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  • Splanchnic  (2)
  • Alzheimer  (1)
  • Key words Mibefradil  (1)
  • subthalamic nucleus
  • Deep brain stimulation
  • Inorganic Chemistry
  • Springer  (4)
  • 1
    ISSN: 1573-6903
    Keywords: Prothrombin ; ELISA ; cerebrospinal fluid ; blood-CSF barrier ; Alzheimer ; neurological disorders
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prothrombin, known to be expressed in brain and to possess growth modulating properties, has been suggested to be involved in the pathogenesis of Alzheimer's disease (AD). We studied prothrombin concentration in lumbar CSF (L-CSF) in patients with AD (n = 25), neurologic disease controls (NDC; n = 33) covering a wide range of neurologic disorders, and subjects with Guillain-Barré syndrome (GBS; n = 4) as well as in samples of non-pathological ventricular CSF (V-CSF; n = 4). The results were evaluated with respect to CSF flow rate, as indicated by the albumin quotient (QAlb). The concentrations of prothrombin in L-CSF in NDC (mean: 0.46 mg/l, range: 0.21–0.96), and AD (mean: 0.6 mg/l, range: 0.19–1.2) were in the normal range reported previously. Expectedly, prothrombin concentration in L-CSF of GBS was increased (mean: 6.3 mg/l, range: 2.3–9.7) corresponding to the increased QAlb in this group (mean 54.6 × 10−3, range: 17–88.1). The concentrations of both prothrombin and albumin were 5.5-fold higher in L-CSF than in V-CSF (mean QAlb : 1.1 × 10−3, mean concentration of prothrombin: 0.088 mg/l). In conclusion, CSF prothrombin in all conditions evaluated here is exclusively derived from blood.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 21 (1995), S. 352-355 
    ISSN: 1432-1238
    Keywords: Liver ; Metastasis ; Splanchnic ; Oxygen consumption ; Sepsis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Metastatic liver disease can modify the metabolic response to critical illness. Systemic lactic acidosis may arise from an increased production due to inadequate peripheral tissue oxygen transport, altered metabolic function such as depressed pyruvate oxidation or insufficient hepatic clearing capacity due to tumor replacement of functional liver mass. Hepatic venous catheterization in a patient with extensive metastatic melanoma to the liver and adult respiratory distress syndrome indicated a marked disparity between whole body and liver oxygenation which may arise due to a markedly stepped up splanchnic oxygen utilization unmatched by a proportionate rise in regional oxygen delivery. Since some neoplasms may exhibit increased metabolic activity, it is suspected that these metastatic lesions may have contributed to the observed regional hypermetabolism thereby worsening hepatic hypoxia and exacerbating lactic acidosis. This case also illustrates the difficulties in interpreting global indicators of metabolic function and oxygenation in critically ill patients.
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  • 3
    ISSN: 1432-1238
    Keywords: Venous oxygen saturation ; Oxygen transport ; Splanchnic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Central mixed venous oxygen saturation (S $$\mathop v\limits^ - $$ O2) monitoring in critically ill patients to estimate adequacy of peripheral perfusion is gaining increasing popularity. However, a number of unexpected responses, one of which is marked depression of regional (splanchnic) venous oxygen saturation which may coexist with normal or high S $$\mathop v\limits^ - $$ O2, makes interpretation pretation of this parameter difficult. The S $$\mathop v\limits^ - $$ O2 and hepatic venous oxygen saturation levels in seven injured (postoperative) and 15 septic patients were measured. No substantial differences between central and hepatic venous oxygen saturation were noted in nonseptic patients, however, septic subjects exhibited a normal S $$\mathop v\limits^ - $$ O2 of 70.5%±8.7% at a time when the hepatic venous saturation was 55.6%±14.4% which is a significant (p〈0.05) reduction. This reduced oxygen saturation was noted to arise from an increased regional metabolic rate rather than reduced perfusion. Nevertheless, we conclude that a flow limited regional oxygen consumption may potentially exist despite the presence of a normal S $$\mathop v\limits^ - $$ O2 in certain patient subgroups such as septic subjects. Therefore, a normal S $$\mathop v\limits^ - $$ O2 should not be considered as sole criteria to insure optimal oxygen delivery in critically ill patients.
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  • 4
    ISSN: 1432-1041
    Keywords: Key words Mibefradil ; Low-density lipoprotein oxidation ; Calcium channel blocker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: Mibefradil is a novel calcium channel antagonist that selectively blocks T-channels. It acts to reduce hypertension, is cardioprotective and reduces ischemic episodes. Oxidative modification of low-density lipoproteins (LDL) is well known to contribute to coronary atherosclerosis and we therefore investigated to see whether mibefradil had antioxidative action on LDL. Methods: Human LDL were isolated by ultracentrifugation. In vitro oxidation of LDL (0.1 μmol · l−1 protein) in the presence of various concentrations of mibefradil was initiated by 3.2 μmol · l−1 copper ions. The kinetics of formation of conjugated dienes was followed photometrically. Malondialdehyde and lipoperoxides were determined at maximum oxidation. LDL (0.3 μmol · l−1) were also pre-incubated with mibefradil (120 μmol · l−1). Excessive mibefradil was separated by column technique. The resultant LDL were oxidized using copper ions or (AAPH) 2,2′-azobis(2-amidinopropane) hydrochloride. Results: The presence of mibefradil in the concentration range from 10 to 200 μmol · l−1 had dose-dependent effects. These were protection of LDL against oxidation measured as prolongation of the lagtime up to 250%, and reduction in the formation of malondialdehyde down to 65% and of lipoperoxides to 20%. Pre-incubation of LDL with mibefradil prolonged the lagtime of Cu-mediated oxidation up to 132% and of AAPH-mediated oxidation up to 138%. Conclusion: In addition to the T-channel blocking and antiproliferative effects, our results provide arguments for a protective role of mibefradil (10–200 μmol · l−1) on LDL against in vitro oxidation. This was shown with three independent parameters (lagtime, malondialdehyde and lipoperoxides) and in different oxidation models.
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