Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although a number of lines of evidence hint that an elevation of intracellular calcium leads to myocardial injury, the cellular consequences of transient Ca overload remain unclear. To determine the contractile, histologic, and metabolic sequelae of transient Ca overload, we measured developed pressure (DP) in isovolumetric Langendorff-perfused ferret hearts at 37 degrees C before and 20 min after three 5 min periods of perfusion with a 10 mM [Ca]o, 1 mM [Mg]o solution (high-Ca group, n = 8) without ischemia, and in control hearts (n = 5) exposed transiently to the same total divalent cation concentration without a change in [Ca]o (9 mM [Mg]o, 2mM [Ca]o). DP, measured at various [Ca]o (0.5 to 5 mM), was depressed in the high-Ca group relative to control (p less than .001). Representative hearts from the control group were histologically normal, whereas hearts from the high-Ca group exhibited rare foci of predominantly "reversible" injury (mitochondrial swelling, glycogen deposition, and clumping of nuclear chromatin). Maximal Ca++-activated pressure (MCAP), measured from tetani after exposure to ryanodine, was also decreased in the high-Ca group (230 +/- 4 vs 262 +/- 6 mm Hg, p less than .001). Cao sensitivity, determined by normalization of the DP-[Ca]o relationship to the corresponding MCAP, was shifted to higher [Ca]o in the high-Ca group. Phosphorus nuclear magnetic resonance spectra were obtained in four high-Ca hearts. [ATP] declined by 30% to 40% after exposure to high [Ca]o, but inorganic phosphate, phosphocreatine, and pH remained unchanged. These results indicate that transient exposure to high [Ca]o without ischemia leaves behind distinctive contractile, metabolic, and histologic sequelae. The possible implications for the pathogenesis of postischemic contractile dysfunction are discussed.
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PMID:Contractile dysfunction and ATP depletion after transient calcium overload in perfused ferret hearts. 334 94

Cerebral energy metabolism was studied in cats subjected to fluid-percussion brain trauma followed immediately by 30 minutes of controlled hypoventilation for the purpose of simulating a more realistic model of human head injury. The cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2) and glucose (CMRGl) were measured, with simultaneous phosphorus-31 magnetic resonance spectroscopy quantifications of cerebral tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi). Hypoventilation alone did not produce marked changes in CMRGl, tissue pH, or PCr:Pi ratios. When hypoventilation was combined with trauma, marked alterations in CBF, CMRGl, PCr:Pi ratio, and tissue pH were seen, indicating relative ischemia. The alterations of cerebral energy metabolism produced by combining trauma and hypoventilation are more severe than those caused by fluid-percussion trauma alone, and may provide a more realistic model of human head injury.
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PMID:Effect of posttraumatic hypoventilation on cerebral energy metabolism. 335 89

To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug. The heart was then isolated and perfused by the Langendorff technique. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor myocardial energy metabolism and intracellular pH during control perfusion and 30 min of total ischemia (37 degrees C), followed by 30 min of reperfusion. Pretreatment with anipamil altered neither left ventricular developed pressure under normoxic conditions nor the rate and extent of depletion of adenosine triphosphate (ATP) and creatine phosphate during ischemia. Intracellular acidification, however, was attenuated. On reperfusion, hearts from anipamil-pretreated animals recovered significantly better than untreated hearts with respect to replenishment of ATP and creatine phosphate stores, restitution of low levels of intracellular inorganic phosphate and recovery of left ventricular function and coronary flow. Intracellular pH recovered rapidly to preischemic levels, whereas in untreated hearts a complex intracellular inorganic phosphate peak indicated the existence of areas of different pH within the myocardium. It is concluded that anipamil pretreatment protects the heart against some of the deleterious effects of ischemia and reperfusion. Because this protection occurred in the absence of a negative inotropic effect during normoxia, it cannot be attributed to an energy-sparing effect during ischemia. Therefore, alternative mechanisms of action are to be considered.
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PMID:Protective effect of pretreatment with the calcium antagonist anipamil on the ischemic-reperfused rat myocardium: a phosphorus-31 nuclear magnetic resonance study. 335 27

