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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Nuclear Instruments and Methods in Physics Research Section A: 294 (1990), S. 602-605 
    ISSN: 0168-9002
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Nuclear Instruments and Methods in Physics Research Section A: 278 (1989), S. 202-205 
    ISSN: 0168-9002
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Nuclear Instruments and Methods in Physics Research Section A: 276 (1989), S. 568-572 
    ISSN: 0168-9002
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 367 (1976), S. 151-156 
    ISSN: 1432-2013
    Keywords: Interstitial pH of working muscle ; pH microelectrodes ; Metabolic alkalosis ; Metabolic acidosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In isolated gastrocnemius muscles from 19 dogs the interstitial H+ activity ([H+]int) was measured with bulb-type buffer-filled glass minielectrodes. The muscles were working isotonically and perfused with blood. In addition arterial and venous pH, venous O2 saturation, muscle temperature, and blood flow were measured continuously at rest, during 12 min of sustained exercise, and in the recovery period. Lactate (LA−) release and O2 consumption were calculated by the Fick principle. The experiments were performed under normal acid-base conditions and during artificially induced metabolic acidosis and alkalosis. 1. In normal acid-base balance [H+]int at rest was 54±3.3 neq/l (=pH 7.27), while venous H+ ([H+]ven) was 45±4.7 neq/l (=pH 7.34) A[H+] gradient was always observed between interstitial fluid and venous blood. 2. Immediately after onset of exercise [H+]int decreased transiently. After about 15 s [H+]int increased rapidly up to values of 105±7 neq/l (=pH 6.98). In the recovery period [H+]int diminished and reached control values after about 20–30 min. [H+]ven increased up to 74.4±8.1 neq/l (=pH 7.13). Maximal gradients between [H+]int and [H+]ven were 36 neq/l (=pH 0.2). 3. During repeated exercise the decrease in [H+]int at the onset of exercise was more extensive, while the subsequent increase was lowered. These changes correspond to a smaller LA− release. 4. During metabolic alkalosis at the onset of exercise [H+]int decreased less, during metabolic acidosis more than under normal acid-base conditions. Thereafter during metabolic alkalosis maximal values of 95.4±12 neq/l (=pH 7.03), during metabolic acidosis of 180±8.6 neq/l (=pH 6.74) were reached. This led to [H+] gradients between interstitial fluid and venous blood which were much higher in metabolic acidosis than in normal acid-base balance or in metabolic alkalosis. In metabolic acidosis [H+]int decreased very slowly during recovery. 5. During metabolic acidosis the muscle fatigues more rapidly than during metabolic alkalosis or during normal acid-base conditions. It is concluded that the H+ activity measured is that within the interstitial space. Exercise hyperemia is not caused by changes of [H+]int. Mechanisms are discussed which may explain H+ gradients between interstitial fluid and venous blood and rapid changes of [H+]int at the onset of exercise.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1434-3932
    Keywords: Schlüsselwörter Kompartmentsyndrom ; Fasziektomie ; Ulcus cruris ; Arthrogenes Stauungssyndrom ; Kompartmentdruckmessung ; Key words Compartment syndrome ; Crural fasciectomy ; Crural ulceration ; Arthrogenic congestion syndrome ; Compartment pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The chronic compression syndrome of the crural fascia is defined as a new pathological entity. Multifactorial influences lead to hardening of the connective tissue of the crural fascia, which then in turn determines the further course of the disease. The main symptom is leg ulcer, which is as yet incurable. By means of crural fasciectomy, the ulcers could be cured in 17 of 18 patients, some of whom had endured several decades of failed conservative therapy; the treatment of the last patient has not yet been completed. The follow-up time ranged from 10 to 36 months (mean 14.6 months). Crural fasciectomy affects the underlying cause of the disease by significantly reducing the pathologically raised pressures within the compartments from 21.1 mmHg in the lying and 62.5 mmHg in the standing position to 15.5 mmHg and 34.5 mmHg respectively (p = 0.172 and p = 0.003 respectively).
    Notes: Zusammenfassung Das chronische Faszienkompressionssyndrom wird als neue Krankheitsentität definiert. Durch multifaktorielle Einflüsse der Mikrozirkulationsstörung kommt es zu einer bindegewebigen Erstarrung der Fascia cruris, die ihrerseits dann den weiteren Krankheitsverlauf bestimmt. Als Kardinalsymptom gilt das bisher unheilbare Gamaschenulkus. Die krurale Fasziektomie führte nach teilweise jahrzehntelanger Erfolglosigkeit der konservativen Therapie in 17 von 18 Fällen zur Abheilung der Ulzera, wobei die Behandlung des letzten Patienten noch nicht abgeschlossen ist. Die Zeit der Nachbeobachtung betrug 10 bis 36 (Mittel 14,6) Monate. Die krurale Fasziektomie greift kausal in das Krankheitsgeschehen ein, indem die pathologisch erhöhten Drücke in den dorsalen Kompartments entscheidend von 21,2 mmHg im Liegen und 62,5mmHg im Stehen auf 15,5 bzw. 34,5 mmHg herabgesenkt werden (p = 0,172 bzw. p = 0,003).
    Type of Medium: Electronic Resource
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