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

31P-NMR spectroscopy has been used to study the energy metabolism and the NMR visibility of ATP and intracellular Pi of the C6 glioma cell line and rat astrocyte grown on microcarrier beads with the following results. 1. In vivo NMR spectra of C6 glioma cells and rat astrocytes indicate that these cells were able to maintain their level of ATP resonances during a long anoxic period (more than an hour). Both cell types were sensitive to ischemia which induced a loss of ATP resonances within 40 min. Glucose starvation induced by 40% decrease in ATP resonances correlated to a 50% increase in the intensity of the Pi signal. These changes corresponded to a new steady state which could be reversed by reperfusing the cells with a glucose-containing medium. 2. In contrast to in vivo data, 31P-NMR analyses of perchloric acid extracts of cells incubated in a glucose-free medium showed that their ATP and Pi contents were unchanged during starvation. The changes of NMR visibility of the metabolites in living C6 cells were correlated to modifications of their macroscopic longitudinal relaxation times, evolving from 0.30 +/- 0.08 s and 6.6 +/- 1.5 s in the presence of glucose to 0.68 +/- 0.26 s and 3.2 +/- 0.9 s in the absence of glucose for ATP and Pi, respectively. The changes of the NMR detectability of ATP and Pi indicate that changes in their microenvironment occur during glucose starvation, suggesting the existence of different pools of these metabolites within the cells. 3. Under various experimental conditions, i.e. anoxia, ischemia and glucose starvation, rat astrocytes in primary culture showed a very similar behavior to that of C6 cells, suggesting a similar adaptability to the nature of the energy supply for both the normal and the malignant cell.
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PMID:Phosphorus-31 nuclear magnetic resonance of C6 glioma cells and rat astrocytes. Evidence for a modification of the longitudinal relaxation time of ATP and Pi during glucose starvation. 199 80

The metabolic effects of R-phenylisopropyladenosine (R-PIA), an agonist of adenosine A1 receptors, were studied by in vivo 31P NMR spectroscopy before, during, and after 30 min of reversible forebrain ischemia in the rat. R-PIA had no effect on cerebral metabolism before ischemia. During a 30-min ischemia, R-PIA reduced the decrease in phosphocreatine (43 +/- 11% of the control level at the end of ischemia vs. 27 +/- 9% in the reference group) and ATP (58 +/- 12% vs. 40 +/- 23%) and the increase in inorganic phosphate (672 +/- 210% vs. 905 +/- 229%). The intracellular acidosis elicited by ischemia was also less in the treated group (pH of 6.40 +/- 0.10 vs. 6.30 +/- 0.10). Recirculation was associated with a faster recovery of PCr, ATP, Pi, and pHi to control levels in the treated group than in the reference group. It is concluded that adenosine protects against ischemic injury by mechanisms that include metabolic protection.
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PMID:Metabolic effects of R-phenylisopropyladenosine during reversible forebrain ischemia studied by in vivo 31P nuclear magnetic resonance spectroscopy. 201 53

Larger NMR magnets with relatively high field strengths have become available recently, allowing the application of magnetic resonance spectroscopy (MRS) in larger mammalian organs. The aim of this study was to develop and test a new and simple kidney perfusion model from slaughterhouse swine using a new 4.7-tesla/40-cm diameter system, with the intention behind to provide a human-like mammalian experimental kidney perfusion model, and to avoid sensitive in vivo animal experiments on higher-developed mammalians, 35 pig kidneys obtained 10-15 min post mortem were studied to evaluate and define conditions for optimum metabolic preservation with the following perfusion protocols: (1) immediate plegia with cold Collins solution, 1-3 h cold storage, P-31 MRS; (2) immediate plegia, 1-3 h cold storage, blood reperfusion, P-31 MRS; (3) immediate blood reperfusion, plegia, 1-3 h cold storage, blood reperfusion, P-31 MRS; (4) immediate blood reperfusion, plegia, 24 h cold storage, blood reperfusion, P-31 MRS, P-31 MRS at 81 MHz with a double-tuned surface coil yielded the following results: [table: see text] Blood flow showed a weak correlation with beta-ATP/inorganic phosphate in protocols 3 and 4 of r = 0.64. Repeated reperfusion and ischemia experiments of this model allowed the on-line observation of the metabolic response of the energy phosphate pattern for several hours. In conclusion, slaughterhouse-harvested swine kidneys lend themselves to a simple, low-cost in vitro perfusion model, provided they are reperfused with arterial blood immediately after harvesting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Application of P-31 nuclear magnetic resonance spectroscopy to a new experimental kidney perfusion model using cadaveric porcine kidneys from slaughterhouse. 201 76

