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

The effect of cerebral hypoxia on protein synthesis was investigated by exposing rats to 5% O2, and examining polypeptide synthesis and size distribution profiles of ribosomes. The findings were compared with the results from cerebral anoxia (decapitation) and hypoglycemia. In cerebral hypoxia there was suppression of polypeptide synthesis, though to a lesser extent than in cerebral anoxia, while no effect was detected in hypoglycemia. Among 4 different ribosomal fractions used for polypeptide synthesis, the microsome was the most sensitive for hypoxia and anoxia, and the polyribosome after short centrifugation was the least sensitive. The size distribution profiles of 3 different ribosomes revealed an increase in the size of the monomere-dimer complex and a decrease of the polysome peak both in cerebral hypoxia and anoxia. Comparison of the energy state and the extent of lactic acidosis in cerebral hypoxia, anoxia and hypoglycemia available in the literature and the functional and structural state of polyribosomes in the present investigation suggests that intracellular acidosis may be the main cause of the suppression of polypeptide synthesis and disaggregation of polyribosomes in hypoxia, and the depletion of energy reserve may be the main cause in anoxia-ischemia.
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PMID:Protein synthesis in rat brain in hypoxia, anoxia and hypoglycemia. 42 Nov 33

We used intracellular microelectrodes to study the electrophysiological effects of combinations of components of ischemia and their relation to the occurrence of ventricular arrhythmias in the specialized conducting system of isolated canine right ventricles. The middle area of the free wall was exposed to various test solutions in the center compartment of a three-chambered bath; the base and apex of the preparation were superfused with normal Tyrode's solution in the outer control compartments. Hypoxia (Po2 40 mm Hg), lactic acidosis (pH 6.5), and orciprenaline (10(-6) M), either alone or combined, failed to affect the action potential amplitude or the conduction velocity of the subendocardial fibers, and no arrhythmias occurred. The action potential duration and the effective refractory period were markedly prolonged by lactic acidosis. Exposure of the test regions to 15 mM K+ plus orciprenaline resulted in marked decreases in action potential amplitude and conduction velocity. Abnormalities of impulse transmission through the depressed area included high degrees of rate-dependent block, one-way block, warming-up phenomenon, and the Wenckebach phenomenon. Such conditions regularly provoked the appearance of single, sustained, or concealed reentrant depolarizations. The combined effects of hypoxia, 15 mM K+, and orciprenaline resulted in further depression of the already depressed action potential in the depolarized fibers. Our results indicate that regional increases of extracellular K+ may be the predominant factor of the components of ischemia we studied which facilitates the initiation of reentrant arrhythmias.
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PMID:Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system. 42 79

The authors studied the effect on cortical metabolites of intracranial hypertension produced by the infusion of mock cerebrospinal fluid into the cisterna magna in rabbits subjected to 15 minutes of cerebral oligemia (20 torr) or 15 minutes of complete ischemia. In both groups high-energy metabolites were exhausted within the first 5 minutes of the 15-minute insult. Significant recovery of the high-energy intermediates occurred within 15 minutes of reperfusion, well before return of electroencephalogram (EEG) activity. Continued reperfusion, during which electrical activity and function were returning, brought only moderate improvement in energy metabolites. In contrast, severe lactic acidosis persisted at least 15 minutes after insult, but was reduced by the time EEG activity returned. At no time were there striking differences in metabolites between the oligemic and ischemic groups. These results indicate that recovery in general, and the significantly earlier recovery of oligemic as compared to ischemic animals, cannot be explained on the basis of energy supply. Whether the persistence of lactic acidosis is an important factor limiting return of function requires further study.
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PMID:Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 3: Brain energy metabolism. 115 68

Clinical use of profound hypothermia and total circulatory arrest has been accompanied by occasional postoperative neurological abnormalities. In a series of infant baboons, surface cooling to 32 degrees C (brain) followed by perfusion cooling by cardiopulmonary bypass with a membrane oxygenator and heat exchanger to 18 degrees C was carried out, after which the circulation was stopped for 30 minutes. The animal was rewarmed to 35 degrees C. Marked alterations in the regional cerebral circulation were observed during perfusion cooling and rewarming. Regional cerebral ischemia was negatively correlated with jugular outflow (total cerebral blood flow) during rewarming, while regional hyperemia showed positive correlation both following perfusion cooling and after rewarming. A higher degree of ischemia in brain ischemic samples was found during rewarming than during cooling. These alterations in regional cerebral perfusion were associated with lactacidosis and hyperglycemia after rewarming, and may be considered potentially responsible for posthypothermic cerebral dysfunction.
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PMID:Cerebral effects of profound hypothermia (18 degrees C) and circulatory arrest. 115 33

