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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

After 30 s ischemia induced by decapitation, the contents of ATP and phosphocreatine (PC) in mouse brain reduced, while that of lactic acid (LA) increased. When mexiletine (3.1-50 mg.kg-1) was injected ip 30 min before decapitation, the brain ATP and PC reduction, and LA accumulation were both alleviated in a dose-dependent manner. These findings suggested that mexiletine was effective in ameliorating the energy exhaustion in the ischemic brain.
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PMID:[Effect of mexiletine on energy metabolism of ischemic brain in mice]. 145 59

Localized water suppressed proton spectroscopy has opened up a new field of pathophysiological studies of severe brain ischemia. The signals obtained with the pulse sequences used so far are both T1 and T2 weighted. In order to evaluate the extent to which changes in metabolite signals during the course of infarction can be explained by changes in T1 and T2 relaxation times, eight patients with acute stroke were studied. STEAM sequences with varying echo delay times and repetition times were used to measure T1 and T2 of N-acetyl-aspartate (NAA), creatine plus phosphocreatine (Cr+PCr) and choline containing compounds (CHO) in a 27-ml voxel located in the affected area of the brain. Ten healthy volunteers served as controls. We found no difference in T1 or T2 of the metabolites between the patients and the normal controls. The T2 of CHO was longer than that of NAA and Cr+PCr. Our results indicate that spectra obtained in brain infarcts and normal tissue with the same acquisition parameters are directly comparable with respect to relative signal intensities as well as signals scaled with internal and external standards.
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PMID:In vivo relaxation of N-acetyl-aspartate, creatine plus phosphocreatine, and choline containing compounds during the course of brain infarction: a proton MRS study. 146 Oct 96

Using 31P nuclear magnetic resonance, the following parameters were determined in the resting musculus erector spinae of five patients suffering from chronic low back pain, five patients with fibromyalgia, and five healthy controls: Inorganic phosphate (Pi), phosphocreatine (PCr), ATP gamma, ATP alpha, ATP beta. The intracellular pH was derived from the chemical shift of Pi referenced to the PCr resonance. In addition, the Pi-Index was calculated according to the formula: Pi/(Pi + PCr). We discovered a tendency towards a shift of the Pi resonance in the alcalic direction, which was the larger, the stronger muscle spasm was found on palpation. The pH showed the most reliable relationship to the clinical status of muscle spasm. The surprising finding that there is no acidification within the spasmed muscle indicates that generalized hypoxia does not exist in this tissue. This has already been shown with PO2 measurements. An intracellular acidification is only recorded during maximal isometric contraction. Thus, ischemia cannot be responsible for pain experienced during muscle spasm.
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PMID:[Recording muscle spasm in the musculus erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies]. 147 7

We investigated the effect of reversible ischemia, leading to persistent contractile dysfunction (stunning), on myocardial energy metabolism. The balance of energy metabolism is expressed by the phosphorylation state of cytosolic nucleotides. This variable cannot be measured directly because of nucleotide compartmentation, but in the isolated heart it can be estimated by the release of purine catabolites. We have previously shown that increased energy consumption or impaired energy production cause purine release to increase, while primary reduction in energy consumption has the opposite effect. Isolated working rat hearts were reperfused after 10 min of global ischemia, measuring hemodynamic variables, tissue high energy phosphate compounds and purine release. In post-ischemic recovery, aortic flow and minute work decreased to 82 +/- 3% and 77 +/- 4% of control, adenine nucleotide pool was reduced by 4.6 mumol/g dry wt, phosphocreatine to creatine ratio increased significantly and purine release decreased to 42 +/- 6% (P < 0.01). The rate of purine salvage, as evaluated by the incorporation of exogenous 3H-adenosine and 14C-hypoxanthine into tissue nucleotides, was much lower than net purine release, and was unchanged after ischemia and reperfusion. The adenine nucleotide pool could be depleted to the same extent as in the stunned myocardium by prolonged (60 min) aerobic perfusion. In this group the hemodynamic variables were unchanged and purine release averaged 87 +/- 9% of control (P = NS). In other experiments prolonged perfusion was combined with preload reduction in order to decrease energy demand. This protocol reproduced the effects of ischemia-reperfusion: aortic flow and minute work averaged 79 +/- 4% and 73 +/- 9% of control, adenine nucleotide depletion was 4.4 mumol/g dry wt and purine release decreased to 38 +/- 5% (P < 0.01). Our findings support the view that stunning is not due to adenine nucleotide depletion or to impairment in energy production, which would cause purine release to increase, but rather to primary reduction in energy utilization.
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PMID:Energy metabolism in myocardial stunning. 147 19

Experiments were conducted on a model of an isolated functioning rat heart to study myocardial protection by normothermic cardioplegic reperfusion (NCR) with phosphocreatine (PC) in 30-minute total ischemia at 37 degrees C. Five series of experiments were performed: (1) cardioplegia (K+ 30 mM/l, Mg2+ 15 nM/l, osmolarity 330 MOSM/l), ischemia, NCR not applied; (2) the same solution was introduced in the preischemic period, ischemia, NCR (K+ 15 mM/l, Mg2+ 15 mM/l, osmolarity 360 MOSM/l); (3) with the same experimental schedule, PC (10 mmol/l) was added to the cardioplegic solution in the preischemic period; (4) in a similar experiment PC was added in the stage of NCR; (5) PC administered in the preischemic stage and in NCR. Restoration of heart functional parameters, rate and ejection of lactate dehydrogenase into the perfusate were compared. The results of the experiment bear evidence that NCR protects the myocardium from reperfusion damage in normothermic ischemia. The optimal cardioprotective effect of PC is produced when it is administered in the preischemic stage. PC added to the solution for NCR has no positive effect on the restoration of heart functional parameters.
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PMID:[The effect of normothermic cardioplegic reperfusion with phosphocreatine on the recovery of the cardiac functional indices after total ischemia]. 148 92

