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

31P NMR was used to continuously monitor ATP and inorganic phosphate levels in perfused mouse liver. Under "optimal" conditions, the time resolution of the technique was approximately 1 min. In the absence of any metabolic perturbations the ATP level remained constant for at least 2 hr and decreased by only approximately 20% in 18 hr. Both ATP and inorganic phosphate levels responded to alterations in the oxygen supply to the liver. The half-time for this response was approximately 1 min, and the response to short periods of hypoxia or ischemia was partially reversible. The addition of insulin caused only a minor decrease in the ATP level but significantly decreased the rate of response of ATP and phosphate levels to hypoxia and ischemia.
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PMID:Rapid ATP assays in perfused mouse liver by 31P NMR. 29 54

A study by pulsed NMR techniques in living liver tissue has led to the discovery that the observed longitudinal relaxation decay behavior is strongly multicomponent. After death of the experimental animal, the relaxation decay curves evolve toward a single-component behavior. These changes can also be observed within a few minutes after the liver is excised and placed in a test tube, and they involve a high degree of quantitative and qualitative regularity and reproducibility. An excellent description of all observed NMR behavior is obtained from a dynamic two-compartment model. Rapidly relaxing volumes exchange water molecules with slowly relaxing volumes; associating only an increasing water molecule exchange rate with increasing ischemia accounts in quantitative detail for all observed changes. The exchange-rate values and their variation with tissue deterioration are in good agreement with that estimated for intra- to extracellular water exchange as limited by cell-membrane osmotic permeabilities. Possible applications of these results in different biomedical areas are discussed.
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PMID:NMR relaxation behavior in living and ischemically damaged tissue. 100 99

In order to investigate the energetic status of the aged heart during ischemia and reperfusion we perfused female Wistar rats 6, 12 and 24 month old. The hearts were subjected to 15 min of global total ischemia plus 30 min of reperfusion. NMR spectra were collected during the entire experimental period to have the in vivo monitoring of the changes in intracellular pH and intracellular ATP, PCr and Pi contents. In the first 8 min of ischemia the fall of pH was similar in the 3 groups of rats, while at the end of the ischemic period the young rat hearts showed an intracellular pH significantly lower than aged rat hearts. At the end of reperfusion, ATP and PCr contents appeared significantly higher in the adult and aged hearts as compared to the young. The Pi content, on the contrary, was significantly lower in aged than young rat hearts. We suggest that the hearts of adult and aged animals, at the end of reperfusion, showed larger energetic recovery, in our experimental conditions of brief ischemia, than young hearts.
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PMID:[A 31P-NMR spectroscopic study of the changes in energy metabolism induced by cardiac ischemia and reperfusion in rats of different ages]. 129 70

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

Fluorine NMR spectroscopy of sequestered perfluorocarbon emulsion has been used to measure myocardial oxygen tension. This novel application provides a rapid noninvasive assessment of changes in oxygen tension in response to ischemia and reperfusion. Rats were predosed with Oxypherol-ET (emulsion of perfluorotributylamine). Following vascular clearance of the emulsion the heart was excised and perfused using the Langendorff retrograde technique. 19F spin-lattice relaxation time measurements provided an accurate estimate of myocardial pO2. Using a two-point determination with a time resolution of 1 s, the loss of oxygen was found to be complete within 40 s of the onset of global ischemia. The fall in oxygen tension correlated closely with an observed loss of ventricular pressure. Magnetic resonance imaging showed that perfluorocarbon was distributed throughout the heart; thus, this reporter molecule provides a global measurement of oxygen tension.
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PMID:A noninvasive assessment of myocardial oxygen tension: 19F NMR spectroscopy of sequestered perfluorocarbon emulsion. 133 4

We investigated the effect of 30 degrees C whole body hypothermia on neuronal injury, astroglial reactivity and intracellular pH in rats subjected to 15 min of forebrain ischemia. Experimental groups included: (1) normothermic ischemia (n = 8), ischemia induced under 37 degrees C body temperature, (2) hypothermic ischemia (n = 6), ischemia induced under 30 degrees C body temperature. Cerebral intracellular pH was measured using in vivo 31P NMR spectroscopy over 7 days. Neuronal injury and astrocytic reactivity were evaluated using hematoxylin and eosin staining, and immunoreactivity to glial fibrillary acidic protein, respectively. Normothermic animals revealed significant alkalosis (P less than 0.01) at 48 h after ischemia compared to the pre-ischemic value. No significant intracellular pH change was detected after ischemia in the hypothermic group. Ischemic neuronal injury was prevented in the hypothermic animals, compared to the severe neuronal injury found in the normothermic animals (P less than 0.01). The marked astrocytosis of normothermic animals was significantly inhibited in the hypothermic animals (P less than 0.01). Our data indicate, that hypothermia significantly inhibits neuronal injury as well as post-ischemic alkaloids and astrocytosis, induced by 15 min of forebrain ischemia in the rat.
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PMID:Neuronal damage, glial response and cerebral metabolism after hypothermic forebrain ischemia in the rat. 138 61

