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

Focal blood flow was measured in the lateral funiculus and center of the spinal cord in the rhesus monkey both before and after a 600 gm-cm injury at T-10. Measurements made by the hydrogen clearance technique showed that blood flow in the lateral funiculus more than doubled within 4 hours after injury, returned to normal by 8 hours, and remained in the normal range for 24 hours. At no time was a hypoperfusion in the lateral funiculus present. Blood flow in the center of the spinal cord, at the level of the lesion, began to fall within 1 hour following injury and continued to fall for 4 hours. These data challenge the notion that spreading ischemia of the white matter is an important factor in the pathophysiology of experimental spinal cord injury.
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PMID:Local spinal cord blood flow in experimental traumatic myelopathy. 111 48

Cerebral ischemia was induced in gerbils by bilateral carotid ligation for periods of 10 to 40 minutes. Cerebral blood flow (CBF) was measured by hydrogen clearance. Following ischemia, ultimate clinical and electroencephalogram recovery could be predicted in every case within the first five minutes by recovery could be predicted in every case within the first five minutes by recovery of CBF to at least 100% of the control level. In animals without EEC recovery, the postischemic CBF was always less than 80% of control and progressively declined to zero. Residual flow during ischemia appeared to minimize the likelihood of brain death. The determination of ultimate brain death appeared to coincide with a major circulatory abnormality that is probably microvascular.
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PMID:Cerebral blood flow. A predictor of recovery from ischemia in the gerbil. 113 11

The degree of recovery of the somatosensory cortical evoked response following a period (15 to 65 minutes) of partial ischemia, produced by temporary occlusion of the middle cerebral artery (MCA), was assessed in baboons and related to the local tissue blood flow and PO2 before, during and after the occlusion. Flow was measured using the technique of two-minute hydrogen clearance. Failure of complete recovery of the evoked response was associated with significantly greater depths of ischemia and tissue hypoxia during occlusion, and with significantly greater and persisting tissue hypoxia after occlusion, than complete recovery. Complete recovery of the evoked response also was associated with tissue hyperoxia after occlusion. The reduced postocclusive PO2 levels associated with incomplete recovery of the evoked response suggest that reduced perfusion during ischemia was sufficiently severe to cause some degree of irreversible anoxic damage. The effect of a brief (three to ten minutes) period of ventilation with air (instead of oxygen) under such low-flow conditions was to depress the evoked response significantly further; normally perfused brain, however, was unaffected by this procedure. This finding has clinical implications in regard to normobaric oxygen therapy.
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PMID:Recovery of the cortical evoked response following temporary middle cerebral artery occlusion in baboons: relation to local blood flow and PO2. 126 8

Capsaicin (10 microM), KCl (80 mM) or superfusion with a low pH medium (pH 5 or 6) produced a significant increase of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) outflow from the superfused rat isolated soleus muscle. CGRP-LI outflow produced by capsaicin or pH 5 medium was totally abolished in a calcium free medium containing EDTA (1 mM) and the effect of pH 5 medium was prevented by a previous application of capsaicin. Ruthenium red (10 microM) produced a marked inhibition of CGRP-LI release produced by capsaicin or pH 5 medium (69 and 84%, resp.), without affecting that evoked by KCl. These findings demonstrate that protons activate capsaicin-sensitive primary afferents in rat skeletal muscle through a Ruthenium red-sensitive mechanism. Proton-induced CGRP-LI release in skeletal muscle could be of relevance during exercise and/or skeletal muscle ischemia.
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PMID:Release of calcitonin gene-related peptide-like (CGRP-LI) immunoreactivity from rat isolated soleus muscle by low pH, capsaicin and potassium. 127 75

