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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 823-828 
    ISSN: 1432-1440
    Keywords: Diabetes mellitus ; Plasma norepinephrine ; Blood pressure regulation ; Diabetes mellitus ; Plasmanoradrenalin ; Blutdruckregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das Verhalten von Blutdruck, Plus und Plasmanoradrenalin während verschiedener Stimulationsmanöver sympathisch nervöser Aktivität sowie das vaskuläre Reaktionsvermögen auf infundiertes Noradrenalin (50, 100 und 200 ng/kg−1/min−1,t=15 min) wurde bei 17 Diabetikern und 6 gesunden Probanden untersucht. Unterschieden wurden Diabetiker 1) ohne Zeichen autonomer Dysfunktion und ohne periphere Neuropathie (n=6), 2) ohne Zeichen autonomer Dysfunktion jedoch mit schwerer peripherer Neuropathie (n=6) und 3) mit autonomer Dysfunktion, mit (n=3) und ohne (n=2) peripherer Neuropathie. Während eines „Cold pressor tests“ (2 min), mechanischer Hautirritation (10 min) und Orthostase (10 min) zeigten Diabetiker ohne klinische Zeichen autonomer Dysfunktion ein den gesunden Kontrollpersonen vergleichbares Verhalten von Blutdruck, Plus und Plasmanoradrenalin, während Diabetiker mit autonomer Dysfunktion unabhängig vom Bestehen einer peripheren Neuropathie während der Orthostase, nicht jedoch während des „Cold pressor tests“ und mechanischer Hautirritation eine deutlich herabgesetzte Noradrenalinfreisetzung (P〈0.05) aufwiesen. Normalpersonen und Diabetiker ohne autonome Dysfunktion unterschieden sich bezüglich ihres Blutdruckverhaltens während Noradrenalininfusion nicht, während Diabetiker mit autonomer Dysfunktion auf die Verabreichung von exogenem Noradrenalin (200 ng/kg/min) mit einem gegenüber Normalpersonen verstärkten (P〈0.05) Blutdruckanstieg reagierten. Störungen der Noradrenalinfreisetzung und der adrenergen Blutdruckregulation scheinen somit, unabhängig vom Bestehen einer peripheren Neuropathie, nur bei Diabetikern mit klinischen Zeichen autonomer Dysfunktion aufzutreten. Der Nachweis derartiger Störungen gelingt jedoch nur bei Anwendung von Stimuli größerer Intensität wie Orthostase oder Infusion einer hohen Noradrenalindosis.
    Notes: Summary Changes in blood pressure (BP) and plasma norepinephrine (NE) following various stimuli of the sympathetic nervous system were studied in six healthy subjects and in 17 diabetic patients. The latter were subdivided in three groups: (1) six patients with neither peripheral neuropathy nor autonomic dysregulation, (2) six patients with severe peripheral neuropathy without autonomic dysregulation, and (3) five patients with autonomic dysregulation, three of whom suffered also from peripheral neuropathy. The following procedures were performed: (1) cold pressor test (2 min), (2) mechanical irritation of the skin by suction (0.75 kg/cm2, 10 min), (3) orthostasis (10 min), and (4) i.v. infusion of NE (50, 100, 200 ng kg−1 min−1 for 15 min each). Both the stimulated endogenous plasma NE levels and BP response to exogenous NE were the same in normal subjects, in diabetic controls and in diabetics with peripheral neuropathy without autonomic dysregulation. In contrast, diabetics with postural hypotension showed a less pronounced release of NE to standing (P〈0.05), but not to cold pressor test and mechanical skin irritation. Furthermore, they showed increased vasoreactivity to the highest dose (P〈0.05), but not to the lower doses of exogenous NE. Thus NE release and adrenergic BP regulation seem to be altered only in diabetics with clinical signs of autonomic dysregulation. These alterations can only be evaluated when patients are exposed to stimuli of higher intensity, such as orthostasis or infusion of a high NE dose.