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

The authors report on an acute compartment syndrome occurring symmetrically in the extensors of both forearms. The etiology of this unique compartment syndrome, not previously described, could be attributed to the inhalation of a propane-butane gas mixture, low in oxygen, while sleeping, in combination with external compression of both forearms, due to the patient's head lying on both forearms while sleeping. Ischemic damage to muscles was precisely located using non-invasive MRI (Magnetic Resonance Imaging). The extent of cellular damage due to ischemia after fasciotomy and healing by secondary intention was quantitatively assessed using non-invasive 31P-MRS (Phosphorus Magnetic Resonance Spectroscopy). The results correlate with the clinical and histological findings and indicate a bioenergetic regeneration of the ischemic skeletal muscle's cells.
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PMID:[Monitoring of an acute compartment syndrome of unusual etiology using MRI (magnetic resonance tomography) and MRS (magnetic resonance spectroscopy)]. 222 41

Electrical burns or ischemia (induced by vascular ligation) were produced in the legs of 15 anesthetized dogs to study evolution of tissue changes compared with impedance alterations. After the application of 1-ampere currents at 60 Hz, animals were monitored from 1 to 4 days. Muscle impendance was measured with frequency sweeping to determine tissue destruction. Nuclear magnetic resonance spectroscopy (phosphorus 31) was used to assess metabolic activity, and results were compared to impedance measurements. In burned limbs, 70% reduction in muscle impedance was seen, which corresponds to decreased metabolic activity (absent organic phosphates) and suggests necrosis. Visually viable tissue had impedance decreases of 25% and levels of organic phosphates slightly lower than normal. Relaxation frequencies in dogs with severe burns exceeded 80 kHz; in viable tissue, 30 to 40 kHz (normal: 30 kHz). In ischemic muscle, organic phosphates decreased rapidly (1 to 2 hours); impedance changes evolved more slowly (1 day), but they ultimately reached the same degree of severity. Measurement of impedance may be a valuable adjunct in the evaluation of electrical burns, since significant changes strongly suggest nonviability.
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PMID:Determination of tissue viability in experimental electrical injuries. 228 5

We measured cerebral intracellular pH using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy during 1 week after forebrain ischemia or sham operation in eight and seven rats, respectively. Mean maximum pH was significantly higher (p less than 0.003) in the ischemic group than in the sham-operated group (7.34 +/- 0.03 and 7.19 +/- 0.02, respectively). The difference between mean maximum pH and baseline pH (7.08 +/- 0.01 in each group) was significantly greater (p less than 0.02) in the ischemic group than in the sham-operated group. In the ischemic group, alkalosis occurred primarily after 48-72 hours of recirculation. We speculate that brain tissue alkalosis occurring chronically after ischemia is associated with delayed ischemic neuronal death.
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PMID:Chronic cerebral intracellular alkalosis following forebrain ischemic insult in rats. 230 71

The mechanisms responsible for changes in myocardial contractility during regional ischemia are unknown. Since changes in high-energy phosphates during ischemia are sensitive to reductions in myocardial blood flow, it was hypothesized that myocardial function under steady-state conditions of graded regional ischemia is closely related to changes in myocardial high-energy phosphates. Therefore, phosphorus-31 nuclear magnetic resonance spectroscopy was employed in an in vivo porcine model of graded coronary stenosis. Simultaneous measurements of regional subendocardial blood flow, high-energy phosphates, pH, and myocardial segment shortening were made during various degrees of regional ischemia in which subendocardial blood flow was reduced by 16-94%. During mild reductions in myocardial blood flow (subendocardial blood flow = 83% of nonischemic myocardium), only the ratio of phosphocreatine to inorganic phosphate (PCr/Pi), Pi, and [H+] were significantly changed from control. PCr, ATP, and PCr/ATP were not significantly reduced from control with mild reductions in blood flow. Changes in myocardial segment shortening were most closely associated with changes in PCr/Pi (r = 0.94). Pi and [H+] were negatively correlated with segment shortening (r = -0.64 and -0.58, respectively) and increased over twofold when blood flow was reduced by 62%. Thus, these data demonstrate that PCr/Pi is sensitive to reductions in myocardial blood flow and closely correlates with changes in myocardial function. These data are also consistent with a role for Pi or H+ as inhibitors of myocardial contractility during ischemia.
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PMID:Relationship between myocardial metabolites and contractile abnormalities during graded regional ischemia. Phosphorus-31 nuclear magnetic resonance studies of porcine myocardium in vivo. 231 22

