was found in the neocortex, the striatum, the hippocampal CA1 sector and the thalamus at 5-24 h of recirculation, but, a slight inhibition was detectable in the hippocampal CA1 sector in one of six animals. This inhibition had fully recovered at 48 h of recirculation. Following 3-min ischemia, severe impairment of protein synthesis was found in the neocortex, striatum, the whole hippocampus and the thalamus. After 5-24 h of recirculation, the protein synthesis in these regions had gradually recovered, except that complete lack of amino acid incorporation was seen in the hippocampal CA1 subfield. This impairment of protein synthesis in the hippocampal CA1 sector was not recovered at 48 h of recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional impairment of protein synthesis following brief cerebral ischemia in the gerbil. 232 49

Transient ischemia does not induce myocardial necrosis but may be associated with prolonged contractile dysfunction ("stunned" myocardium). It has been suggested that alteration of the excitation-contraction coupling system (sarcoplasmic reticulum) could be responsible for this phenomenon. We tested this hypothesis by characterizing sarcoplasmic reticulum (SR) function in an isolated rat heart model of "stunned" myocardium (hearts reperfused after 10 min of normothermic global ischemia). At the end of the ischemic period oxalate-supported Ca-uptake was depressed either in the whole homogenate or in isolated SR (to 47% and 22% of control values, respectively). During reperfusion Ca-uptake of the whole heart homogenate recovered almost completely whereas slight but significant depression persisted in isolated SR (48 +/- 2 vs 67 +/- 4 nmol/min x mg, P less than 0.01). In the presence of ruthenium red or ryanodine, two inhibitors of SR Ca-release channels, Ca-uptake was stimulated. Both in the whole heart homogenate and in isolated SR, such stimulation was remarkably smaller after reperfusion than in control conditions (P less than 0.001) suggesting reduced conductivity state of the SR Ca-release channels. Ca-stimulated, magnesium-dependent ATPase activity was remarkably reduced during ischemia and postischemic reperfusion induced only incomplete recovery (93 +/- 18 vs 169 +/- 14 nmol ATP/min x mg protein, P less than 0.05). We conclude that complex modifications of SR function occur in the "stunned" myocardium and could contribute to the contractile impairment found in this condition.
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PMID:Sarcoplasmic reticulum function in the "stunned" myocardium. 247 59

Evaluation of degree of muscle ischemia of a limb and its reversibility is a poorly resolved practical problem, and it has not been clarified whether vasodilatory and circulatory spasmolytic substances possess, in addition to an effect of increasing irrigation, any direct action on muscle cell energy metabolism. An experimental study used histochemical techniques to evaluate oxidative enzyme activity of tissues. The compound tetrazolium nitro-blue (NBT), when reduced by tissue dehydrogenases, has the property of producing a dense non-crystalline blue pigment designated "formazan". During muscle ischemia, the time of appearance of this reaction increases with degree of ischemia through the bias of the decrease or disappearance of succinate-dehydrogenases. Transient ischemia of hindpaw, over 3, 6, 9, 12, 15 and 18 hours, was provoked by tourniquet in 49 rats treated with a vasodilator (naftidrofuryl) and 21 untreated (control) rats. Spontaneous revascularization occurred after removal of the tourniquet. Muscles were studied by microsurgical removal of specimens on removal of tourniquet and 1 and 12 hours and 3, 7 and 14 days after its removal (fig. 1 and 2). Times for staining of muscles with tetrazolium were measured and curves of comparative times established (fig. 3 and 4). Histopathologic specimens were also obtained at the same periods (fig. 5, 6, 7). Results of histochemical studies with tetrazolium and with quantitative determination of degree of cellular anoxia showed the action of naftidrofuryl to be related to mitochondrial metabolism of skeletal muscle, specifically for succinate-dehydrogenase. Clinical application in the determination of therapy and of functional prognosis of an ischemic limb is a possibility by the use of the NBT test in vascular surgery.
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PMID:[Histochemical quantification of muscular ischemia: effect of treatment with naftidrofuryl]. 339 80

