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

Neonatal encephalopathy of early onset, plausibly related to hypoxia and ischemia remains one of the main problems in perinatal medicine. Efforts are necessary to find new non-invasive methods for assessing brain oxygenation. Near-infrared spectroscopy (NIRS) provides information on the concentrations of the oxygenated and reduced forms of hemoglobin, as well as the redox state of cytochrome aa3. Different important variables can be derived through hemoglobin measurement, such as cerebral blood volume and flow, and the responses of these to changes in pCO2. Changes in cytochrome aa3 may provide immediate information on intracellular oxygen utilization. Various studies have shown the feasibility of NIRS in preterm infants. Methodological and technical problems of this method are discussed.
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PMID:Near-infrared spectroscopy in newborn infants. 151 51

In order to investigate the role of the outer medulla in acute ischemic renal failure (Epstein FH, Balaban RS, Ross BD: Redox state of cytochrome aa3 in isolated perfused rat kidney. Am J Physiol 1982;243: F356-F363), the distribution of ATP in the in vivo porcine kidney and its relationship to Na transport and to ischemia was examined by using localized 31P magnetic resonance spectroscopy. Renal cortex (ATP) was higher than medulla. Reduction in Na transport produced by partial renal arterial occlusion ("hypofiltration"), resulted in a 13% increase in the ATP/Pi ratio of the whole kidney (from 2.61 +/- 0.26 to 2.96 +/- 0.27; P less than 0.03). This increase was accounted for by a statistically significant increase in (ATP) in the cortex, with medulla contributing to an insignificant extent. Further occlusion of the renal artery to reduce GFR to zero ("hypoperfusion") resulted in a 70% fall in ATP/Pi ratio. (ATP) was reduced most in the cortex, but pH fell equally in cortex and medulla. After release of arterial occlusion, cortical ATP recovered less completely than medulla ATP. Intracellular pH and Pi were restored in both cortex and medulla. It was concluded that cortex and medulla contribute equally to the pattern of disordered energy metabolism in acute renal failure. Sparing of ATP during hypofiltration may reflect the reduced energy requirements of active Na transport.
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PMID:Renal corticomedullary metabolite gradients during graded arterial occlusion: a localized 31P magnetic resonance spectroscopy study. 195 32

1H MRI permits detection of edema in the brain. In a middle cerebral artery stroke model in the cat, we found a significant correlation between an edema index based on MRI and a sensitive metabolic index of ischemia, the in vivo oxidation status of mitochondrial cytochrome aa3 determined by near-infrared reflectance spectrophotometry (r = -0.70, alpha = 0.001). This result suggests that a simple, noninvasive study using MRI can provide an index of the extent of ischemic damage in an experimental acute stroke model.
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PMID:MRI quantitation of edema in focal cerebral ischemia in cats: correlation with cytochrome aa3 oxidation state. 215 26

Myocardial oxygenation may be altered markedly by changes in tissue blood flow. During brief ischemia and reperfusion produced by transient occlusion of the left anterior descending artery in 10 open-chest dogs, changes in the oxygenation of tissue hemoglobin (Hb) plus myoglobin (Mb) and the oxidation-reduction (redox) state of mitochondrial cytochrome aa3 were monitored continuously using near-infrared spectroscopy. The nondestructive optical technique indicated that coronary occlusion produced an abrupt drop in tissue oxygen stores (tHb02 + Mb02), tissue blood volume (tBV), and the oxidation level of cytochrome aa3. Changes in the cytochrome oxidation state were related inversely to transmural collateral blood flow within the ischemic region (r = 0.77) measured with radiolabeled microspheres. Furthermore, there was a direct relationship (r = 0.91) between collateral blood flow and the tissue level of desaturated Hb and Mb (tHb + Mb). Reperfusion after 2 min of ischemia led to a synchronous overshoot of baseline in coronary flow and tBV followed by supranormal increases in tHb + Mb02 and the oxidation level of cytochrome aa3. The tHb + Mb level increased transiently during reperfusion. This response correlated inversely with collateral flow during ischemia (r = 0.91). Accordingly, the time required to reach peak tHb + Mb levels was shortest in dogs with high collateral flows (r = 0.75). Thus collateral blood flow partially sustains myocardial oxygenation during coronary artery occlusion and influences tissue reoxygenation early during reperfusion.
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PMID:Dynamic mechanisms of cardiac oxygenation during brief ischemia and reperfusion. 217 24