The effects of dichloroacetate (DCA) on brain lactate, intracellular pH (pHi), phosphocreatine (PCr), and ATP during 60 min of complete cerebral ischemia and 2 h of reperfusion were investigated in rats by in vivo 1H and 31P magnetic resonance spectroscopy; brain lactate, water content, cations, and amino acids were measured in vitro after reperfusion. DCA, 100 mg/kg, or saline was infused before or immediately after the ischemic period. Preischemic treatment with DCA did not affect brain lactate or pHi during ischemia, but reduced lactate and increased pHi after 30 min of reperfusion (p < 0.05 vs. controls) and facilitated the recovery of PCr and ATP during reperfusion. Postischemic DCA treatment also reduced brain lactate and increased pHi during reperfusion compared with controls (p < 0.05), but had little effect on PCr, ATP, or Pi during reperfusion. After 30 min of reperfusion, serum lactate was 67% lower in the postischemic DCA group than in controls (p < 0.05). The brain lactate level in vitro was 46% lower in the postischemic DCA group than in controls (p < 0.05). DCA did not affect water content or cation concentrations in either group, but it increased brain glutamate by 40% in the preischemic treatment group (p < 0.05). The potential therapeutic effects of DCA on brain injury after complete ischemia may be mediated by reduced excitotoxin release related to decreased lactic acidosis during reperfusion.
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PMID:Effect of dichloroacetate on recovery of brain lactate, phosphorus energy metabolites, and glutamate during reperfusion after complete cerebral ischemia in rats. 135 94

Metabolic acidosis immediately after surgical operation is followed by metabolic alkalosis. Hormonal change by surgical stress and anaerobic glucolysis due to tissue ischemia cause initial lactic acidosis. Later alkalosis may be caused by secondary aldosteronism and bicarbonate production from lactate and citrate supplied by massive infusion and transfusion. Postoperative complications, such as respiratory insufficiency, renal failure and hypovolemic or septic shock, cause acidosis. In the gastrointestinal surgery, acidosis can be caused by starvation and loss of bicarbonate contained in bile, pancreatic juice or intestinal fluid, and alkalosis can be caused by loss of HCl in gastric juice. Severe acidosis can be caused by extracorporeal circulation, hypothermia, low output syndrome or declamping shock in cardioaortic surgery.
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PMID:[Acid-base disturbances in surgical operation]. 143 18

Preischemic hyperglycemia, which raises tissue lactate content during ischemia, is known to aggravate ischemic brain damage. To explore the possibility that the enhanced lactic acidosis gives rise to osmotic damage, we studied the influence of a varied preischemic plasma glucose concentration on the early postischemic edema. Brain edema was measured by the specific-gravity technique. Brain and plasma osmolality were measured with a vapor pressure osmometer. We examined different brain regions in hyperglycemic and moderately hypoglycemic rats subjected to 15 min of forebrain ischemia, followed by recirculation for 5, 15, and 30 min. The decrease in specific gravity was compared with the increase in osmolality, to study whether the edema formation in the different groups correlated to the increase in tissue osmolality. We found edema formation to be most pronounced in frontoparietal cortex. In this structure and in hippocampus, statistically significant decreases of specific gravity were seen at all recirculation times studied. In caudoputamen, significant edema was seen only in the groups with 5 and 15 min of recirculation. Contrary to expectations, no difference was found between hyperglycemic and hyperglycemic animals. Tissue osmolality increased during ischemia in both the low and high glucose groups, but to a higher level in the latter (hypoglycemia 311 +/- 1 mmol kg-1, hyperglycemia 328 +/- 10 mmol kg-1; mean +/- SD, p less than 0.05). In the hyperglycemic group, brain osmolality remained elevated for the first 15 min of recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of preischemic hyperglycemia on osmolality and early postischemic edema in the rat brain. 150 45