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: Preoptic ; anterior hypothalamic area ; GABA ; Muscimol ; Norepinephrine turnover ; LH ; Prolactin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of intraventricular injections of the highly specific gamma-amino-butyric acid (GABA) agonist muscimol (5 nmol/animal) on blood LH and prolactin levels were measured in ovariectomized (ovx) and in ovx estrogen-progesterone (OEP) primed rats. While the drug stimulated pituitary prolactin release in both experimental groups, pituitary LH release was significantly inhibited in the ovx animals. Muscimol was without any effect on LH levels in ovx-OEP primed rats. Bilateral implantation of tubes containing a muscimol-mannitol mixture into the medial preoptic/ anterior hypothalamic (MPO/AH) area abolished pulsatile LH release whereas blood prolactin values were elevated. The intraventricular injection of GABA (8 μmol) also reduced LH and increased prolactin levels in the blood. Measurements of catecholamine turnover rates in the MPO/AH and in the mediobasal hypothalamus (MBH) yielded reduced preoptic but unchanged hypothalamic norepinephrine (NE) and stimulated hypothalamic dopamine (DA) turnover. In view of the well known stimulatory involvement of the NE system in the mechanism of pulsatile LH release and the inhibitory effect of GABA and its agonist muscimol on pulsatile LH release, it is suggested that GABA inhibits NE release in the MPO/AH by the mechanism of presynaptic inhibition. The observation that muscimol is unable to suppress LH release in vox OEP-primed rats may indicate that those estrogen receptive neurons in the MPO/AH which mediate the negative feedback action of the steroid may use GABA as neurotransmitter and that they are the neurons which inhibit NE release. The inhibitory effect of locally implanted muscimol into the MPO/AH also supports this hypothesis. The facilitatory action of this implanted GABAergic drug on prolactin release points to the involvement of control mechanisms for the regulation of prolactin secretion which reside in the MPO/ AH. The stimulatory effect of intraventricularly injected GABA on hypothalamic DA turnover makes it likely that other than dopaminergic mechanisms are involved in mediating the stimulatory effect of GABA on prolactin release.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1459
    Keywords: Human β-endorphin ; Cerebrospinal fluid ; Simplified RIA-determination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Beta-human-Endorphin-like immunreaktive Substanzen (β h -EI) im menschlichen Liquor (CSF) wurden radioimmunologisch bestimmt. Die Kreuzreaktivität des von uns eingesetzten Antikörpers gegen Beta-human-Endorphin (β h -E) zum Beta-human-Lipoprotein (β h -LPH) betrug 40%, während sie zu Leu- und Met-Enkephalin, Alpha- und Gamma-Endorphin, Fraktion I und II nach Terenius [10], Substanz P und Alpha-MSH geringer war als 1%. Vor der radioimmunologischen Bestimmung wurde eine Adsorption von β h -EI aus CSF an Kieselsäure mit anschließender Desorption mittels eines Gemisches aus Aceton/Salzsäure durchgeführt. Diese Methode wurde gewählt, weil sich dadurch das Verhältnis von β h -LPH zu β h -E im Desorbat zugunsten von β h -E aufgrund der unterschiedlichen Recoveries R ( $$R_{\beta _h - LPH} $$ =33%, $$R_{\beta _h - E} $$ =66%) verschob. Damit wird einerseits eine erhöhte Spezifität bei der Bestimmung von β h -EI und andererseits eine Abtrennung von eventuell vorhandenen Peptidasen erreicht. Eine Adsorption/Desorption aus 2 ml CSF genügt, um β h -EI von 20–150 pg/ml (6–48 fmol/ml) nachzuweisen. Patienten (n=28) mit verschiedenen neurologischen Erkrankungen wiesen Werte von 20–70 pg/ml auf. Vier Liquores unter 20 pg/ml stammten von Meningitis-Patienten, welche unter einer Corticoidtherapie standen. Ein käuflicher RIA-Kit wurde auf seine Eignung zur Bestimmung von β h -E untersucht und verworfen.
