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

To investigate the role of tissue oxygenation as one of the control factors regulating tissue respiration, 31P-nuclear magnetic resonance spectroscopy (31P-NMR) was used to estimate muscle metabolites in isolated working muscle during varied tissue oxygenation conditions. O2 delivery (muscle blood flow x arterial O2 content) was varied to isolated in situ working dog gastrocnemius (n = 6) by decreases in arterial PO2 (hypoxemia; H) and by decreases in muscle blood flow (ischemia; I). O2 uptake (VO2) was measured at rest and during work at two or three stimulation intensities (isometric twitch contractions at 3, 5, and occasionally 7 Hz) during three separate conditions: normal O2 delivery (C) and reduced O2 delivery during H and I, with blood flow controlled by pump perfusion. Biochemical metabolites were measured during the last 2 min of each 3-min work period by use of 31P-NMR, and arterial and venous blood samples were drawn and muscle blood flow measured during the last 30 s of each work period. Muscle [ATP] did not fall below resting values at any work intensity, even during O2-limited highly fatiguing work, and was never different among the three conditions. Muscle O2 delivery and VO2 were significantly less (P < 0.05) at the highest work intensities for both I and H than for C but were not different between H and I. As VO2 increased with stimulation intensity, a larger change in any of the proposed regulators of tissue respiration (ADP, P(i), ATP/ADP.P(i), and phosphocreatine) was required during H and I than during C to elicit a given VO2, but requirements were similar for H and I.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A 31P-NMR study of tissue respiration in working dog muscle during reduced O2 delivery conditions. 144 18

31P NMR spectroscopy was used to assess the cerebral ischemia status in rats by measuring the relative levels of phosphate metabolites. Partial cerebral ischemia was induced in 49 rats by reversible occlusion of the carotid arteries. Rats were intubated and mechanically ventilated on a hypoxic gas mixture. Physiological parameters such as temperature and arterial pressure were strictly controlled during the experiments. 31P spectra were acquired at 7 T during basal observation, for 15-20 min after the induction of ischemia, and for 1 hr after reperfusion. Depletion and increase in PCr and Pi levels, respectively, were already observable in the collected spectra within few minutes after the onset of ischemia. No appreciable changes were found in the ATP levels.
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PMID:Partial cerebral ischemia assessed by "in vivo" 31P NMR spectroscopy in rats. 146 Oct 71

Sodium spectroscopy and imaging sequences designed to emphasize fast T2 decay or the multiple quantum signal have previously demonstrated a high contrast between normal and pathologic tissue which may be due to changes in intracellular versus extracellular sodium distribution. Since alterations in the amount of signal with fast T2 decay have previously been shown to occur with changes in intracellular sodium content, this study investigated the fast T2 relaxation characteristics of extracellular sodium during pathologic interventions on nonsubmerged perfused rat hearts. T2 data on total sodium content were obtained while global ischemia (stopping all perfusate flow) and extracellular edema (due to long perfusion times) were induced in the heart. The data were fit to a biexponential, with Mf(T2f) the magnitude (time constant) of the fast component of decay. Mf increased significantly in both pathologies (to 319 +/- 26%, n = 3, of baseline for ischemia and to 527 +/- 284%, n = 3, of baseline for edema); the increase with edema was demonstrated to be due to extracellular sodium by intermittently perfusing the heart for a short period with shift reagent. When shift reagent was not used until the conclusion of the edema experiment, Mf increased to 169 +/- 35% of baseline, also due mainly to extracellular sodium. T2f did not exhibit any trends with these experiments, with values ranging from 1.7 to 5.5 ms. We believe that these results indicate that compartmental sodium content will most likely not be quantifiable in pathologic states in the heart with relaxation-based techniques. However, correlations between the pathologic state of the tissue and the sodium NMR signal obtained with pulse sequences or images that emphasize a particular aspect of relaxation may prove to be useful.
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PMID:Characteristics of extracellular sodium relaxation in perfused hearts with pathologic interventions. 146 Nov 13