Postischemic reperfusion injury can be modified by transient low calcium (Ca2+) reperfusion, although the data on the optimal [Ca2+] are controversial. High-energy phosphates and contractile function of isolated perfused rat hearts (37 degrees C, 300 beats/min) were studied simultaneously during global ischemia (30 min) and reperfusion (10 min at [Ca2+] = 1.3, 0.05, 0.1, 0.3, 0.5 and 0.7 mmol/l, followed by 20 min at [Ca2+] = 1.3 mmol/l), using phosphorus-31 nuclear magnetic resonance (31P NMR) spectroscopy. Reperfusion with 1.3 mmol/l Ca2+ after 0.05 or 0.1 mmol/l Ca2+ largely abolished the recovery of ATP obtained during initial low Ca2+ reperfusion (calcium paradox effect). A [Ca2+] of 0.3 mmol/l was sufficiently high to prevent this detrimental effect; at the same time this concentration was sufficiently low to cause a substantial recovery of ATP, which was maintained upon switching to 1.3 mmol/l Ca2+. Recovery of ATP did not correlate with recovery of contractile function.
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PMID:A phosphorus-31 nuclear magnetic resonance study of myocardial ATP content during postischemic low calcium reperfusion. 202 52

To evaluate changes in coronary blood flow during allograft rejection, 16 beagles with cervical cardiac allografts from mongrel donors were immunosuppressed postoperatively for 7 days with cyclosporine (20 mg/kg orally) and prednisone (0.5 mg/kg orally). They were weaned from immunosuppression over 3 days and then treated with methylprednisolone (30 mg/kg/day IV), cyclosporine (20 mg/kg orally), and prednisone (0.5 mg/kg orally) for 4 days. Previous experiments with this model have suggested the utility of phosphorus 31 nuclear magnetic resonance spectroscopy (31P NMR) in the diagnosis of rejection. Therefore in 10 dogs (NMR group) bioenergetic changes during rejection were assessed using the 31P NMR index of the ratio of phosphocreatine to inorganic phosphate (PCr/Pi). To correlate coronary blood flow and graft ischemia with allograft rejection, six dogs (FLOW group) underwent placement of a magnetic flow probe on the left anterior descending coronary artery to determine mean and peak coronary flow. In both NMR and FLOW groups, grafts were evaluated by endomyocardial biopsy (grading 0 to 8 for increasing rejection), and measurement of lactate production and left ventricular end-diastolic pressure. During the initial 7 days of immunotherapy, cellular rejection was effectively suppressed, and the bioenergetic status of the grafts remained stable (day 7: PCr/Pi = 70% of baseline, biopsy score = 2.0). During weaning of immunotherapy, however, the metabolic profile of the grafts decayed (day 10: PCr/Pi = 45% of baseline, biopsy score = 5.8; p less than 0.05 vs day 0). After 4 days of augmented immunosuppression, PCr/Pi recovered to 83% of baseline; this metabolic recovery corresponded with an improvement in mean biopsy score to 3.2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary blood flow does not decrease during allograft rejection in heterotopic heart transplants. 203 21

Using an isolated perfused heart preparation of the rat, the effects of lidocaine (Na+ channel blocker) on ischemic derangements of the mechanical function and energy metabolism of the ventricular myocardium were studied. The myocardial tissue levels of creatine phosphate (CP), ATP, inorganic phosphate (PI) and pH were determined using 31P-NMR. Global ischemia was induced by cross-clamping the aortic inflow line for 20 min, which resulted in a fall in CP, ATP, and pH, and a rise in Pi. The test hearts were perfused with a lidocaine-containing solution (10(-7) M) for 20 min prior to the induction of global ischemia and for 80 min after reperfusion. No significant decline of the myocardial mechanical function expressed as "left ventricular pressure x heart rate" was observed in lidocaine-treated hearts. Lidocaine significantly suppressed the fall in the myocardial ATP and pH during ischemia. Furthermore, in the reperfusion phase, restoration of high ATP levels was observed with the lidocaine-treated heart. These results manifest the beneficial effect of lidocaine on ischemia-induced cell injury.
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PMID:Protective effect of lidocaine on the ischemic-reperfused rat heart: a phosphorus 31 nuclear magnetic resonance study. 203 91

An effect on normothermic ischemia on the rat liver metabolism was examined using in vivo 31P-NMR spectroscopy. Energy metabolism was monitored by measuring the ratio of beta-ATP/Pi and changes were compared between two groups, untreated rats (Group A) and rats of which spleens were subcutaneously transposed to perform portosystemic collaterals (Group B). In group A, beta-ATP/Pi reduced to 0.18 after occlusion of both portal vein and hepatic artery for 10 min, and recovered to 0.97 at 120 min after reperfusion was initiated. In the case of 30 minischemia, however, it recovered only to 0.53 even at 120 min after reperfusion. In contrast to group A, it recovered to 0.81 at 120 min after reperfusion following 30 min-ischemia in group B. Furthermore, when 10 min-ischemia was repeated 3 times with intervals of 10 min-perfusion in group B, it recovered to 0.87 as early as 20 min after initiation of reperfusion. These results clearly indicate that the prevention of the portal congestion improves recovery from energy metabolic disorder and, in addition, division of total ischemic time with moderate intermission is effective to diminish the metabolic disorder due to occlusion of both hepatic artery and portal vein. However without the prevention of the portal congestion the effect of division of total ischemic time was significantly reduced.
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PMID:[31P-NMR study on the high energy phosphate metabolism in warm ischemic rat liver caused by hepatic artery and portal vein occlusion]. 204 51

