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  • 1
    ISSN: 1432-1440
    Keywords: Uremia ; Renal osteodystrophy ; Bone collagen metabolism ; Bone mineralization ; Urämie ; Renale Osteodystrophie ; Knochenkollagenstoffwechsel ; Skelettmineralisation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die renale Osteodystrophie reflektiert als chronischer Summationsschaden der Struktur und Funktion des Skeletts komplexe Veränderungen im hormonalen Bereich und der Calciumbilanz. Dem Morphologen zeigt sie sich als Mischbild verschiedener histologischer Befunde, unter denen vor allem die Fibro-Osteoclasie eine fortschreitende Destruktion des Knochens verursacht. Unter dem zusätzlichen Einfluß des gestörten Kollagenstoffwechsels des Knochens und der ungenügenden Bildung druckstabiler Mineralkristalle leiden auch die mechanischen Eigenschaften des Skeletts. Offenbar stört die Urämie per se die Kollagenreifung, als weitere pathogenetische Faktoren werden der Einfluß des sekundären Hyperparathyreoidismus sowie Störungen im Vitamin D3-Metabolismus diskutiert.
    Notes: Summary Important sequelae of uremia are hormonal changes in calcium homeostasis combined with chronic calcium imbalance causing structural alteration and functional insufficiency of bone. Morphological findings of the so called renal osteodystrophy are osteomalacia, osteitis fibrosa and osteoporosis. Osteitis fibrosa and abnormal skeletal metabolism (changes of collagen turnover, insufficient maturation of stable bone crystals) impair the mechanical qualities of bone. Probably the uremia per se influences the collagen metabolism; additional factors such as secondary hyperparathyroidism and deficiency of vitamin D3 are discussed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 795-801 
    ISSN: 1432-1440
    Keywords: Mental stress ; Hypertension ; Plasma catecholamine ; Sympathetic lesion ; Tetraplegia ; Paraplegia ; Mentaler Streß ; Hypertonie ; Plasmakatecholamine ; Sympathikusschädigung ; Tetraplegie ; Paraplegie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die durch mentalen Streß induzierte Kreislaufreaktion ist bei Patienten mit irreparabler Halsmarkschädigung und Tetraplegie untersucht worden, indem durch Vergleich mit einem Kollektiv mit distaler Rückenmarkschädigung und Paraplegie und einem Kontrollkollektiv das Verhalten von Blutdruck, Herzfrequenz und der Plasmakatecholaminwerte vor, während und nach mentalem Streß geprüft wurde. Eine pressorische Reaktion war bei Patienten mit kompletter Halsmarkschädigung nicht mehr nachweisbar, die Herzfrequenz stieg lediglich insignifikant über ihr Ausgangsniveau an, eine Konzentrationsänderung der Plasmakatecholamine war kaum noch zu erkennen. Bei paraplegischen Patienten fand sich dagegen eine überhöhte Zunahme der Herzfrequenz. Die Ergebnisse dieser Untersuchung belegen die Aufhebung mental auslösbarer Kreislaufveränderungen bei Patienten mit Sympathikusschädigung im Halsmarkbereich.
    Notes: Summary In ten patients suffering from complete chronic cervical spinal cord lesion, the effect of mental stress was studied. Before, during and after stress, variations of blood pressure, heart rate and plasma catecholamines were tested. The study showed a loss of hemodynamic reactions under mental stress in tetrapiegics, namely the pressure response, the typical increase in heart rate and in plasmanoradrenalin and adrenalin. It is concluded, that changes in sympathectomized man inferfere with the acute hemodynamic stress reaction and impair the blood pressure homeostasis.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 61 (1983), S. 633-640 
    ISSN: 1432-1440
    Keywords: Calcium antagonists ; Nifedipine ; Verapamil ; Diltiazem ; Effects in experimental and essential hypertension ; Side effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Calcium antagonists (nifedipine, verapamil, diltiazem) are potent vascular smooth muscle relaxants. Experimental and clinical investigations provide growing evidence that they are effective in acute and (sub)chronic therapy of arterial hypertension by lowering peripheral vascular resistance and improvement of altered hemodynamics — independent from pathogenesis of hypertension. Due to its prompt and profound hypotensive action, sublingual or oral nifedipine has been used successfully in hypertensive crises. The hypotensive effect usually correlates closely with the severity of hypertension and is nearly absent in normotensive controls. Since the blood pressure drop may occasionally result in absolute or relative hypotension, the initial dose should be as low as possible. The activation of the adrenergic and renin angiotensin systems seen after nifedipine administration is less pronounced after chronic administration of the drug and is nearly