The aim of this study was to detect early renal changes in the rat. Female Wistar rats received oral doses of cyclosporine (12.5, 25 or 50 mg/kg daily). The duration of the experiment was 1, 2, and 3 weeks. Controls received the vehicle only (olive oil). The following alterations were seen by light microscopy: Hypertrophy of the juxtaglomerular apparatus (PAS stain). Cytoplasmic droplets of neutral fat (Oil Red 0) in clusters of cortical tubules, probably belonging to the same nephron. Both the above phenomena increased with dosage and duration of treatment and were absent in controls. In the fat containing tubulus (FCT) brush border staining (alkaline phosphatase) was decreased or absent. Since after PAS the brush border was visualized in many FCT, it is concluded that many FCT were proximal tubulus (PT) of which the brush border has been damaged. In FCT mitochondrial staining (Cytochrome oxidase activity) was strongly decreased or absent. Mean lysosomal volume (acid phosphatase and dipeptidase II) is increased in the PT; in some cyclosporine animals, lysosomes were enlarged, while in others they were comparable to controls. Electron microscopy showed in some PT cells an increased number of empty vacuoles and focal alteration of mitochondria. Normal mitochondria were present next to grossly altered mitochondria. Autophagocytosis of mitochondria was clearly present. The lysosomes appeared swollen and contained electron dense material, not organised in the typical 50 A pattern of myeloid figures. These morphological changes suggest a defect of mitochondrial metabolism, leading to lipid deposition in PT. The mitochondrial metabolism can be disturbed by a direct toxic effect of cyclosporine or indirectly via ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporine nephrotoxicity: comparative cytochemical study of rat kidney and human allograft biopsies. 301 37

Changes in tissue oxygenation of forearm muscles were measured by near infrared (NIR) spectrophotometry in 10 healthy adults during tourniquet ischemia and venous outflow restriction. Muscle O2 stores were depleted rapidly by forearm ischemia manifest by a progressive decrease in tissue oxyhemoglobin and oxymyoglobin over 4-5 min. Muscle ischemia significantly decreased the oxidation level of cytochrome aa3, to below resting base line after only 1.5 min, and the enzyme became fully reduced after 6.5 min. After 8 min of ischemia, tourniquet release was accompanied by a transient increase in muscle blood volume due to influx of oxyhemoglobin. The cytochrome aa3 oxidation level increased above resting base line within 1 min after tourniquet release. Transcutaneous PO2 measurements recorded simultaneously from the same forearm correlated poorly with the kinetics of O2 availability and cytochrome oxidation in the underlying muscle tissue; this was not unexpected because overlying skin did not contribute significantly to NIR muscle signals. Venous outflow restriction without inflow obstruction increased muscle deoxyhemoglobin and tissue blood volume but did not change muscle O2 stores or cytochrome aa3 oxidation level. The ability of the NIR technique to detect dynamic trends in tissue oxygenation reveals that muscle O2 is rapidly consumed during tourniquet ischemia and rapidly restored by hyperemic responses after brief ischemia.
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PMID:Near infrared monitoring of human skeletal muscle oxygenation during forearm ischemia. 340 28

Polarographic measurements show that activity of cytochrome oxidase (CO), assayed as ascorbate plus TMPD oxidase, is decreased in the mitochondria (M) from postischemic areas of rabbit heart 1, 6, and 9 days after temporary (1-hr) coronary artery occlusion (CAO). This effect is observable only in the absence of added cytochrome c. Cytochrome oxidase activity in the cytochrome c-containing medium was not different from the control level. Levels of cytochromes c + c1 and a were substantially lower in tissue from postischemic areas and elevated in the intact tissue 1 and 6 days after temporary CAO as compared with control hearts. Stoichiometry of the cytochromes was not changed. After 1 or 4 hr of permanent CAO, CO activity (plus cytochrome c) of ischemic M was equal to that of M from intact area; CO activity (with or without cytochrome c) was reduced after 0.5 and 1 hr but elevated after 3 or 4 hr of in vitro ischemia as compared with control. The changes of CO activity in infarcted human heart M were similar to those in rabbits after temporary CAO; CO activity was restored after addition of cytochrome c. The data suggest that leakage of cytochrome c occurs during isolation of M and is more pronounced in ischemia-damaged M.
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PMID:Cytochrome oxidase activity of mitochondria from ischemic and reperfused myocardium. 630 31