Concurrent 23Na and 31P nuclear magnetic resonance spectroscopy has been employed to study the effects of ischemia upon the high-energy phosphagens and sodium ion concentration within the in vivo rat liver. High-energy phosphates in the form of ATP were depleted within 10 min of the onset of ischemia when measured by NMR. However, similar liver samples subjected to analytical biochemistry retained 27 +/- 12% of their ATP after a similar 10-min ischemic insult. Time-dependent 23Na NMR measurements, obtained in the presence of the shift reagent Dy(TTHA) to distinguish intracellular from extracellular sodium, revealed a rapid rise in the intracellular sodium when the liver was made ischemic. Intracellular and extracellular sodium concentrations approached equilibrium with an exponential time constant of 14.7 +/- 7 min. The initial rate of sodium influx was calculated to be 1.50 meq.l-1.min-1. The results indicate that the ischemic liver has a high passive sodium permeability and that NMR detectable 31P signals reflect the actual availability of cytosolic high-energy phosphates to enzymes, in this instance the membrane-bound [Na+, K+]-ATPase.
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PMID:Sodium flux and bioenergetics in the ischemic rat liver. 204 16

The mechanism responsible for heterogeneity in tissue pH was investigated in perfused rat hearts subjected to ischemia/reperfusion insult, by correlating the time course of pH changes to the severity of vascular impairment. In 25 perfused hearts, myocardial pH was monitored by 31 P-NMR spectra. During ischemia, pH, which was 7.1 at the beginning of ischemia, progressively decreased and reached a steady level of 5.9 (5.9-compartment) after 40 minutes. In addition, another define peak of pH 7.1 (7.1-compartment) became evident after 50 min of ischemia. The 7.1-compartment grew higher with ischemic time and was only observed after 180 min of ischemia. Although reperfusion after 20 min of ischemia recovered pH, ATP, and creatine phosphate, reperfusion after 50 min left two Pi peaks, the 5.9- and 7.1-compartments; the former gradually decreased with a concomitant increase of the latter. Reperfusion after 180 min of ischemia with various pH levels did not shift the Pi peak from pH 7.1, suggesting that the perfusate did not reach that compartment, the impaired flow region. High coronary resistance and a heterogeneous staining pattern concomitant with a late appearance of the 7.1 component further supported this hypothesis. Myocardial coenzyme Q10 radical, an indicator of the tissue redox state, was also low in those hearts which were reperfused after 50 min of ischemia. Thus, the splitting of the Pi peak, caused by reperfusion after prolonged ischemia, represents the existence of a no-reflow region.
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PMID:The mechanism underlying heterogeneous pH in ischemic and reperfused myocardium. 206 3

The visibility of ATP and ADP to NMR was studied by comparing simultaneous measurements of freeze-trapped tissue sections from perfused rat liver under normoxia and ischemia using a modified 31P-cryo-NMR method and biochemical assay. The 31P-cryo-NMR method provides good time resolution and allows the quantitation of absolute metabolite concentrations. Prior to 31P-cryo-NMR measurements, freeze-trapped tissues were thawed in the presence of cryoprotectant and EDTA. With this sample preparation procedure, the integrity of the plasma and mitochondrial membranes was not maintained, inducing homogeneous microviscosity and chelation of intracellular divalent cations, thereby increasing the visibility of metabolites compared to the in vivo NMR measurement. With ischemic stress, total cellular ATP concentration decreased significantly (P less than 0.001). While ADP concentrations measured by cryo-NMR and biochemical analysis were consistent during normoxia and ischemia, ATP concentrations measured by cryo-NMR were significantly lower (P less than 0.05) than those obtained by biochemical analysis. The amount of invisible ATP (0.42 +/- 0.10 mumol/g wet weight: mean +/- S.E.) did not change after the induction of ischemia. The results of this study suggest that ATP invisibility to cryo-NMR is not due to compartmentation into regions of high paramagnetic ion concentrations or high microviscosity, but is influenced by other factors.
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PMID:Visibility of ATP and ADP in freeze-trapped tissue from perfused rat liver during normoxia and ischemia using 31P-cryo-NMR. 206 82


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