A comparative study of 24 hr preservation at 4 degrees C of excised rat livers with Euro-Collins and hydroxyethyl starch-free University of Wisconsin (UWm) solutions has been conducted based on the assessment of (1) the cellular energy status determined by 31P NMR spectroscopy and (2) cellular injury estimated from the loss of purine compounds (inosine, hypoxanthine, xanthine, and uric acid) during cold ischemia and reperfusion measured by HPLC, the leakage of intracellular enzymes, and the modifications of parenchyma established by light microscopy. Recovery of nucleosides di- and triphosphate was greater in the UWm group (80 +/- 6% vs. 58 +/- 6%) while inorganic phosphate formation was comparatively reduced. During hypothermic storage, the UWm groups generated a higher amount of inosine and hypoxanthine (in relation to the presence of adenosine in the protective solution) while no xanthine or uric acid was detected due to the inhibitory effect of allopurinol. Conversely, large quantities of xanthine and uric acid were found in the reperfusate of the EC group, pinpointing the cytotoxic role of oxygen-derived free radicals in the generation of cellular damage, as also illustrated by a higher aspartate aminotransferase leakage in the EC group (devoid of allopurinol and glutathione. Light microscopy indicated no histological alterations in the UWm group and mild alterations in the EC group that showed ballooning of hepatocytes (no lactobionate and raffinose in EC) and an alternation of clarifications and eosinophilic condensations. This study clearly confirms and illustrates the overall superiority of UWm solution in liver transplant preservation.
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PMID:Twenty-four-hour hypothermic preservation of rat liver with Euro-Collins and UW solutions. A comparative evaluation by 31P NMR spectroscopy, biochemical assays, and light microscopy. 141 50

31P-NMR spectroscopic studies were performed in vivo on brains of rats administered cocaine. Cocaine.HCl (1-5 mg/kg) administered systemically to lightly anesthetized rats resulted in significant and progressive deficits in whole brain intracellular free Mg ([Mg2+]i). Intracellular pH (pHi) also fell in a progressive manner but only after a significant fall in brain [Mg2+]i was noted. Both [Mg2+]i and pHi returned to normal in most rats. Brains of rats that exhibited stroke-like events, however, demonstrated continued intracellular acidosis associated with progressive loss of phosphocreatine and elevation of Pi up until death. These observations are consistent with the tenet that injection of cocaine can result in severe cerebral vasospasm, ischemia and rupture of cerebral blood vessels as a consequence of depletion of brain [Mg2+]i.
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PMID:Cocaine induces intracellular free Mg deficits, ischemia and stroke as observed by in-vivo 31P-NMR of the brain. 142 Feb 62

Mannitol has a beneficial effect on ischemic injury following a short-duration forebrain ischemic insult in rats. Using the same animal model, we attempted to show that this effect of mannitol could be traced (via an improvement in cerebral blood flow) to a tempering of the collapse in the high-energy phosphates that occurs during the insult. A 10 min ischemic insult was induced by bilateral carotid artery occlusion followed by a reduction of the blood pressure to 50 mmHg through removal of blood via a tail catheter. 31P NMR spectroscopy was used to monitor the energy state and the pH prior to, during, and after the insult. The studies show that mannitol administered in doses of 0.25 g kg-1 or 1.0 g kg-1 prior to the insult has no significant effect on the high-energy phosphate levels or on the cerebral pH during ischemia, or on their post-ischemia recovery.
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PMID:Mannitol does not affect energy metabolism in forebrain ischemia. 142 Oct 96

The effects of high dose allopurinol (ALLOP) pretreatment on the cerebral energy metabolism of unanesthetized 7-day-postnatal rats during exposure to 3 h of cerebral hypoxia-ischemia were serially quantitated using non-invasive 31P NMR spectroscopy. Adenosine triphosphate, integrated over the last 2 h of hypoxia and expressed as a fraction of baseline, was 0.73 +/- 0.16 with ALLOP pretreatment (200 mg/kg s.c.) compared to 0.52 +/- 0.05 for saline pretreatment (P = 0.001). Inorganic phosphate/phosphocreatine (Pi/PCr), integrated over the same time interval, was 2.63 +/- 1.23 relative to baseline with ALLOP versus 5.13 +/- 1.45 for saline-treated pups (P less than 0.0005). We suggest that the neuroprotection achieved with high dose ALLOP pretreatment may be attributed in part to preservation of energy metabolites.
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PMID:Allopurinol preserves cerebral energy metabolism during perinatal hypoxia-ischemia: a 31P NMR study in unanesthetized immature rats. 143 87


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