absent after verapamil and diltiazem. Plasma aldosterone concentrations remain constant or are slightly decreased. In contrast to classic vasodilators, the long-term administration of calcium antagonists usually does not result in tachycardia (nifedipine), but slight sinus bradycardia (verapamil, diltiazem). Peripheral edema may occasionally occur after nifedipine. A tolerance has been observed during long-term treatment of hypertension. Combining these drugs (verapamil, diltiazem) with betablockers is not recommended due to the negative inotropic and bathmotropic effects. Simultaneous administration of nifedipine and beta-blockers enhances the hypotensive action, but favours the development of peripheral edema and in rare cases (especially in severe coronary heart disease) results in a dramatic drop in blood pressure and/or congestive heart failure. Further clinical evaluation and long-term trials of calcium antagonists as antihypertensive agents will be needed before definite conclusions can be drawn.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 948-958 
    ISSN: 1432-1440
    Keywords: Alcoholism ; Fetal alcohol syndrome ; Genitourinary tract malformations ; Phosphate and magnesium depletion ; Rhabdomyolysis ; Acute renal failure ; Hypertension ; Alkohol ; Alkoholische Embryopathie ; Urogenitaltraktschädigung ; Phosphatund Magnesiumdepletion ; Rhabdomyolyse ; Akutes Nierenversagen ; Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Nephrologisch wichtige Störungen des schwereren Alkoholismus manifestieren sich auf verschiedenen Ebenen. Eine direkte Schädigung der Nieren und abführenden Harnwege ist bislang ausschließlich bei alkoholischer Embryopathie nachgewiesen. Beim Erwachsenen dominieren unspezifische und komplexe Elektrolytstörungen mit Akzentuierung im Alkohol-Entzugssyndrom. Die Niere ist nicht selten primäre Ursache verschiedener Störungen, sie trägt ferner zur — oft inadäquaten — Kompensation extrarenal entstandener Stoffwechselstörungen (z.B. Phosphatmangel, Hypoglykämie) bei. Der alkoholassoziierten Uratretention, hervorgerufen durch Hyperlaktatämie oder Erhöhung derβ-Hydroxybuttersäure, kommt — wegen meist mäßiger Ausprägung — für die Entwicklung einer hyperurikämischen Nephropathie nur geringe Bedeutung zu. Alkoholexzeß (akut oder chronisch) prädisponiert zur Rhabdomyolyse mit konsekutivem Nierenversagen. Möglicherweise ist bei schwerem Alkoholismus und Myopathie die Vulnerabilität der Nieren für andere Noxen gesteigert. Bei der Ratte wird das Glyzerin-induzierte akute Nierenversagen durch Alkoholvorbehandlung verstärkt. Alkohol begünstigt ferner bei Normotonikern und Hypertonikern einen Blutdruckanstieg, der seinerseits das Risiko einer Nierenschädigung erhöht.
    Notes: Summary Different nephrological derangements are observed in severe alcoholics. Until now the direct toxicity of ethanol is only shown in the fetal alcohol syndrome with various malformations of the genitourinary tract. In the adult the kidney is often involved in the development, maintenance and counterregulation of complex electrolyte disturbances like phosphate and potassium hypoglycemia etc. The alcohol associated retention of urate, induced by hyperlactatemia and/or increasedβ-hydroxybutyrate concentration is only rarely complicated by urate nephropathy. Alcohol intoxication (acute and chronic) predisposes to rhabdomyolysis with the risk of acute renal failure. There are some hints that chronic alcoholism with myopathy increases the vulnerability of the kidney for further toxic agents. In rats glycerol induced renal failure is enhanced by alcohol pretreatment. Finally, regular alcohol consumption raises the blood pressure, which per se is a risk factor for renal damage.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 58 (1980), S. 105-116 
    ISSN: 1432-1440
    Keywords: Toxic nephropathy ; Acute tubular necrosis ; Acute interstitial nephritis ; Chronic nephropathy ; Toxische Nephropathie ; Akute Tubulusnekrose ; Akute interstitelle Nephritis ; Chronische Nephropathie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei der Elimination von Arzneimitteln oder ihrer Metaboliten wird gelegentlich die Niere selbst in Mitleidenschaft gezogen. Der Ablauf solcher nephrotoxischer Reaktionen läßt sich nach klinischen und morphologischen Gesichtspunkten meist in voneinander gut abgrenzbare Störungen gliedern. Diese Störung der Funktion oder Alteration der Struktur der Niere sind Folge direkt toxischer Wirkungen oder einer Hypersensitivitätsreaktion, auch übergeordnete metabolische Veränderungen sowie ein chronischer Medikamentenabusus können Ausgangspunkt schwerer Nierenfunktionsstörungen werden. Der pathogenetische Mechanismus der nephrotoxischen Reaktionen wird anhand ihrer chemischen Auslöser diskutiert.
