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

The dynamics of rat skeletal muscle energy metabolism in response to ischemia and reperfusion have been investigated by in vivo 31P NMR spectroscopy. The time course of changes in the phosphocreatine, inorganic phosphate, ATP peaks and in intracellular pH during 2 and 4 h of tourniquet ischemia followed by up to 24 h of tissue reperfusion have been determined. Furthermore, the ATP and IMP concentrations in the soleus and tibialis muscles have been determined by high performance liquid chromatography analysis in response to ischemia and subsequent reperfusion. The results demonstrate an initial overshoot in the pH during the first minutes of ischemia. It is also shown that the muscles recover completely after 2 h of ischemia whereas the energy state of the muscle cell is not restored after 4 h of ischemia followed by up to 24 h of reperfusion. However, the soleus muscle recovers better than the tibialis. The results are discussed in terms of oxygen availability, reperfusion injury, IMP accumulation and different response between muscles with different fibre composition.
NMR Biomed 1990 Apr
PMID:Dynamics of skeletal muscle energetics during ischemia and reperfusion assessed by in vivo 31P NMR. 239 Apr 56

The influence of iloprost, PGE1 and of the combined application of iloprost and PGE1 on high energy phosphate contents was investigated in isolated rat hearts perfused aerob at 37 degrees C in Langendorff mode. Changes in creatine phosphate, ATP and inorganic phosphate were registered during 20 minutes of global ischemia and 56 minutes of reperfusion with 31P-NMR-spectroscopic methods starting drug application prior to ischemia simultaneously with onset of heart perfusion. Most effective in preservation of high energy phosphates was the combined application of PGE1 and iloprost resulting in a creatine phosphate/inorganic phosphate ratio of 103.2 +/- 30.9% of pre-ischemia values compared to 52.5 +/- 6.1% in control group without drug application 0-5 minutes after onset of reperfusion, 148.8 +/- 24.8% vs 78.8 +/- 15.2% at 6-11 minutes of reperfusion and 116.6 +/- 16% vs 68.9 +/- 12.7% at 12-17 minutes of reperfusion. The same trend was observed employing ATP/inorganic phosphate ratio. The improved energy state in reperfused hearts following application of PGE1 and iloprost in combination is presumed to be supported by a reduction of the loss of high energy phosphates (HEP) during global ischemia and by a cytoprotective effect of iloprost immediately after starting reperfusion.
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PMID:Action of iloprost and PGE1 on global ischemic and reperfused myocardium: a 31P-NMR-study. 247 Mar 51

The influence of PGE1, iloprost and a combination of both on high energy phosphate levels in isolated rat hearts reperfused 1 h following 20 min of global ischemia was investigated employing 31P-NMR-spectroscopy. Whereas PGE1 induced a slight reduction in the decline of the creatine phosphate/inorganic phosphate. ATP/inorganic phosphate ratio and NMR-energetic index during ischemia, iloprost application was followed predominantly by a temporary but marked improvement of the creatine phosphate/inorganic phosphate ratio during the early period of reperfusion. The best results in preservation of high energy phosphates were achieved after simultaneous application of PGE1 and iloprost. It is presumed that the accelerated normalization of the heart function observed immediately after ischemia in the eicosanoid treated hearts is related to the more rapid recovery of intracardial high energy phosphate level.
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PMID:PGE1 and iloprost affect the high energy phosphates in the global ischemic and reperfused rat heart: a 31P-NMR study. 247 19

There is controversy regarding the use of alkalinizing agents during reperfusion after cardiac arrest. The potential deleterious effects of sodium bicarbonate (bicarb) administration, including paradoxic cerebral acidosis, have led to the search for alternative agents. Tromethamine (tris) is a non-CO2-generating buffer that has been proposed for use during cardiopulmonary resuscitation. The purpose of this experiment was to compare the ability of tris with bicarb to correct brain pH (pH B) during reperfusion after a 12-minute cardiac arrest. Adult mongrel dogs were instrumented and placed in the bore of a Bruker Biospec 1.89 tesla superconducting magnet system. Ventricular fibrillation was induced; after 12 minutes, cardiopulmonary bypass was initiated and maintained for two hours with minimum flows of 80 mL/kg/min. Bicarb (n = 5) or tris (n = 5) were administered to correct arterial pH as rapidly as possible. 31P NMR spectra were obtained at baseline and throughout ischemia and reperfusion. The pH B was determined with the inorganic phosphate relative to the phosphocreatine resonance signal shift. Profile analysis indicates a difference between groups (P less than .02) related to an initial delay in pH B correction in the tris group. By 48 minutes of reperfusion, pH B did not differ between the groups. Moreover, there was no evidence of paradoxic cerebral acidosis in the bicarb group. Although tris corrects blood pH as quickly as bicarb, it is less effective in correcting pH B. Absence of paradoxic acidosis may be caused by efficient elimination of CO2 by cardiopulmonary bypass.
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PMID:The effect of CO2 and non-CO2-generating buffers on cerebral acidosis after cardiac arrest: A 31P NMR study. 253 65