    Notes: Summary Human β-endorphin-like immunoreactive substances (β h -EI) in human cerebrospinal fluid (CSF) were determined radioimmunologically. The cross reactivity of the antibodies to human β-endorphin (β h -E) amounted to 40% for human β-lipotropin (β h -LPH) whilst it was less than 1% for leu-and metenkephalin, α- and γ-endorphin, fraction I and II [5], substance P and α-MSH. Prior to radioimmunological determination, an adsorbtion of β h -EI from CSF with silicic acid was carried out and followed by a desorbtion, using a mixture of aceton/hydrochloric acid. This method was chosen because the ratio of β h -LPH to β h -E in the desorbat can be shifted in favour of β h -E owing to the variation in recoveries r ( $$r_{\beta _h - LPH} $$ =33%, $$r_{\beta _h - E} $$ =64%). On the one hand, this enables a more specific determination of β h -E and, on the other hand, and separation of any peptidase than may be present [9]. An adsorbtion/desorbtion of 2 ml CSF suffices to prove the presence of 20–150 pg/ml (6–48 fmol/ml) of β h -EI. The CSF of 28 patients with various neurological diseases was examined and 24 of them had concentrations of 20–70 pg/ml β h -EI. The remaining four, which had concentrations less than 20 pg/ml, came from meningitis patients undergoing corticoid therapy. A purchasable RIA kit was tested for its determination of β h -E and was found to be unsuitable.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 7 (1981), S. 77-87 
    ISSN: 1432-1238
    Keywords: Burn toxins ; Immunotherapy ; Liver damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Modern intensive care combined with current improvements in the specific, systemic and local therapy of burns has delayed the mortal effects of severe burns. Nor has there been any significant improvement in this mortality during the last decade. The occurrence of uncontrollable infection and sepsis due to gram-negative bacteria or fungi as the basic cause of death was not a satisfactory explanation. So, progress should only be expected from a new concept in burn treatment. This new concept should be to view the burn disease as being caused by toxic factors induced by thermal injury to the skin. Electron-microscope studies in mice and rats have revealed similar mitochondrial alterations in hepatocytes after either a sublethal controlled burn injury or an intraperiotoneal application of an equivalent dose, of a cutaneous burn toxin. The intraperitoneal injection of different amounts of the burn toxin indicated, that the extent of the mitochondrial changes correlated directly with the dose of toxin. Investigations of liver metabolism suggested an inhibition of the oxygenation chain. The incubation of isolated liver cells together with the burn toxin demonstrated by scanning electron microscopy a direct cytotoxic effect of the burn toxin. In animal tests the pathogenic effect of the burn toxin could be prevented by treatment with an antitoxic IgG generated in sheep. The fatal sepsis of severely burned patients is the consequence of a decreased host defence against infections, which is caused by a primary and general toxic alteration of the whole organism. One important aspect of treatment should therefore be the elimination of burn toxins. To achieve this management should include primary excision of the burns, local application of nonabsorbable protein-complex-binding substances and specific passive immuno-therapy with an antitoxic IgG.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Graefe's archive for clinical and experimental ophthalmology 221 (1983), S. 78-80 
    ISSN: 1435-702X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tonography of the eye was performed after administration of 10 mg edrophonium chloride (Tensilon) in 13 patients with clinically diagnosed myasthenia gravis. In ten of these patients repetitive nerve stimulation was used to examine the function of the motor end-plate. A significant pressure rise (more than 2 mm Hg) within the 1st min after edrophonium administration was observed in three patients (four eyes), whereas eight of the ten patients who underwent nerve stimulation showed positive results. The edrophonium tonogram test does not seem to be significant enough to define the diagnosis in early myasthenia gravis. Beyond this, these tests might have lost some of their value due to the introduction of antibody analysis against acetylcholine receptors, which serve as a very sensitive diagnostic tool now.
    Type of Medium: Electronic Resource
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