Depletion of high-energy phosphates, accumulation of inorganic phosphate and intracellular acidosis have each been proposed as important events in the transition from reversible to irreversible ischemic injury. To assess whether each variable is predictive of functional recovery on reperfusion, these were measured in the isolated isovolumic rat heart using 31P NMR. Perfused hearts were subjected to either 10, 12 or 40 min of normothermic ischemia followed by 40 min of reperfusion. Hearts were then freeze-clamped for further analysis of phosphate metabolites by NMR and ion chromatography. High-energy phosphates, Pi, phosphomonoesters and pH were measured by 31P NMR spectroscopy at 2 minute intervals. Heart rate and developed pressure were monitored simultaneously. All hearts undergoing 10 min of ischemia and 40% of hearts subjected to 12 min of ischemia demonstrated good functional recovery. The remainder of hearts ischemic for 12 min went into contracture on reperfusion with little return of function. Hearts subject to 40 min of ischemia went into ischemic contracture and showed no recovery on reperfusion. Intracellular pH, [ATP], and [Pi] measured prior to reperfusion did not predict the extent of recovery. However, phosphomonoesters were detected prior to reperfusion in all hearts that did not recover well, but were not observed in hearts that showed good mechanical recovery. Analysis of tissue extracts by 31P NMR and ion chromatography indicated that the most prominent components of the phosphomonoesters were glucose 6-phosphate, alpha-glycerol phosphate and AMP. In conclusion, of the various phosphorus metabolites that can be measured by 31P NMR, only one group, the phosphomonoesters, was predictive of functional recovery.
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PMID:Predicting functional recovery from ischemia in the rat myocardium. 148 87

The 31P NMR visibility of ATP of the perfused rat liver was tested over a wide range of metabolic conditions, including normoxic and hypoxic perfusions, fructose loads, and various intervals of normothermic ischemia, for both ad libitum fed and 24-h fasted rats. The 31P NMR signal of ATP was compared to the concentration of ATP determined by enzymatic assays on liver biopsies performed at the end of NMR acquisition. In a first series of experiments, the NMR resonance of intracellular ATP was quantitated in absolute terms by applying the 1H NMR water signal as internal reference: during normoxic and hypoxic perfusions, a constant amount of ATP (0.43 +/- 0.19 mM, mean +/- SD), approximately 12% of the cellular ATP, is not detected by NMR. Nevertheless, there is a high correlation (slope = 0.96 +/- 0.09; r2 = 0.93) between the measurements of ATP by 31P NMR spectroscopy and by biochemical analysis. In a second series of experiments, there was a highly significant correlation between the NMR and analytical biochemical measurements of ATP for whole range of metabolic states, i.e., fructose loads (1.0-10 mM) and various intervals of normothermic ischemia (ranging from 2 to 12 min), indicating unchanged ATP visibility. Thus, as opposed to the studies of Murphy et al. [Murphy, E., et al. (1988) Biochemistry 27, 526-528], it is concluded that ATP at 37 degrees C remains almost entirely visible in the perfused rat liver, also during ischemia.
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PMID:The 31P NMR visibility of ATP in perfused rat liver remains about 90%, unaffected by changes of metabolic state. 151 Sep 35

Relative concentrations of inorganic phosphate [Pi]r, creatine phosphate [CP]r, adenosine triphosphate [ATP]r, and intracellular pH (pHi) were determined by 31P-NMR spectroscopy in the flexores digitorum muscles. The measurements were performed at rest, during bouts of rhythmic exercises at different powers, including one with restricted blood supply, and during recovery. Normal subjects (N) and subjects with previous histories of exercise hyperthermia (EH) were compared. No significant difference was found between N and EH subjects at rest. During exercise [ATP]r was not affected, except in EH subjects exercising under partial muscle ischemia (P less than 0.001); in both N and EH, [CP]r and pHi decreased, and the higher the load the more pronounced the reduction. These changes were significantly larger in EH patients than in N (P less than 0.05), and the differences were dramatically increased by reducing blood supply (P less than 0.001). During recovery, the return to the control values was much slower in EH patients than in N, in particular for pHi after the exercise under partial ischemia. In conclusion, the fact that metabolic disorders are still patent long after the EH occurrence supports the possibility of latent myopathy and of a persistent metabolic disorder. Thus, 31P-NMR spectroscopy could be a useful noninvasive test to detect EH susceptibility in at-risk subjects.
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PMID:Long-term relationship between acute rhabdomyolysis and abnormal high-energy phosphate metabolism potentiated by ischemic exercise. 154 23

The purpose of this study was to investigate the energy movement of the normothermic ischemic liver. Liver ischemia was induced in normal and cirrhotic rats, by cross-clamping portal vein and hepatic artery, bypassing the portal blood to the jugular vein through a shunt tube. The levels of ATP of the hepatic tissue was measured before and after hepatic ischemia, by HPLC and 31P-NMR. Before hepatic ischemia, the levels of ATP was greater in normal liver than in cirrhotic liver, but after ischemia it was significantly smaller in normal liver than cirrhotic liver. Generally they say that the greater is the ATP of the tissue, the greater is the viability of the tissue. But this experiment showed the contrary. Cirrhotic liver can't use glucose sufficiently, therefore acetyl-CoA, which is used in TCA-cycle, is derived from the resolution of fatty acid. As a result, free fatty acid and acyl-CoA increase in cirrhotic liver, and suppress Na(+)-K(+)-ATPase. I conclude that the cirrhotic liver can't effectively use ATP to maintain the potential of the liver cells, maybe, because of it's abnormal metabolism of glucose. Therefore, the levels of ATP was greater in cirrhotic liver than in normal liver after hepatic ischemia.
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PMID:[Investigation of hepatic energy metabolism in normothermic hepatic ischemia--comparison between normal and cirrhotic rat liver]. 154 96