Rat leg muscles, rendered ischaemic 1 hour previously by ligation of the femoral artery, were submitted to 20 minutes exercise by electrical stimulation of the sciatic nerve. 31P-NMR spectroscopy was used to monitor the changes in high-energy phosphate content of the muscles before, during, and after exercise. Fifteen of the 35 studied muscles evolved toward total necrosis, whereas the others showed signs of recovery over a 2-5-hour postexercise period. Those muscles which did not subsequently recover contained significantly more inorganic phosphate (Pi) at rest (before exercise) than those which recovered. It is suggested that under acute ischaemic conditions the Pi level at rest is correlated with the extent of blood flow restriction and can be used to predict the severity of the ischemia.
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PMID:Prediction by 31P-NMR of the irreversibility of ischemic injury in rat skeletal muscle after ligation of the femoral artery. 254 75

The N-methyl-D-aspartate receptor antagonist MK801 has been reported to prevent neuronal change in models of ischemia in adult animal systems. We studied the hypothesis that blockade of the N-methyl-D-aspartate receptor would prevent the depression of cerebral high-energy phosphates found in perinatal asphyxia without producing alterations in cerebral blood flow, and thus prevent neuropathologic damage. Newborn beagle puppies were anesthetized, tracheotomized, ventilated, and randomized to asphyxial insult (I = discontinuation of ventilatory support for 5 min) or no insult (NI) and drug treatment with MK801 (10 mg/kg intravenously) or an equal volume of saline (S). Puppies received MK801 or saline 15 min prior to I/NI. In S/I pups during insult, blood flow increased to brainstem structures but decreased elsewhere. MK801 had no effect on cerebral blood flow in either control or insulted puppies. 1H NMR studies demonstrated no effect of the MK801 on NI brains. Phosphocreatine levels were 1.7 +/- 0.1, 0.6 +/- 0.1, and 0.9 +/- 0.1 mmole/kg (mean: +/- S.D.) for the S/NI, S/I, and MK801/I pups, respectively. Cerebral lactate was 1.3 +/- 0.2, 3.0 +/- 0.7, and 2.0 +/- 0.4, respectively. The pH fell 0.8 units in the S/I puppies, compared to 0.4 units in the MK801/I puppies. We conclude that pretreatment with the N-methyl-D-aspartate receptor antagonist MK801 in part protects the developing brain against severe metabolic insult.
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PMID:Beagle puppy model of perinatal asphyxia: blockade of excitatory neurotransmitters. 255 28

The Langendorff perfused rat heart was used to investigate whether myocardial damage during ischemia and reperfusion could be protected by free radical scavengers, calcium antagonist and adenosine. Myocardial high energy phosphates were measured by phosphorus-31 NMR spectroscopy during normal perfusion, 20 min of ischemia and 20 min of reperfusion. In hearts, which were treated both with free radical scavengers (FRS) (Superoxide dismutase): 24 IU/ml and catalase 22 IU/ml) and verapamil (10(-7) M), beta-ATP was significantly higher than that of FRS at the end of ischemia. However, beta-ATP recovered only to 83% of baseline value at the end of reperfusion. In view of myocardial metabolism, verapamil treated hearts were good for recovery of creatine phosphate (PCr) but not ATP at the end of reperfusion. Hearts which were treated with only adenosine did not differ from control hearts. However, when hearts were treated with both verapamil and adenosine (10(-4) M), recovery of both ATP and PCr content was significantly greater than that of control hearts. These results suggested that pretreatment with both verapamil and adenosine before and after global ischemia could protect ischemic myocardium, but, further studies are necessary to clarify the precise mechanism of protection.
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PMID:Effects of calcium antagonists and free radical scavengers on myocardial ischemia and reperfusion injury: evaluation by 31P-NMR spectroscopy. 260 Oct 5

