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

Previous investigations have shown that preischemic hyperglycemia worsens cerebral outcome. This study sought to delineate the temporal relations between postischemic brain edema and the development of spontaneous epileptic activity. Fasted rats were subjected to 10 minutes of forebrain ischemia. One-half of the animals were made hyperglycemic by glucose infusion prior to ischemia. At serial recirculation intervals regional specific gravity and cortical electrolytes were measured. Normoglycemic animals showed a biphasic increase in brain water content that was fully resolved by 96 hours and had no convulsive activities. Hyperglycemic brains, although displaying a slower resolution from an initial transient decrease in specific gravity, also developed an interval with normal water content that persisted at 18 hours postischemia. At 24 hours, an increase in water content recurred and was soon followed by the onset of seizure activity. Cortical electrolyte changes were unremarkable until seizures occurred. Significant increases in total Na+, Cl-, and Ca2+ and a decrease in K+ were then seen. We conclude that while the normoglycemic brain is capable of resolving postischemic edema in this model, the hyperglycemic brain develops a delayed secondary increase in water content followed by the onset of seizure activity accompanied by a deterioration of ionic homeostasis.
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PMID:Ischemia in normo- and hyperglycemic rats: effects on brain water and electrolytes. 356 5

To determine if moderate hyperglycemia produced by dextrose administration was detrimental in normothermic renal ischemia, 15 halothane-anesthetized mongrel dogs underwent right nephrectomy and 60 minutes of left renal artery and vein occlusion. Six dogs received 1 L of lactated Ringer's solution (LR) and six others received 1 L of 5% dextrose in lactated Ringer's solution (D5LR). Three sham-operated dogs received 1 L of D5LR and underwent right nephrectomy but no occlusions. All dogs received 500 mL of fluid before occlusion and 500 mL after occlusion. The blood glucose concentration for the LR group was 7.6 mmol/L (137 mg/dL) after 500 mL and 7.2 mmol/L (130 mg/dL) after 1000 mL. In the D5LR group, the blood glucose concentration was 21.5 mmol/L (387 mg/dL) after 500 mL and 20.2 mmol/L (363 mg/dL) after 1000 mL. In the sham-operated group, the blood glucose concentration was 22.8 mmol/L (410 mg/dL) after 500 mL and 20.7 mmol/L (373 mg/dL) after 1000 mL. At 30 hours, the plasma creatinine concentration rose from 70 to 300 mumol/L (0.8 to 3.4 mg/dL) in the LR group and from 90 to 500 mumol/L (1.0 to 5.8 mg/dL) in the D5LR group; the increase for the D5LR group was significantly greater than that for the LR group. In the sham-operated group, the plasma creatinine concentration was stable throughout the 30-hour period. This study demonstrates a significant detrimental effect of dextrose administration on renal function during normothermic ischemia.
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PMID:Dextrose administration exacerbates acute renal ischemic damage in anesthetized dogs. 359 69

To study whether transient ischemia is influenced by hyperglycemia, the middle cerebral artery was occluded for 5, 10 and 15 min in normo- and hyperglycemic rats. Five-minute ischemia induced minor lesions in both groups. After 10-min ischemia a significant greater infarct volume was found in hyperglycemia compared with normoglycemia (29 +/- 9 mm3 vs 4 +/- 4 mm3, P less than 0.001). Fifteen-minute artery occlusion induced even more damage in both hyper- and normoglycemia (63 +/- 20 mm3 vs 13 +/- 12 mm3, P less than 0.006). The lateral part of striatum was infarcted in all hyperglycemic animals exposed to 10 or 15 min of ischemia. In the same area selective neuronal injury occurred in 6 out of 9 normoglycemic animals. The findings show that hyperglycemia increases brain damage during transient ischemia by conversion of selective neuronal injury into cerebral infarction.
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PMID:Transient focal ischemia in hyperglycemic rats is associated with increased cerebral infarction. 359 32