The authors studied the ultrastructure of the brain tissue in "symptom negative" clawed jirds (M. unguiculatus) in the presence of permanent and transient circulatory ischemia caused by ligation of the right common carotid artery and by a 3-minute occlusion of the left common carotid artery which was unattended by any clinical manifestations signifying cerebral ischemia. The formation of oedema and dystrophic changes in the right hemisphere differed from that in the left one. Permanent ischemia was associated with the typical picture of hypoxic damage to the neural tissue with the development of cytotoxic oedema. Transient ischemia was predominantly characterized by an impairment of the blood-brain barrier with the development of marked vasogenic oedema. The study made it possible to closely follow the differences in the formation of an early stage of brain damage in permanent and transient ischemia and to establish the possibility of the damaging effect of blood recirculation in the hemisphere previously affected with ischemia.
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PMID:[Features of the ultrastructure of the brain tissue of Meriones unguiculatus after cerebral ischemia and postischemic recirculation]. 382 89

Transient ischemia arising from proximal events in epicardial coronary arteries causes important symptoms, such as angina pectoris, and is usually studied in the hospital with provocative tests. However, Holter monitoring of ST-segment disturbances in patients out of the hospital has shown frequent asymptomatic evidence of ischemia that is surprisingly prolonged and that is not associated with the obvious tachycardia of exercise or stress. Positron emission tomography has been developed to measure the regional myocardial uptake of a cation (rubidium-82) in order to assess repeatedly the directional changes in regional coronary blood flow during these events. This method has been used to show that both symptomatic and asymptomatic episodes of ST depression are reliably associated with disturbances in regional myocardial perfusion. The daily activities of patients have been analyzed and reproduced in the hospital to assess the effects of cold stimulation, mental arithmetic, cigarette smoking, and exercise. Physical exercise was associated with angina, ST-segment change, and regional abnormalities of myocardial perfusion, including decreased perfusion in poststenotic segments. The other tests caused the same disturbances in myocardial perfusion; these perfusion disturbances were mostly asymptomatic and surprisingly prolonged, with periods of recovery that were two to five times longer than the ST-segment disturbance and the pain. Current studies using a structured diary indicate that the episodes of transient ischemia occurring out of the hospital are more frequently associated with different levels of mental arousal than with any other activity. Physical exercise is a relatively infrequent cause of transient ischemia. The examination of coronary blood flow using provocative tests derived from the patients' own activities out of the hospital have confirmed that, irrespective of the pattern of angina, patients have frequent episodes of asymptomatic transient ischemia that are surprisingly prolonged and that these episodes occur in response to previously unsuspected ordinary daily activities. The disturbances in coronary blood flow usually include a regional decrease in myocardial perfusion that can only be explained by pathophysiologic events in the proximal epicardial coronary arteries.
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PMID:Clinical problems in coronary disease are caused by wide variety of ischemic episodes that affect patients out of hospital. 405 Aug 20

This study evaluates the effects of Indomethacin (IND), Prostaglandin E1 (PGE1), and Ibuprofen (IBP) in a bowel ischemia model. Laparotomy was performed in 80-gram rats (n = 260). Transient ischemia was induced by a one minute occlusion of the superior mesenteric artery. Animals were placed in five experimental groups: (I) ischemic controls (n = 80), (II) PGE1, 80 micrograms/kg IV (n = 20), (III) IBP, 12.5 mg/kg IV (n = 60), (IV) IND 15 mg/kg IV (n = 80) and (V) PGE1 + IND (n = 20). All medications were given just prior to laparotomy. Animals were evaluated for survival, length of survival and the presence of bowel necrosis and/or perforation at seven days. Survival was 18% in controls and was reduced to 5% by IND (p less than .005). Improved survival was observed with PGE1 (35%), TBP (31%) and PGE1 + IND (35%). IND resulted in early death, while PGE1, IBP, and PGE1 + IND all increased the length of survival (p less than .05). IND-treated rats had a high incidence of bowel perforation (greater than 40%). PGE1 reversed this effect when given concomitantly with IND. IBP had a significantly lower incidence of intestinal necrosis. These data suggest that infants treated with IND who are at risk for NEC should be carefully monitored for evidence of bowel necrosis. PGE1 and IBP may have a cytoprotective role in subjects at risk for bowel ischemia.
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PMID:Comparative effects of indomethacin, prostaglandin E1, and ibuprofen on bowel ischemia. 668 9