Concentrations of phosphocreatine, creatine, ATP, ADP, AMP, glucose and lactate in the whole brain did not differ between the mice intoxicated with acrylamide and the controls. When the brain was made ischemic, these concentrations changed to the same extent in both groups. The only difference was the lower pyruvate in acrylamide-intoxicated mice under the ischemia. Thus, as far as the whole brain is concerned, acrylamide does not cause gross alterations of energy metabolites, even under ischemia.
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PMID:Brain energy metabolites in mice intoxicated with acrylamide: effects of ischemia. 150 5

31-phosphorous magnetic resonance spectroscopy was used in a rat model of 10 min severe incomplete forebrain ischemia (two-vessel occlusion with hypotension) to assess the effect of hyperglycemia on intracellular pH and high energy phosphates during ischemia and early reperfusion. One group (n = 8) with preischemic hyperglycemia (serum glucose 20 mmol.l-1) showed an increased intracellular acidosis (pH 6.35) during ischemia compared to 6.55 in the normoglycemic control group (n = 7, P less than 0.001), but the recovery of phosphocreatine and ATP in early reperfusion was the same in the two groups. Another group (n = 7) was normoglycemic during ischemia, but received an i.v. bolus of glucose during the first minute of reperfusion. In this group the recovery of intracellular pH in early reperfusion was slower than in the control group (0.034 +/- 0.006 pH units per minute compared to 0.052 +/- 0.11 in the controls, +/- s.d. and P less than 0.01).
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PMID:Hyperglycemia in global cerebral ischemia and reperfusion: a 31-phosphorous NMR spectroscopy study in rats. 153 75

The age-related response of the myocardium to 30 min of 37 degrees C global ischemia and 120 min of 37 degrees C reperfusion, measured by phosphorus-31 magnetic resonance spectroscopy and the recovery of isovolumic function, was evaluated by using perfused neonatal (3-8 days old, n = 10), immature (24-30 days old, n = 10), and adult (2-4 mo old, n = 5) rabbit hearts. Basal intracellular pH (pHi) was highest in neonatal hearts and decreased with age. The basal phosphocreatine (PCr)-to-ATP ratio differed in each group, increasing with age. Rapid depletion of PCr occurred in all groups during ischemia; ATP retention was greater in adults than in neonates. Reperfusion resulted in no measurable recovery of ATP in any group. Postischemic pHi stabilized above preischemic values in neonatal and immature hearts and below preischemic values in adult hearts. Recovery of PCr and cytosolic Pi (Pcyi) content, heart rate, and coronary flow during reperfusion was greater in neonatal and immature than in adult hearts. During the final 20 min of ischemia, pHi was lower in immature than in neonatal or adult hearts. Postischemic recovery of left ventricular maximum rate of pressure rise (+dP/dtmax) was depressed in immature compared with neonatal and adult hearts. These results demonstrate increased tolerance of the neonatal heart and increased susceptibility of the immature heart to unprotected normothermic ischemic injury relative to the adult heart and suggest that maturational changes in myocardial pHi regulation may be responsible for the observed age-related response.
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PMID:Age-related response of rabbit heart to normothermic ischemia: a 31P-MRS study. 153 98

In vivo 31P nuclear magnetic resonance (NMR) spectroscopy of the right ventricular (RV) free wall was employed to determine (a) whether phosphorus energy metabolites vary reciprocally with workload in the RV and (b) the mechanisms that limit RV contractile function in acute pressure overload. In 20 open-chest pigs, phosphocreatine (PCr)/ATP ratio (an index of energy metabolism inversely related to free ADP concentration), myocardial blood flow (microspheres), and segment shortening (sonomicrometry, n = 14) were measured at control (RV systolic pressure 31 +/- 1 mm Hg), and with pulmonary artery constriction to produce moderate pressure overload (RV systolic pressure 45 +/- 1 mm Hg), and maximal pressure overload before overt RV failure and systemic hypotension (RV systolic pressure 60 +/- 1 mm Hg). With moderate pressure overload, PCr/ATP declined to 89% of control (P = 0.01), while contractile function increased. Adenosine (n = 10, mean dose 0.16 mg/kg-min) increased RV blood flow by an additional 41% without increasing PCr/ATP, indicating that coronary reserve was not depleted and that the decrease in PCr/ATP from control was not due to ischemia. With maximal pressure overload and incipient RV failure, PCr/ATP fell further to 81% of control and RV blood flow did not increase further, even with adenosine. Thus: (a) The decline in PCr/ATP with moderate RV pressure overload, without evident ischemia or contractile dysfunction, supports the positive regulation of oxidative phosphorylation by ATP hydrolysis products. (b) Depletion of RV coronary flow reserve accompanies the onset of RV failure at maximal pressure overload.
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PMID:Energetics of acute pressure overload of the porcine right ventricle. In vivo 31P nuclear magnetic resonance. 154 81


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