Magnesium (Mg2+) is an important regulator of cell energy metabolism, since only MgATP can serve as a substrate for ATP utilizing processes. We used 31P NMR spectroscopy to determine the complexation of ATP with Mg2+ and intracellular free Mg2+ (Mgf) in isolated rat hearts during control perfusion, ischemia and reperfusion. Atomic absorption spectrophotometry was used to determine preischemic and postischemic tissue Mg2+ and release of Mg2+ into the coronary effluent during reperfusion. Mgf increased from 0.60 mmol/l during control perfusion to greater than 6.5 mmol/l after 15 min of ischemia, while we estimated that at that time 6.7 mmol/l Mg2+ had been liberated from ATP. Less than 2% of cellular Mg2+ was released to the effluent during reperfusion after 30 min of ischemia. From spectra obtained during reperfusion the fraction of ATP that was bound to Mg2+ was calculated to be approximately 96% (compared to 94% during control perfusion), indicating that intracellular Mg2+ did not limit the metabolic use of the newly produced ATP. Mgf remained elevated during reperfusion (0.85 mmol/l). We conclude that intracellular Mg2+ deficiency due to leakage of Mg2+ to the extracellular space does not play a role in the poor postischemic recovery in this isolated rat heart model. Nevertheless, high Mg2+ prior to ischemia or during reperfusion may well be protective, due to interactions of Mg2+ with the sarcolemma or intracellular sites, affecting Ca2+,K+ and Na+ distribution and fluxes.
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PMID:Intracellular magnesium during myocardial ischemia and reperfusion: possible consequences for postischemic recovery. 260 49

The peculiarities of brain energy metabolism were studied in male rats before and during cerebral ischemia of various severity elicited by bilateral common carotid arteries ligation. A multidimensional analysis was applied. In the rats which died after the ischemia, the NAD + NADH+/phosphocreatine (PCr) ratio and ATP content before ligation were higher than those in the surviving group. Also the strength of relationships between parameters of NMR spectra in each correlation matrix were 10 times higher and the variability of elements in each matrix was significantly lower in victims than those in the surviving group. The development of severe ischemia and the animals death were accompanied by an increase in the inorganic phosphate content, decrease in pH and stepwise disappearing of PCr and ATP. In animals surviving the same brain ischemia model, the changes in 31P spectra parameters pointed to some increase in the ratio of NAD + NADH+ only to ATP + ADP but not to PCr, and to an increase in summarized strength of correlation between 31P spectra parameters with the variability of elements decreased within each correlation matrix. Detection of these changes can be helpful in the diagnosis of mild ischemia without neurological deficit which already needs preventive therapy against more severe ischemia.
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PMID:[Changes in energy metabolism in the brain in experimental cerebral ischemia of different degree of severity (nuclear magnetic resonance-spectroscopic study)]. 260 23

The molecular order of synthesis and mobilization of glycogen in the perfused heart was studied by 13C NMR. By varying the glucose isotopomer ([1-13C]glucose or [2-13C]glucose) supplied to the heart, glycogen synthesized at different times during the perfusion was labeled at different carbon sites. Subsequently, the in situ mobilization of glycogen during ischemia was observed by detection of labeled lactate derived from glycolysis of the glucosyl monomers. When [1-13C]glucose was given initially in the perfusion and [2-13C]glucose was given second, [2-13C]lactate was detected first during ischemia and [3-13C]lactate second. This result, and the equivalent result when the glucose labels were given in the reverse order, demonstrates that glycogen synthesis and mobilization are ordered in the heart, where glycogen is found morphologically only as beta particles. Previous studies of glycogen synthesis and mobilization in liver and adipocytes [Devos, P., & Hers, H.-G. (1979) Eur. J. Biochem. 99, 161-167; Devos, P., & Hers, H.-G. (1980) Biochem. Biophys. Res. Commun. 95, 1031-1036] have suggested that the organization of beta particles into alpha particles was partially responsible for ordered synthesis and mobilization. The observations reported here for cardiac glycogen suggest that another mechanism is responsible. In addition to examining the ordered synthesis and mobilization of cardiac glycogen, we have selectively monitored the NMR properties of 13C-labeled glycogen synthesized early in the perfusion during further glycogen synthesis from a second, differently labeled substrate. During synthesis from the second labeled glucose monomer, the glycogen resonance from the first label decreased in integrated intensity and increased in line width.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ordered synthesis and mobilization of glycogen in the perfused heart. 261 Dec 59


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