Unlike adult rats, glucose supplementation of immature rats does not lead to accentuated hypoxic-ischemic brain damage. To explore the reason for this age-specific paradox, we subjected 7-day postnatal rats to unilateral common carotid artery occlusion followed by a subcutaneous injection of either 0.1 ml 50% glucose or normal saline. They were then exposed to hypoxia with 8% oxygen, during which they received 2.5 microCi 2-[14C]-glucose or were quick-frozen for brain metabolite analysis. During hypoxia-ischemia, glucose transport into the ipsilateral cerebral hemisphere of the hyperglycemic rats was greater (+100-150%) than in normoglycemic animals. However, glucose consumption was similar in the two groups. Glucose concentrations in brain were lower during hypoxia-ischemia in the normoglycemic animals, whereas lactate increased to similar levels in the two groups. The high-energy phosphate reserves, ATP and phosphocreatine, were depleted to a similar extent. Thus, hyperglycemia combined with hypoxia-ischemia, although associated with increased glucose transport into brain, does not lead to enhanced glucose utilization or lactate accumulation by brain over that of hypoxia-ischemia alone.
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PMID:Cerebral metabolic responses of hyperglycemic immature rats to hypoxia-ischemia. 360 71

The effects of transient ischemia on the metabolic responsiveness of a well-defined brain circuit were investigated with [14C]2-deoxyglucose autoradiography. Rats underwent 30 min of severe forebrain ischemia followed by postischemic recirculation periods of 1, 2, 3, 5, and 10 days. At these times, unilateral whisker stimulation was carried out, resulting in the metabolic activation of the whisker barrel circuit. An altered pattern of glucose utilization within both stimulated and nonstimulated circuit relay stations was observed at 1, 2, and 3 days following ischemia. At 1 day, stimulus-evoked increases in metabolic activity were severely depressed within both the ventrobasal thalamus and layer IV of the cortical barrel field region. Baseline metabolic rate within nonstimulated relay areas was also severely depressed at this time. At postischemic days 2 and 3, moderate levels of increased glucose utilization were apparent overlying cortical layer IV and the superficial half of layer VI, while layers I, II, III, and V appeared less responsive to metabolic activation. By day 5, whisker stimulation resulted in normal levels of increased glucose utilization within the activated ventrobasal thalamus and layer IV of the cortical barrel field region. Glucose utilization within nonactivated relay stations, depressed at earlier time periods, had also returned to control levels by day 5. At both 5 and 10 days, an altered laminar pattern of elevated glucose utilization was apparent within the activated barrel field region, with local CMRglu being depressed in layer V compared with control values. These results demonstrate that periods of transient ischemia produce both reversible and longer-lasting effects on the ability of the CNS to respond to peripheral activation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of transient cerebral ischemia on metabolic activation of a somatosensory circuit. 373

Seven-day postnatal rats were rendered hyperglycemic by the SC injection of 50% glucose, following which they were exposed to hypoxia with 8% oxygen. The glucose-treated animals survived more than twice as long as saline-treated littermates. Other hyperglycemic and control rat pups were subjected to hypoxia-ischemia by unilateral common carotid artery occlusion combined with 2 hours of hypoxia. Neuropathologic analysis of recovered animals at 30 days of age showed that the brains of the glucose-treated animals were no more damaged than those of the saline controls (p greater than 0.05). The finding indicates that, unlike adults, glucose supplementation and its associated hyperglycemia in the immature rat does not increase the extent of hypoxic-ischemic brain damage.
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PMID:Glucose and perinatal hypoxic-ischemic brain damage in the rat. 373 79

Incomplete forebrain ischemia of 15-min duration was induced in rats made hyperglycemic or moderately hypoglycemic prior to ischemia. Tissue CO2 tension, CO2 content, labile tissue metabolites, and extracellular pH (pHe) were measured, and intracellular pH (pHi) was derived by calculation on the assumption that cerebral intracellular fluids can be lumped into one space. In hypoglycemic animals, mean tissue lactate content increased from 2 to 10 mumol g-1. Tissue CO2 content was virtually unchanged and the CO2 tension increased from approximately 50 to approximately 145 mm Hg. In hyperglycemic animals, tissue lactate content rose to 20 mumol g-1, and the CO2 content decreased by 25%, demonstrating that some CO2 was lost to the blood supplied by the remaining perfusion. Accordingly, tissue CO2 tension did not rise above 200 mm Hg. pHe was reduced in proportion to the amount of lactate accumulated, the values obtained in hypo- and hyperglycemic animals showing relatively little scatter (6.76 +/- 0.03 and 6.25 +/- 0.04, respectively). In hypoglycemic animals the extracellular HCO-3 concentration was virtually unchanged, demonstrating that any influx of lactic acid from the cells must have been accompanied by H+ efflux and/or HCO-3 influx via independent routes. In hyperglycemic animals [HCO-3]e fell by greater than 10 mumol ml-1. In both groups [HCO-3]e was reduced during the first 5 min of recovery. Recovery of pHe was slower in hyper- than in hypoglycemic animals. During ischemia calculated pHi fell to 6.37 +/- 0.04 and 5.95 +/- 0.06 in hypo- and hyperglycemic animals, respectively. Differences in pHi were maintained for the first 15 min of recovery, but in both hypo- and hyperglycemic animals pHi had normalized after 30 min. It is concluded that preischemic hyperglycemia leads to a more pronounced intra- and extracellular acidosis than normo- and hypoglycemia, an acidosis that also resolves more slowly during recirculation.
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PMID:Changes in extra- and intracellular pH in the brain during and following ischemia in hyperglycemic and in moderately hypoglycemic rats. 376 41