    Notes: Summary Direct tubular damage, hypersensitivity reaction, metabolically mediated kidney disturbances, and chronic nephropathies are important sequelae of several drugs or their metabolites. In this review the drug-induced kidney disease is discussed from a clinical, histological, and pathogenetic point of view. The knowledge of possible nephrotoxic reactions and their underlying toxins are essential for prevention of this kidney disease.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1440
    Keywords: Phosphate-clearance ; Hypernatriuresis ; Hyperparathyreoidism ; Phosphat-Clearance ; Hypernatriurese ; Hyperparathyreoidismus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Phosphat-Clearance (CPO4) des nieren-, kreislauf- und stoffwechselgesunden Erwachsenen beträgt unter Standardbedingungen am frühen Vormittag 8,9±3,2 ml/min. Im 6. und 7. Dezennium besteht eine Tendenz zum Anstieg. Patienten mit essentiellem Hochdruck weisen unter den gleichen Bedingungen — unabhängig vom Verhalten der Nierenfunktion — eine signifikant erhöhte CPO4auf. Ursächlich könnte nach Frick (1969) eine momentane Parathormonfreisetzung infolge der zur Clearance-Untersuchung üblichen Kochsalzinfusion bedeutsam sein. Hypertoniker reagieren bekanntlich bereits auf kleinere Volumenbelastungen empfindlicher als Kreislaufgesunde. Bei renovasculärem Hochdruck ist die Hyperphosphaturie mit einer rückläufigen Plasmakonzentration verknüpft. Denkbar wäre, daß die Phosphatreabsorption dieser Patienten schon unter Basalbedingungen durch das aktivierte Renin-Angiotensin-Aldosteron-System negativ beeinflußt wird. Von den Patienten mit entzündlicher Nephropathie ist bei Pyelonephritis — selbst im normotonen Krankheitsstadium — eine beschleunigte C PO4 bemerkenswert. Im Unterschied hierzu besteht bei Glomerulonephritis ausschließlich bei kompliziezierendem Hochdruck eine Ausscheidungssteigerung. Die Phosphatrejektion ist indes in allen Krankheitsgruppen — offenbar durch den Einfluß eines regulativen Hyperparathyreoidismus — hochgradig gesteigert.
    Notes: Summary In 194 patients the renal clearance of inorganic phosphorus, sodium, inulin and p-aminohippuric acid (CP, CNa, CIn, CPAH) have been studied with standard techniques in the early morning. In the normal group of men the CP averaged 8.9±3.2 ml/min. With increasing age (6th to 7th decade) there was a tendency to a higher CP. In essential hypertension the CP was significantly elevated. According to Frick (1969) this effect might be induced by an increased parathormone sceretion, which occurs after saline loading. Patients with renovascular hypertension showed similar hyperphosphaturia. Since their plasma phosphorus level was slightly reduced, tubular phosphorus reabsorption might be partly diminished due to an activation of the renin-angiotensin-aldosterone-system. In pyelonephritis CP was slightly elevated even when the blood pressure was normal. Combination with hypertension resulted in a further increase of CP. In glomerulonephritis CP was elevated only the hypertensive state. Tubular rejection fraction was markedly increased in both inflammatory kidney diseases, which is possibly due to a secondary hyperparathyreoidism.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 61 (1983), S. 773-783 
    ISSN: 1432-1440
    Keywords: Hypercalcemia ; Malignant discases ; Parathyroid hormone ; Prostaglandin ; Osteoclast activating factor ; Osteopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hypercalcemia accompanies often malignant diseases. The majority of cases of malignancy complicated by hypercalcemia is induced by metastases involving bone, hypercalcemia may also accompany localised tumors. Various hormones have been implicated in the genesis of malignant hypercalcemia: ectopic secretion of parathyroid hormone by tumor or orthotopic secretion by concomitant primary hyperparathyroidism, prostaglandin activating osteoclasts, production of hypercalcemic factor other than these hormones. This review summarizes current knowledge about endocrine-mediated mechanisms which produce hypercalcemia and about its frequency and mechanism in different types of tumors.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1440
    Keywords: Granulocyte lysosomal factors ; Elastase ; Acute and chronic uremia ; Catabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In uremic intoxication proteolytic activity in plasma and striated muscle is enhanced. To get further insights into the underlying mechanisms the lysosomal factors of polymorphonuclear (PMN) leukocytes and the plasma elastase-α 1-proteinase inhibitor complex were investigated in patients with acute and chronic renal failure. Lysosomal activity was evaluated in peripheral blood smears by the lysis of erythrocytes and plasma (halo formation) around each neutrophil induced by 0.25 M NaCl borate buffer. In about half of the patients with chronic renal insufficiency on dietary treatment lysosomal activity of PMN leukocytes was reduced. The plasma concentration of elastase-α 1-proteinase inhibitor