Changes in phosphorus metabolites and intracellular pH in acute liver failure induced by D-galactosamine (GAL) were evaluated non-destructively and continuously using 31P-NMR spectroscopy. Furthermore, changes in these parameters under ischemia were also examined. GAL(1.0g/kg) was injected intravenously to male Wistar rats. NMR measurements in perfused livers were performed with a GX-270FT NMR spectrometer (JEOL). Typical changes in 31P-NMR spectra were observed after GAL administration. ATP levels decreased to 57.4 +/- 12.4% at 12 hours and to 65.4 +/- 7.7% at 24 hours after the administration compared with that in control rats. Pi levels increased remarkably to 632.1 +/- 76.4% at 3 hours and recovered to 127.5 +/- 22% at 24 hours. NAD+/NADH and UDP-sugar levels gradually increased to 253.5 +/- 33.4 and 456.3 +/- 60.9%, respectively, at 24 hours. In GAL treated livers, ATP levels fell rapidly and Pi levels rose correspondingly during ischemia, and they rapidly recovered by reperfusion. The intracellular pH decreased to 7.16 +/- 0.032 from 7.38 +/- 0.065 at 3 hours after GAL administration. However, significant changes in pH were not observed until 24 hours. In GAL treated livers, slight changes in pH were observed under ischemia. These results indicate that 31P-NMR is a useful method to evaluate the damage of acute liver failure, and to diagnose liver diseases involving the intrahepatic energy metabolism.
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PMID:[31P nuclear magnetic resonance study of intrahepatic energy metabolism in acute liver failure]. 231 84

The changes in cerebral phosphorus metabolites, intracellular pH, and lactate during 30 min of complete global ischemia and 2 h of reperfusion were monitored by time-shared 1H and 31P in vivo NMR spectroscopy in rats. After the induction of ischemia, intracellular pH decreased from 7.14 +/- 0.01 to 6.32 +/- 0.10, and lactate concentration increased from 1.6 +/- 0.4 to 15.8 +/- 2.5 mumol/g; ATP and phosphocreatine were totally depleted, while inorganic phosphate increased 715 +/- 47%. Within 1 h after blood flow was restored, high-energy phosphates and lactate levels had recovered close to baseline levels. The changes in intracellular pH and lactate levels during ischemia and reperfusion correlated well.
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PMID:Cerebral metabolite dynamics during temporary complete ischemia in rats monitored by time-shared 1H and 31P NMR spectroscopy. 231 35

The dose-response relation between plasma glucose and brain lactate and the relation of these parameters to intracellular pH during severe cerebral ischemia have not been well characterized over a wide range of plasma glucose levels. Experiments to delineate these relations in the gerbil model of global ischemia were performed by using phosphorus-31 nuclear magnetic resonance spectroscopy to measure intracellular pH and a new method to measure brain lactate. Ischemia increased final brain lactate linearly 4 mumol/g for every 100 mg/dl increase in plasma glucose up to 650 mg/dl (p = 0.0001, r2 = 0.9); beyond 650 mg/dl, saturation of the glucose transport-glycolysis system occurred. Plasma glucose correlated better with ischemic intracellular pH than did brain lactate. However, when brain lactate levels are compared with intracellular pH during ischemia, the relation may be threshold rather than linear. A narrow transition zone, during which ischemic intracellular pH decreased precipitously with increasing brain lactate, was observed between 17 and 22 mumol/g; below 17 mumol/g, intracellular pH remained stable at 6.8-6.9, whereas above 22 mumol/g, intracellular pH decreased maximally to about 6.2. The marked decrease in intracellular pH that occurs when brain lactate surpasses 17 mumol/g suggests that this sudden drop in intracellular pH may account for the "lactate threshold" for increased cerebral ischemic damage.
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PMID:Relationship between plasma glucose, brain lactate, and intracellular pH during cerebral ischemia in gerbils. 234 98