Regional changes in myocardial function and oxidative metabolism during acute coronary artery occlusion were recorded spectrophotometrically by incorporating fiber optics in the isolated rat heart perfused by Langendorff's procedure. Oxygen saturation of myoglobin, reduction of cytochrome aa3, and the dynamic wall thickness of the left ventricle were continuously and concurrently measured from absorbancy increments at 581-592 nm, 605-630 nm, and 568-592 nm, respectively. In contrast to a gradual decrease in the extent of systolic wall thickening in anoxia, observed decreases in both the extent and the duration of systolic wall thickening and the appearance of a late systolic bulge occurred within 5 s after the onset of regional ischemia. After 10 s of both anoxia and regional ischemia, oxygen saturation of myoglobin decreased by 50%, but fluorescence of nicotinamide adenine dinucleotide remained at aerobic level which indicated that mitochondrial oxidative energy production might still be maintained. Thus early and pronounced dysfunction of the ischemic region appeared to precede a substantial loss of ATP production.
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PMID:Regional myocardial function and metabolism during acute coronary artery occlusion. 709 58

The survival of infants with congenital heart disease has improved dramatically. However, the incidence of neurological injury in infants surviving cardiac surgery remains considerable. These neurological sequelae are attributable at least in part to hypoxia-ischemia/reperfusion, which inevitably accompanies infant heart surgery with deep hypothermia, cardiopulmonary bypass, and circulatory arrest. To begin to identify mechanisms of brain injury during infant cardiac surgery, we used near-infrared spectroscopy to study the relationship between cerebral intravascular (hemoglobin) and mitochondrial (cytochrome aa3) oxygenation in 63 infants (aged 1 day to 9 months) undergoing deep hypothermic repair of congenital heart defects, throughout the intraoperative period. Moreover, we assessed the effect of postnatal age on these changes. The cerebral concentration of oxidized cytochrome aa3 decreased from the onset of deep hypothermic cardiopulmonary bypass, despite apparent abundant intravascular oxygenation manifested by a simultaneous increase in the cerebral concentration of oxyhemoglobin. During this interval infants older than 2 weeks had a greater decrease in oxidized cytochrome aa3 than did infants 2 weeks old or younger. During deep hypothermic circulatory arrest, cerebral levels of oxidized cytochrome aa3 remained depressed while those of oxyhemoglobin declined. With reperfusion following circulatory arrest, the recovery of oxidized cytochrome aa3 was delayed, despite a rapid recovery of intravascular oxygenation (HbO2). After rewarming and 60 minutes of reperfusion, only 46% of infants recovered to the baseline level of cerebral oxidized cytochrome aa3. These findings demonstrate a paradoxical dissociation of changes in intravascular and mitochondrial oxygenation during hypothermic cardiopulmonary bypass; a pronounced decrease of mitochondrial oxygenation is established during induction of hypothermia and a delay in recovery of mitochondrial oxygenation occurs following circulatory arrest. These effects were more pronounced in infants older than 2 weeks than in younger infants. The data suggest potentially deleterious impairments of intrinsic mitochondrial function or of delivery of intravascular oxygen to the mitochondrion or both, effects previously undetected and apparently influenced by cerebral maturation.
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PMID:Cerebral oxygen supply and utilization during infant cardiac surgery. 771 85

The rapid changes in extracellular oxygenation and intracellular oxidation during ischemia and reflow were measured in deep liver tissue by a novel method combining tissue near-infrared spectroscopy with multicomponent curve-fitting analysis. This method enabled us to make real-time measurements of oxygen saturation (SO2) and amount (THB) of hemoglobin in the liver sinusoid as parameters of extracellular oxygenation state and of redox transition of cytochrome aa3 as intracellular oxidation state. Clamping of the hepatic artery in rabbit decreased the THB with a transient fall of SO2. Clamping of the portal vein decreased both SO2 and THB. The decreases of SO2 and THB caused by Pringle's maneuver were larger than the sum of decreases by hepatic artery and portal vein. These changes in SO2 were correlated with intramitochondrial oxidation state as measured by cytochrome aa3. These results indicate the presence of an interrelationship of oxygen supply by hepatic artery and portal vein. This method was clinically applied during and after clamping of hepatic artery and portal vein in 19 cases of hepatic resection with or without chronic hepatic diseases. The decrease in SO2 values before and after clamping (SO2D) and the slope of SO2 recovery (SO2R) after release were calculated. SO2D and SO2R values of the portal vein in cirrhotics were significantly higher and lower, respectively, than those in the normal liver. These data indicate that the present method provides a rapid and reliable method of quantifying hepatic oxygenation during liver surgery and its perioperative management.
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PMID:Interrelationship of oxygen supply by hepatic artery and portal vein: rapid analysis of ischemia-reflow-induced changes in hepatic oxygenation in experimental and clinical subjects by tissue near-infrared spectroscopy. 785 60


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