Hyperglycemia aggravates brain pathologic outcome following middle cerebral artery (MCA) occlusion in cats. We presently determined if hyperglycemia during occlusion leads to high lactic acid accumulations in the ischemic MCA territory. We measured brain metabolite concentrations in 14 MCA territory sites at 0.5 and 4 h following occlusion in hyper- (20 mM) and normoglycemic (5 mM) cats and correlated these results with previous brain pathologic findings. Hyper- versus normoglycemia during MCA occlusion resulted in significantly higher lactate concentrations in the ischemic territory and more numerous loci with lactates greater than 17 mumol/g. At 0.5 h of occlusion, ATP levels were lower in normoglycemic cats, while at 4 h, ATP was similarly reduced (40%) in both glycemia groups. At 4 h, PCr was more reduced in hyperglycemics secondary to a greater brain tissue acidosis. Carbohydrate substrates at 0.5 h were more markedly depleted in normoglycemics, likely limiting lactate accumulation (34.3% versus only 5.0% of sites in hyperglycemics with glucose less than 0.5 mumol/g). Although lactate was markedly elevated at both 0.5 and 4 h in hyperglycemic ischemic territories, clip release at 4 versus 0.5 h yields a significantly poorer brain pathologic outcome. Correspondingly, intracellular pH, calculated from the creatine kinase equilibrium, was more markedly depressed at 4 than at 0.5 h of occlusion, demonstrating a time-dependent dissociation between tissue lactate and hydrogen ion accumulations. The present findings show that following MCA occlusion (a) hyperglycemia increases the magnitude and topographic extent of marked tissue lactic acidosis, (b) infarct size following 0.5 h of clip release correlates more closely with tissue acidosis than with lactate concentrations, (c) ischemic tissue ATP concentrations correlate poorly with infarct size, (d) normoglycemia limits lactate accumulation during focal ischemia because tissue glucose is depleted, and (e) early during ischemia, tissue buffering or antiport mechanisms may prevent marked increases in intracellular hydrogen ion activity.
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PMID:Hyperglycemic versus normoglycemic stroke: topography of brain metabolites, intracellular pH, and infarct size. 154 94

The effects of hyperglycemia on the time course of changes in cerebral energy metabolite concentrations and intracellular pH were measured by nuclear magnetic resonance (NMR) spectroscopy in rats subjected to temporary complete brain ischemia. Interleaved 31P and 1H NMR spectra were obtained every 5 min before, during, and for 2 h after a 30-min bilateral carotid occlusion preceded by permanent occlusion of the basilar artery. The findings were compared with free fatty acid and excitatory amino acid levels as well as with cations and water content in funnel-frozen brain specimens. One hour before occlusion, nine rats received 50% glucose (12 ml/kg i.p.) and five received 7% saline (12 ml/kg i.p.). Before ischemia, there were no differences in cerebral metabolite levels or pH between hyperglycemic rats and controls. During the carotid occlusion, the lactate/N-acetylaspartate (Lac/NAA) peak ratio was higher (0.73-1.48 vs. 0.56-0.82; p less than 0.05) and pH was lower (less than 6.0 vs. 6.45 +/- 0.05; p less than 0.05) in the hyperglycemic rats than in the controls. Phosphocreatine and adenosine triphosphate were totally depleted in both groups. Within 5-15 min after the onset of reperfusion, the Lac/NAA peak ratio increased further in all rats; however, only in extremely hyperglycemic rats (serum glucose greater than 960 mg/dl) did the lactic acidosis progress rather than recover later during reperfusion. Total free fatty acid and excitatory amino acid levels, but not cation concentration or water content, in brain correlated with serum glucose levels during and after ischemia and with NMR findings after 2 h of reperfusion. Although profound hyperglycemia (serum glucose of 970-1,650 mg/dl) appears to be associated with progression of anaerobic glycolysis and failure of cerebral energy metabolism to recover after temporary complete brain ischemia and with postischemic excitotoxic and lipolytic reactions thought to participate in delayed cellular injury, severe hyperglycemia (490-720 mg/dl) was associated with recovery of energy metabolism.
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PMID:Effects of hyperglycemia on the time course of changes in energy metabolism and pH during global cerebral ischemia and reperfusion in rats: correlation of 1H and 31P NMR spectroscopy with fatty acid and excitatory amino acid levels. 156 39

Eight cases of transient reversible segmental asynergy of the left ventricle thought not to be related to coronary artery lesions are reported. Three cases were associated with inflammatory reactions of unknown origin, and one each with lactic acidosis, abdominal surgery, hypoglycemia, tetanus and pneumonia. None of the patients had symptoms suggestive of ischemic heart disease before or after these episodes. Electrocardiograms before these episodes were all normal. Two-dimensional echocardiography was performed to evaluate abnormal electrocardiograms. Coronary angiography was performed in 4 of 8 cases and was normal in all 4 cases; 2 done as emergencies and 2 non-emergencies. Two ergonovine tests were negative. Left ventricular wall motion abnormalities, present mainly at the apex of the left ventricle, returned to normal in 1 to 4 weeks. Giant negative T waves in the chest leads during this recovery period were characteristic electrocardiographic features and normalized in 6 weeks on average. We believe that these episodes were not related to ischemia due to coronary artery disease, but to some metabolic humoral factors. An excellent prognosis can be expected if these abnormal metabolic circumstances can be resolved.
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PMID:Transient segmental asynergy of the left ventricle of patients with various clinical manifestations possibly unrelated to the coronary artery disease. 174 67


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