Intracellular pH can be measured quantitatively in rat brain in vivo and in vitro using spectrophotometric detection of the vital dye neutral red. This method preserves spatial information and is compatible with microhistochemistry. The intracellular pH indicated by this method is in close agreement with that indicated by 31P-NMR spectroscopy. During ischemia, intracellular acidification is correlated with tissue lactate accumulation. The spatial distribution of pH values becomes more heterogeneous as the tissue becomes more acidic. Resuscitation from total cerebral ischemia produced by cardiac arrest results in rapid intracellular realkalinization. This realkalinization is at least partially inhibited by amiloride pretreatment. Some neuronal populations, especially in the hippocampal CA1 and CA4 regions, may become more acidic during ischemia and realkalinize more slowly after reperfusion than other tissue regions. The intracellular pH of hippocampal brain slice preparations is more alkaline than expected from in vivo studies. The intracellular pH of the brain slice can be acidified to near neutrality by specific inhibitors of the sodium/hydrogen ion exchanger.
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PMID:Intracellular pH in rat brain in vivo and in brain slices. 129 77

The activities of Superoxide Dismutase (SOD), Glutathione Peroxidase (GSH-Px) and Catalase (CAT) in the ischemic cerebral tissue following the unilateral middle cerebral artery occlusion of rats were assessed. In comparison with the sham-operated rats, both SOD and GSH-Px activity in the ischemic area (striatum and fronto-parietal cortex) were significantly reduced by 30 min. of ischemia, GSH-Px activity in the peri-ischemic area (parieto-parasagittal) was significantly reduced as well. It was shown that in the striatum the GSH-Px activity was much higher than that in the cortex. According to our data, it was suggested that in the ischemic condition, cerebral Superoxide (O2-) and Hydrogen Peroxide (H2O2) were accumulated, and thus the polyunsaturated fatty acids in the neuronal membrane were trapped by these free radical. And such a process resulted in neuronal damage. It implicated that the oxygen free radical might be involved in the neuronal damage induced by Dopamine, since the O2- and H2O2 were excessively generated during the oxidative deamination of Dopamine and the free radical scavengers, SOD and GSH-Px were decreased concomitantly in the cerebral ischemic tissue.
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PMID:[A study on the activity of three antioxidant enzymes in the brain of experimental acute cerebral ischemia]. 130 99

Cerebral acidosis occurring during ischemia has been proposed as one determinant of tissue damage. Newborn animals appear to be less susceptible to ischemic tissue damage than adults. One possible component of ischemic tolerance could derive from maturational differences in the extent of acid production and buffering in newborns compared to adults. The purpose of this study was to measure the dependency of acid production on the blood plasma glucose concentrations and acid buffering capacity of piglets at different stages of development. Complete ischemia was induced in 29 piglets ranging in postconceptual age from 111 to 156 days (normal term conception, 115 days). Brain buffering capacity during the first 30 min of ischemia was quantified in vivo, via 31P and 1H nuclear magnetic resonance (NMR) spectroscopy, by measuring the change in intracellular brain pH for a given change in the concentration of compounds that contribute to the production of hydrogen ions. Animals from all four age groups showed a similar linear correlation between preischemia blood glucose concentration and intracellular pH after 30 min of ischemia. For each animal the slope of the plot of intracellular pH versus cerebral buffer base deficit was used to calculate the buffer capacity. Using data obtained over the entire 30 min of ischemia, there was no difference in the mean buffer capacity of the different age groups, nor was there a significant correlation between buffer capacity and age. However, there was a significant increase in buffer capacity for the intracellular pH range 6.6-6.0, compared to 7.0-6.6, for all age groups. No significant differences in buffer capacity for these two pH ranges were observed between any of the age groups. Acid buffering capacity was also measured by performing pH titrations on brain tissue homogenized in the presence of inhibitors of glycolysis and creatine kinase. Plots of homogenate pH versus buffer base deficit showed a nonlinear trend similar to that seen in vivo, indicating an increase in buffer capacity as intracellular pH decreases. A comparison of newborn and 1-month-old brain tissue frozen under control conditions or after 45 min of ischemia revealed no differences that could be attributed to age and a slight decrease in buffer capacity of ischemic brain compared to control brain tissue homogenates. There was no difference between the brain buffering capacity measured in vivo using 31P and 1H NMR and that measured in vitro using brain homogenates.
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PMID:Cerebral acid buffering capacity at different ages measured in vivo by 31P and 1H nuclear magnetic resonance spectroscopy. 131 67