Numerous laboratories have shown that hyperglycemia increases cerebral ischemic damage. This presumably results from increased lactate production and accumulation during ischemia. Although increased tissue lactic acidosis is associated with increased ischemic brain damage, this damage has not been directly linked to glycolytic flux. Because 2-deoxyglucose (2-DG) is a competitive inhibitor of glycolysis we tested its ability to reduce hyperglycemia-exacerbated ischemic brain damage. Severe forebrain ischemia was produced by the four-vessel occlusion model in rats. Four rats received 3 g/kg glucose and saline while a second group (n = 5) was injected with 3 g/kg glucose plus 1.6 g/kg 2-DG. A third group (n = 5) was treated with 1 g/kg glucose plus saline and a fourth group (n = 5) received 1 g/kg glucose and 1.6 g/kg 2-DG. All rats were injected i.p. 10 minutes prior to the ischemic insult with the same volume/kg body weight. All rats receiving the high dose of glucose alone (3 g/kg) were dead within 24 hours postischemia. Rats who received 2-DG in addition to 3 g/kg glucose showed only 40% mortality (p = 0.119 Fisher's Exact). 2-DG completely eliminated convulsions during the initial two hours of recovery which was significant (p = 0.008), however, all rats in both groups showed some convulsions by 24 hours postischemia. Among rats receiving the low glucose dose (1 g/kg), none of the rats receiving 2-DG died or convulsed by 24 hours postischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycolytic inhibition by 2-deoxyglucose reduces hyperglycemia-associated mortality and morbidity in the ischemic rat. 376 73

The adverse effect of a minimal cerebral blood flow (CBF) in models of global ischemia has been noted by many investigators. One factor believed important in this situation is the level of blood glucose, since a continued supply of this metabolite results in increased tissue lactate, decreased brain pH, and increased cell damage. The authors have extended these observations to a model of focal incomplete ischemia. Brain pH was measured in fasted squirrel monkeys in regions of focal incomplete ischemia after transorbital occlusion of the middle cerebral artery (MCA). In both control and hyperglycemic animals, CBF was reduced to less than 30% of baseline. At 3 hours after MCA occlusion, brain pH in the control group was 6.66 +/- 0.68 as compared to 6.27 +/- 0.26 in the glucose-treated group. This difference was statistically significant by Student's unpaired t-test (p less than 0.05). Thus, hyperglycemia results in decreased tissue pH in regions of focal incomplete cerebral ischemia in monkeys.
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PMID:Effect of hyperglycemia on brain pH levels in areas of focal incomplete cerebral ischemia in monkeys. 377 58

The study describes a reproducible model of complete brain ischemia in rats. Rats with different plasma glucose concentrations were exposed to 10 min of complete cerebral ischemia achieved by compression of neck vessels by a pneumatic cuff. All 30 rats, except one, in which pre-ischemic plasma glucose level were lower than 22 mM (range 1.6-22) survived 10 min complete ischemia and made a similar recovery. Ten rats with pre-ischemic plasma glucose levels above 22 mM (range 22-47.2) died from seizures in the post-ischemic period. Post-ischemic treatment of seizures and hyperglycemia in the hyperglycemic rats significantly improved recovery. In conclusion, pre-ischemic hyperglycemia above 22 mM impairs recovery after complete ischemia by inducing seizures, post-ischemic hyperglycemia and lactic acidosis.
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PMID:The effect of glucose upon restitution after transient cerebral ischemia: a summary. 389 8


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