Ischemia leads to intracellular acidosis, the severity of which depends on the availability of glucose for production of lactate and H+. It has been suggested that major compartmentalization of H+ occurs, with glial cells becoming much more acidotic than neurons. Since this issue is of crucial importance for the understanding of mechanisms of ischemic brain damage, we induced complete ischemia by decapitation in hypo-, normo- and hyperglycemic awake rats, yielding brain tissue lactate contents varying between 4 and 27 mumol/g. Using phosphorus nuclear magnetic resonance (NMR) we explored whether a splitting of the phosphorus peak occurred as a reflection of compartmentalization. Forebrains were put in NMR tubes and spectra obtained 15 min after decapitation. Since no such splitting was observed, we conclude that major compartmentalization does not occur in ischemia at the degrees of lactic acidosis studied.
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PMID:Evidence against major compartmentalization of H+ in ischemic rat brain tissue. 336 6

Progressive cerebral ischemia was induced in seven anesthetized hyperglycemic rats by carotid artery ligation and hemorrhagic hypotension. Phosphorus metabolites, intracellular pH, and lactate in the brain were monitored by 31P and 1H magnetic resonance spectroscopy. Under conditions in which blood flow was low, phosphocreatine (PCr) concentration and intracellular pH decreased and the concentration of lactate increased. The decrease in ATP was approximately one-third that of PCr until only 25% PCr remained, after which ATP was lost more rapidly than PCr. These changes were interpreted in terms of three regions observed by the magnetic resonance coil, one of complete ischemia, one of partial ischemia, and one of perfusion sufficient to maintain normal metabolite levels. The extent of the three regions was estimated quantitatively. Broadening and splitting of the inorganic phosphorus (Pi) peak into two components provided further evidence of distinct populations of cells, one very acidic and another less so. Apparent intracellular buffering capacity was calculated as 23.6 +/- 1.3 mumol lactate/g wet wt/pH.
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PMID:Metabolic changes during experimental cerebral ischemia in hyperglycemic rats, observed by 31P and 1H magnetic resonance spectroscopy. 336 94

Phosphorus-31 magnetic resonance spectroscopy (MRS) was used to monitor regional changes in high-energy phosphorus compounds and intracellular pH during 60 min of acute regional ischemia (acute occlusion of left anterior descending artery) and reperfusion in open-chest cats using a 1.2-cm two-turn coil sutured to the myocardium. During the 60-min ischemic phase, phosphocreatine (PCr) intensity was reduced to 47 +/- 4.9% (mean +/- SE) of control (p less than 0.01) by 15 min postocclusion while adenosine triphosphate (ATP) intensity decreased more slowly with the decrease (66 +/- 5.6%) achieving significance (p less than 0.05) only at 60 min postocclusion. Inorganic phosphate (Pi) increased to a maximum of 397 +/- 42% of control (p less than 0.01) while the pH decreased progressively from 7.36 +/- 0.02 to 6.02 +/- 0.14 (p less than 0.01). After release of occlusion PCr intensity recovered to 86 +/- 12% of the initial control value at 15 min postreperfusion but showed a subsequent downward trend to 79 +/- 8.8%. The ATP did not recover but tended to decline further during reperfusion. The Pi intensity decreased to 260 +/- 38% of control while the pH increased to 7.01 +/- 0.23 by 15 min postreperfusion. Thus, the reperfused irreversibly injured myocardium is characterized by persistent depletion of PCr and ATP and elevation of Pi. Phosphorus-31 MRS provides a nondestructive method for characterizing the reperfused irreversibly damaged myocardium.
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PMID:Characterization of high-energy phosphate compounds during reperfusion of the irreversibly injured myocardium using 31P MRS. 339 64

Phosphorus-31 magnetic resonance spectroscopy was used to study the relationship between metabolic and functional alterations during acute regional ischemia in vivo. Phosphocreatine, adenosine triphosphate (ATP), inorganic phosphate, and intracellular pH (pHi) were monitored in 11 pigs at 2-minute intervals during 4 and 20 minutes of acute left anterior descending coronary artery occlusion followed by 20 minutes of reperfusion. In a parallel series of experiments, segment shortening was continuously monitored by sonomicrometry during the early ischemic period. Segment shortening decreased precipitously after coronary occlusion, and systolic expansion was noted within 30 seconds. Phosphocreatine levels decreased rapidly and reached a minimum value of 44 +/- 13% (mean +/- SE) of the control value by 20 minutes of ischemia. Ischemia-induced reduction of ATP was small and not statistically significant. Inorganic phosphate increased rapidly to a peak level of 158 +/- 9% of the control value by 4 minutes of ischemia. Intracellular pH decreased 0.76 +/- 0.04 units during the initial 10 minutes of ischemia and subsequently stabilized. After reperfusion, phosphocreatine, inorganic phosphate, and pHi recovery occurred within 4 minutes and was similar in the 4- and 20- minute ischemia groups. These results indicate that the changes in high-energy phosphates and pHi observed during both 4 and 20 minutes of coronary occlusion are rapidly reversible. The temporal course of metabolic and functional alterations during early ischemia suggests that if these are causally related the decline in contractility is mediated by an increase in inorganic phosphate, a decrease in pHi, or both rather than by loss of ATP.
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PMID:In vivo alterations of high-energy phosphates and intracellular pH during reversible ischemia in pigs: a 31P magnetic resonance spectroscopy study. 341 85