Two-dimensional 1H spectroscopic imaging and magnetic resonance imaging were used to study focal ischemia induced by middle cerebral artery occlusion in rats. A water suppressing spin-echo sequence was used at 4.7 T. Phase encoding during the spin-echo delay (TE = 272 ms) yielded an 8 x 8 array of 35 microL voxels. The injured area of the brain had a higher lactate level and markedly lower N-acetyl aspartate, creatine and choline levels than did the non-ischemic regions. The spectroscopic imaging data clearly showed the localization of the infarct, which agreed well with both magnetic resonance imaging and the histological data obtained post-mortem. This study demonstrates the potential usefulness of combining magnetic resonance imaging and 1H spectroscopic imaging for studying animal models of stroke, and indicates the suitability of the technique for further pharmacological approaches.
NMR Biomed
PMID:Two-dimensional 1H spectroscopic imaging for evaluating the local metabolic response to focal ischemia in the conscious rat. 155 Jul 5

We investigated the effect of moderate post-ischemic hypothermia on neuropathological outcome and cerebral high energy phosphate metabolism, intracellular pH and Mg2+ concentration in the rat. Three groups of animals were investigated: (1) Wistar rats subjected to 12 min of forebrain ischemia under normothermic conditions (n = 17), (2) rats subjected to the identical procedure of ischemia, except that 30 degrees C hypothermia was induced post-ischemia and maintained for 2 h of reperfusion (n = 6), and (3) control hypothermic rats not subjected to ischemia (n = 4). In vivo 31P NMR spectroscopy was performed prior to ischemia, and at intervals up to 168 h after ischemia. Histological analysis of brain tissues was performed 7 days after ischemia. No significant differences in cortical and hippocampal neuronal damage was detected between the two experimental groups. Significantly lower pH values were detected in the hypothermic ischemic animals at 24 h (P = 0.0001) and 48 h (P = 0.018) post-ischemia compared to the normothermic ischemic animals. Normothermic ischemic animals exhibited significantly lower [Mg2+] at 72 h (P less than 0.006) compared to the pre-ischemia level. Our data indicate that post-ischemic hypothermia modifies the profiles of post-ischemic brain tissue pH and Mg2+ concentration, and this modification is not associated with histopathological outcome 7 days after ischemia.
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PMID:The effects of post-ischemic hypothermia on the neuronal injury and brain metabolism after forebrain ischemia in the rat. 156 17

To assess the effect of carteolol, a beta-blocker, on ischemia and reperfusion, changes in the ultrastructure of myocytes and energy metabolism were studied by 31P-NMR in 41 pig hearts without collateral circulation. The left anterior descending coronary artery was occluded for 20 min and reperfused for 120 min in three groups: seven pigs (group 1, no treatment with carteolol; group 2, pre-ischemia treatment with carteolol (10 micrograms/kg); group 3, post-ischemia treatment with carteolol before reperfusion). Other groups of five pigs were killed after 120 min of ischemia (group 4, no treatment; group 5, pre-ischemia treatment) or 20 min of ischemia (group 6, no treatment; group 7, pre-ischemia treatment). After 20 min of ischemia, ATP was higher in groups 2 (76 +/- 9% of the baseline value) than in group 1 (59 +/- 5%) and group 3 (60 +/- 10%). However, the difference disappeared after 30 min of ischemia. After 120 min of reperfusion, ATP showed much better recovery in group 2 (92 +/- 9%) than in groups 1 (66 +/- 7%) and 3 (68 +/- 10%). Ischemic injury, as viewed by light and electron microscopy, was milder in group 7 than in group 6 after 20 min occlusion, but the myocytes were almost normal after 120 min reperfusion in groups 1 to 3. The heart rate, blood pressure and rate pressure product showed no significant difference among the groups. These results indicate that pre-ischemia treatment with carteolol provided protection against ischemic cellular injury and accelerated the repletion of ATP during reperfusion, but the post-ischemia treatment did not lead to recovery of ATP. Therefore, the favorable effect during reperfusion of pre-ischemia treatment with carteolol depends on its protective effect during ischemia.
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PMID:Protective effect of carteolol, a beta-blocker, on myocardial cellular damage in ischemic and reperfused pig hearts: assessment with gated in vivo 31-phosphorus magnetic resonance spectroscopy and electron microscopy. 156 29


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