To determine if there is a quantitative relationship between systolic contraction abnormalities (demonstrated by two-dimensional echocardiography) and reduced myocardial perfusion in a setting of moderate and severe coronary stenosis, we created 70% or 90% reduction in circumflex coronary artery diameter in open-chest dogs. Transient ischemia was induced by superimposing increased myocardial oxygen requirements (i.v. isoproterenol, aortic constriction) in the presence of the stenosis or by decreased coronary perfusion (lowering arterial pressure with i.v. nitroprusside, nitroglycerin, or hemorrhage). Acute systolic wall thinning show by two-dimensional echocardiography or by implanted myocardial sonomicrometers was taken as functional evidence of myocardial ischemia. Myocardial perfusion was determined by radiolabeled microspheres when wall thinning was apparent. Systolic wall thinning could not be induced by these interventions when the degree of coronary stenosis was only 70%. Systolic wall thinning occurred only when increased myocardial oxygen requirements or decreased aortic pressure were superimposed on 90% coronary stenosis. Under these conditions, myocardial perfusion was reduced to 28 +/- 27 ml/100 g/min (mean +/- SD), 15--25% of control. Aortic diastolic pressure was a major determinant of ischemia in that contraction abnormalities produced by a 90% stenosis and vasodilators or hemorrhage could be acutely reversed by superimposing acute aortic constriction, which elevated arterial pressure; myocardial perfusion increased correspondingly. Thus, the demonstration of transient systolic wall thinning by two-dimensional echocardiography during a stressful intervention indicated that severe coronary stenosis was present, and that the perfusion of the acutely dyskinetic myocardial area was 25% of control or less.
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PMID:Two-dimensional echocardiography in experimental coronary stenosis. II. Relationship between systolic wall thinning and regional myocardial perfusion in severe coronary stenosis. 680 69

Transient ischemia results in changes in the cerebral blood flow at the level of microinfarcts, enzymatic and metabolic changes and the development of a cerebral edema; all these disorders regress in the week following ischemia. Besides, the observed functional disorders disappear as the cerebral edema regresses. The brain functional activity is protected by the use of treatments which reduce the development of the cerebral edema and/or a quicker regression of the edema.
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PMID:Short-term memory and cerebral ischemia: pharmacological application. 726 26

To study the involvement of endogenous endothelin (ET) in the development of cerebral ischemia, we measured by radioimmunoassay brain tissue content of immunoreactive (ir)-ET-1 in a model of focal cerebral ischemia in the rat. Permanent occlusion of the middle cerebral artery (OMCA) was accompanied after 24 h by a progressive but marked elevation of ir-ET-1 in the ipsilateral compared with the contralateral hemisphere (119% after 24 h; 184% after 48 h and 459% after 72 h). The pial vessels and the arteries of the circle of Willis did not respond with ir-ET-1 production. The increase in ir-ET-1 content in tissues was first observed in the caudate nucleus (after 24 h) and later in the cortex (after 48 h), which was more variably injured. Transient ischemia followed by recirculation led to a slight increase of ir-ET-1, which also appeared after 24 h of recirculation. This study demonstrates that during permanent OMCA, the tissue content of ir-ET-1 markedly and progressively increases, whereas less severe ischemia (transient) is accompanied by a modest elevation of ir-ET-1 levels. These results suggest that endogenous ir-ET-1 production is involved in the development and the severity of ischemic injury.
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PMID:Elevated tissue endothelin content during focal cerebral ischemia in the rat. 750 72

The effects of transient bilateral carotid occlusion on the physical state of synaptosomal membrane proteins and lipids were studied in adult and aged gerbils employing electron paramagnetic resonance. Transient ischemia was produced in adult and aged gerbils by bilateral occlusion of the common carotid arteries with reperfusion times ranging from 0 to 24 h. Synaptosomes of the cerebral cortices were isolated and labeled with a protein-specific spin probe (2,2,6,6-tetramethyl-4-maleimido-piperidine-1-oxyl) and a lipid-specific spin probe (5-doxylstearic acid). Changes in the physical state of the protein peaked at 60 min reperfusion for both adult and aged gerbil models, with a more intense change in aged, but did not return to control values by 24 h. A biphasic change occurred with the lipid-specific label in both the aged and adult models. The onset of the first phase of change occurred at an earlier time (30 min reperfusion) for aged gerbil tissue than for adult tissue (between 3 and 6 h reperfusion), while the second phase of change occurred at 12 h reperfusion for both adult and aged. These results are consistent with the hypothesis that protein oxidation and lipid peroxidation are direct results of free radicals produced during the reperfusion following ischemia and that protein oxidation may be intensified by peroxidation of the surrounding lipids. Phospholipase A2 activation is implicated to cause changes in membrane phospholipid organization as seen in these studies.
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PMID:Ischemia/reperfusion-induced changes in membrane proteins and lipids of gerbil cortical synaptosomes. 770 17


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