We have employed concurrent 31P- and 23Na-nuclear magnetic resonance (NMR) spectroscopy in conjunction with the paramagnetic shift reagents dysprosium-chelated tripolyphosphate and triethylenetetramine-hexa-acetic acid to observe the intracellular sodium and phosphorus signals in rat leg muscle. With induced ischemia in the leg, we find slowly falling phosphorylation potential. At a critical value of, associated with energetic failure of the Na+-K+ antiport, the intracellular sodium signal begins to increase. We find the following critical values: log, 3.12 +/- 0.32; pH, 6.86 +/- 0.13; Na+ influx with and without ouabain, 5.1 +/- 4.3 and 4.0 +/- 1.3 mol.l-1.h-1, respectively.
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PMID:Intracellular sodium flux and high-energy phosphorus metabolites in ischemic skeletal muscle. 342 18

Lysophosphoglycerides accumulate in ischemic myocardium and induce electrophysiologic alterations in normoxic tissue in vitro closely analogous to those seen during ischemia in vivo. The present study was performed to define the temporal alterations of myocardial phospholipids during the first 3 minutes of ischemia in anesthetized cats and to determine whether the magnitude of the increase in lysophosphoglycerides correlates with the severity of ventricular arrhythmias. Fast-frozen transmural biopsies were obtained simultaneously from the ischemic and non-ischemic zones of the left ventricle. In control animals, values of lysophosphatidylcholine (LPC) did not differ in anterior (2.1 +/- 0.2 nmol/mg protein) compared with lateral (2.2 +/- 0.2 nmol/mg protein) regions of the left ventricular wall. The values for LPC in the anterior and lateral regions were also identical when expressed as % of total phospholipid phosphorus (1.4 +/- 0.1%). Comparing these values to those of all other animals biopsied within 3 minutes of ischemia, no significant increase in LPC was seen (1.7 +/- 0.2%). However, stratification of the animals based on the severity of ventricular arrhythmias showed striking differences. In animals without arrhythmias, no significant change occurred in LPC (1.2 +/- 0.2% phospholipid phosphorus or 2.0 +/- 0.3 nmol/mg protein) compared with the non-ischemic tissue control values (1.4 +/- 0.1% phospholipid phosphorus or 2.1 +/- 0.2 nmol/mg protein). In contrast, in animals with arrhythmias, a striking and significant increase in LPC (to 2.0 +/- 0.2% phospholipid phosphorus or 3.1 +/- 0.3 nmol/mg protein) was seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lysophosphoglycerides and ventricular fibrillation early after onset of ischemia. 343 Jun 44

Phosphorus-31 (31P) nuclear magnetic resonance (NMR) spectroscopic investigations of the rat stomach were performed utilizing a 1-cm2, three-turn, zig-zag coil. A zig-zag coil of this dimension produced an effective B1 field that extends only within a 4-mm distance from the plane of the surface coil, rendering it possible to obtain high-resolution 31P spectra localized to the stomach without contamination from surrounding tissues. Normal stomach showed a characteristic spectral pattern with resonances reflecting inorganic phosphate (Pi), phosphocreatine (PCr), and the alpha-, beta-, and gamma-phosphates of adenosine triphosphate (ATP). Ischemia-induced changes in Pi, PCr, and ATP resonances were readily followed in vivo with a time resolution of 2.13 min. Indomethacin-induced ulcer revealed a low intracellular pH and a decrease in the PCr to Pi ratio indicating the partially ischemic conditions of ulcerative lesions of the stomach as has been previously suggested. The present studies indicate that 31P NMR spectroscopy utilizing a zig-zag coil is a powerful tool to study local pathology of the gastrointestinal (GI) tract. Since zig-zag coils suitable for fiberscopic devices are easily constructed, clinical applications of the present technique are apparent.
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PMID:31P NMR spectroscopy of the stomach by zig-zag coil. 343 5


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