Recovery of myocardial high-energy phosphate (HEP) metabolism after coronary occlusion and reperfusion may vary with ischemic duration and may provide information about the extent of tissue viability. To evaluate the differences between varying durations of ischemia and to attempt to identify metabolic indexes of salvaged viable tissue, intact New Zealand white rabbits underwent either 30 (group 1; n = 8) or 60 (group 2; n = 8) minutes of coronary occlusion followed by reperfusion. HEP metabolism was evaluated with cardiac gated phosphorus 31 (31P) nuclear magnetic resonance (NMR) spectroscopy with a 2.0 T spectrometer. While similar HEP changes were observed during ischemia in both groups, differences in HEP recovery between groups were seen following reperfusion. Group 1 animals demonstrated a gradual decrease in inorganic phosphates (Pi) (p less than 0.05 versus group 2), an immediate recovery of phosphocreatine (PCr) (p = ns versus baseline), and a gradual increase of adenosine triphosphate (ATP) to pre-ischemic levels. Group 2 animals had elevated levels of Pi (p less than 0.05 versus baseline; p less than 0.05 versus group 1), slow recovery of PCr, and continued reduction of ATP (p less than 0.05 versus baseline; p less than 0.05 versus group 1). Group 1 rabbits had a greater extent of viable myocardium than group 2 (77.1 +/- 9.7% of risk area versus 39.4 +/- 9.4%; p less than 0.001). Significant correlations were found between PCr and Pi reperfusion values and myocardial viability (r = 0.59, p less than 0.05; r = 0.73, p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of myocardial viability following ischemic and reperfusion injury using phosphorus 31 nuclear magnetic resonance spectroscopy in vivo. 236 May 15

Changes in high-energy phosphate metabolism may be important in the regulation of myocardial contractile function during ischemia. This study sought to determine the dynamic relation between myocardial contractile function and high-energy phosphate metabolism during and following brief (24-second) coronary occlusion, when large and rapid changes in both parameters occur. Eight anesthetized, open-chest pigs were instrumented with a Doppler flow probe and occluder on the anterior descending coronary artery, segment length crystals in the anterior left ventricular wall, and a surface coil for phosphorus-31 nuclear magnetic resonance spectroscopy. Phosphorus-31 spectra were reconstructed with a 4.8-second time resolution by summing corresponding short blocks of data from multiple occlusions. Metabolic and functional parameters were unchanged during the first 4.8 seconds of occlusion. During the remainder of occlusion, phosphocreatine progressively declined to 66 +/- 3% of control, inorganic phosphate rose to 170 +/- 8% of control, and segment shortening fell to 25 +/- 9% of control. A strong linear correlation was found between dynamic changes in segment shortening and phosphocreatine (r2 = 0.97), inorganic phosphate (r2 = 0.96), and the ratio of phosphocreatine to inorganic phosphate (r2 = 0.98) during occlusion. At any level of the ratio between phosphocreatine and inorganic phosphate, segment shortening was greater during reflow than during occlusion. The close, dynamic relation between segment shortening and phosphorus metabolites supports the regulation of contractility by changes in energy metabolism or its by-products during ischemia. During reactive hyperemia, the high coronary flow rate may be an independent factor modulating contractility.
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PMID:Dynamic relation between myocardial contractility and energy metabolism during and following brief coronary occlusion in the pig. 237 83

The energy metabolism of the brain was measured in three types of ischemic models in the cat using phosphorus-31 magnetic resonance spectroscopy. The cerebral ischemia was produced as follows. In Group 1, two balloons were inflated in the left subclavian artery and the brachiocephalic trunk. In Group 2, the left middle cerebral artery was occluded through a transorbital approach. A combination of the two was employed in Group 3. Phosphorus-31 magnetic resonance spectra were obtained serially during 2 hours of ischemia. Immediately after occlusion, peaks of phosphocreatine and adenosine triphosphate decreased, whereas the peak of inorganic phosphate increased and split in two. Intracellular pH determined by chemical shift of the inorganic phosphate peak decreased. These changes were more pronounced in Group 3 when compared with the other groups. Histological study showed no infarction in Group 1 and infarcted areas in Groups 2 and 3. The size of the infarcted area in Group 3 was larger than that in Group 2. These results suggest that the model of middle cerebral artery occlusion potentiated with the occlusion of the brachiocephalic trunk and the left subclavian artery by balloon catheters is a reliable stroke model and that phosphorus-31 magnetic resonance spectroscopy is useful to understand the pathophysiological state of cerebral ischemia in vivo.
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PMID:Phosphorus-31 magnetic resonance spectroscopy of cerebral ischemia in cats. 238 42


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