complex was normal in most subjects, but increased in three patients with the highest serum creatinine levels (〉13 mg/dl). In the patients with acute renal failure (ARF) of various origin (postoperatively, septicemia, pancreatitis, or dye-induced) halo formation was either reduced or absent. The plasma elastase-α 1-proteinase inhibitor complex was increased in 5/6 of the patients by a factor of two to four. Also in the patients on regular hemodialysis treatment halo formation of PMN leukocytes was substantially reduced, whereas the plasma levels of elastase-α 1-proteinase inhibitor complex was slightly increased. The finding of reduced lysosomal activity of PMN neutrophils in uremia may be partly due to an enhanced release of neutral proteinases into the circulation as indicated by the elevated plasma levels of elastase-α 1-proteinase inhibitor complex in some patients. This release might be in part due to the effect of “uremic toxins”. In the patients on hemodialysis treatment the contact of the blood with the dialyzer (cuprophane) membrane might be an additional factor. Moreover, in the patients with acute renal failure the underlying disease (infection, shock, trauma) contributes to the release of proteinases. These disturbances may be harmful to the patient if the blood concentration or function of the most important proteinase inhibitors (α 1-proteinase inhibitor,α 2-macroglobulin) is reduced.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 59 (1981), S. 715-726 
    ISSN: 1432-1440
    Keywords: Stress ; Emotion ; Hypertension ; Central Nervous System ; Sympathetic nervous system ; Catecholamines ; Streß ; Emotion ; Hypertonie ; Zentralnervensystem ; Sympathicus ; Katecholamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In der multifaktoriellen Genese der Hypertonie wird dem Streß eine wichtige ursächliche Bedeutung zugeschrieben, die Vielfalt der Stressoren, die Komplexität der Streßreaktion sowie die vor allem dem Menschen eigene Fähigkeit der Streßreduktion modifizieren jedoch seinen Stellenwert. In dieser Übersicht werden das Konzept des Stresses, sein Erscheinungsbild und seine zentralnervösen Abläufe eingehender analysiert, die Rolle der Emotion als streßbegleitende Reaktion wird herausgestellt. Als wichtiges funktionelles Bindeglied zwischen Streßreaktion und Hypertonie kann das sympathische Nervensystem angesehen werden, da es auch bei der Borderline-Hypertonie eine übergeordnete Rolle spielt. Die naheliegende Annahme einer direkten ursächlichen Verknüpfung von Streß und Hypertonie wird vor dem Hintergrund experimenteller und epidemiologischer Daten durchleuchtet; offenbar hat Streß nur in der Initialphase der essentiellen Hypertonie einen pathogenetischen Stellenwert, bei manifester Hypertonie jedoch kann er als Auslöser intermittierender Blutdruckanstiege therapeutische Bedeutung erlangen.
    Notes: Summary In current literature stress is assumed to be an import factor in the multifactorial pathogenesis of hypertension. The cardiovascular response might be dependent on the type and severity of stressors, the complexity of stress reaction and the ability of man to counteract stress. In this review the concept of stress, its nature and the participation of the central nervous system are elucidated. The role of emotion is also discussed, as well as a connection to stress mechanisms. The sympathetic nervous system acts as link between stress and hypertension, especially borderline-hypertension. Based on various experimental models as well as epidemiological investigations the hypothesis that stress is a causative factor in the initiation of hypertension is critically discussed. In patients with a genetic predisposition to hypertension, stress may play an important role in early manifestations of chronic blood pressure elevation, and in established hypertension, however, psychological stress contributes to temporary or longer lasting increases of blood pressure.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 575-577 
    ISSN: 1432-1440
    Keywords: Glomerular haematuria ; Glomerulonephritis ; Diuresis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The differentiation between glomerular and non-glomerular haematuria by phase-contrast microscopy has proved to be a useful tool in the diagnosis of glomerulonephritis. In an attempt to evaluate the effect of marked diuresis on the altered red cell morphology in patients with biopsy proven glomerulonephritis, urinary sediments were examined following water or furosemide-induced diuresis. In both diuretic states urine flow increased, urine osmolality decreased and the percentage of glomerular erythrocytes was significantly reduced in the urinary sediment. These data demonstrate that the alteration in urinary red cells in glomerulonephritis is mainly caused by tubular forces. The diagnostic significance is reduced during increased diuresis and the evaluation of urinary red cell morphology should not be performed.
    Type of Medium: Electronic Resource
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