Reactive oxygen metabolites have been reported to be important in the pathogenesis of ischemia/reperfusion-induced and alcohol- and drug-induced liver injuries. We investigated the role of superoxide dismutase, cellular and extracellular, in preventing reactive oxygen metabolite-induced cytotoxicity in cultured rate hepatocytes. Cells were exposed to reactive oxygen metabolites enzymatically generated by hypoxanthine-xanthine oxidase. Cytotoxicity was quantified by measuring 51Cr release from prelabeled cells and lactate dehydrogenase release. Reactive oxygen metabolites caused dose-dependent cytotoxicity. Good correlation was found between the values for 51Cr and lactate dehydrogenase release. Reactive oxygen metabolite-induced cell damage was reduced by catalase but not by superoxide dismutase. Cellular superoxide dismutase and catalase activities were not increased after incubation with exogenous superoxide dismutase and catalase for up to 5 hr. Pretreatment with diethyldithiocarbamate inhibited cellular superoxide dismutase activity without inhibiting other antioxidants such as catalase, glutathione, glutathione reductase and glutathione peroxidase and sensitized cells to reactive oxygen metabolite-induced cytotoxicity. We conclude that hydrogen peroxide is an important mediator in hypoxanthine-xanthine oxidase-induced cell damage and that superoxide dismutase plays a critical role in cellular antioxidant defenses against hypoxanthine-xanthine oxidase-induced cytotoxicity in cultured rat hepatocytes in vitro.
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PMID:Role of cellular superoxide dismutase against reactive oxygen metabolite-induced cell damage in cultured rat hepatocytes. 131 53

Proton nuclear magnetic resonance spectroscopy is a noninvasive technique allowing the localized, in vivo detection of proton-containing brain metabolites. We used this technique to study eight patients with cerebral infarction or ischemia. A stimulated echo-pulse sequence with chemical shift imaging was used to acquire spectra from multiple contiguous 4-cc volumes extending from the site of ischemia to the opposite hemisphere. Six patients had a reduction in the signal from N-acetyl groups (NAG) in the stroke area compared with controls, and those with the lowest NAG to phosphocreatine/creatine ratios had the least recovery of function. Lactate was observed within the infarcted region in two patients at 9 and 11 days after infarction and may have been present in other patients up to 15 weeks after stroke.
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PMID:Multivoxel 1H-MRS of stroke. 132 Feb 20

The association between cigarette smoking and delayed wound healing is well recognized in clinical practice, although extensive controlled studies have yet to be performed. The documented effects of the toxic constituents of cigarette smoke--particularly nicotine, carbon monoxide, and hydrogen cyanide--suggest potential mechanisms by which smoking may undermine expeditious wound repair. Nicotine is a vasoconstrictor that reduces nutritional blood flow to the skin, resulting in tissue ischemia and impaired healing of injured tissue. Nicotine also increases platelet adhesiveness, raising the risk of thrombotic microvascular occlusion and tissue ischemia. In addition, proliferation of red blood cells, fibroblasts, and macrophages is reduced by nicotine. Carbon monoxide diminishes oxygen transport and metabolism, whereas hydrogen cyanide inhibits the enzyme systems necessary for oxidative metabolism and oxygen transport at the cellular level. Slower healing has been observed clinically in smokers with wounds resulting from trauma, disease, or surgical procedures. The reduced capacity for wound repair is a particular concern in patients undergoing plastic or reconstructive surgery. Compared with nonsmokers, smokers have a higher incidence of unsatisfactory healing after face-lift surgery, as well as a greater degree of complications following breast surgery. Smokers should be advised to stop smoking prior to elective surgery or when recovering from wounds resulting from trauma, disease, or emergent surgery.
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PMID:Smoking and wound healing. 132 8


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