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  • 2000-2004  (2)
  • 1985-1989  (5)
  • 1975-1979  (4)
  • 1
    Digitale Medien
    Digitale Medien
    The syndrome of hypertension and hyperkalaemia with normal glomerular function (Gordon's syndrome) (1987)
    Springer
    Pediatric nephrology 1 (1987), S. 473-478 
    Details
    ISSN: 1432-198X
    Schlagwort(e): Tubular function ; Atrial natriuretic peptide ; Hypertension ; Acidosis ; Hyperkalaemia
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract A 14-year-old boy with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome) is described. The patient's clinical symptoms consisted of periodic paralysis, slight metabolic acidosis of the proximal type and hypercalciuria. Prostaglandin excretion was normal. Infusion of atrial natriuretic peptide had no effect on electrolyte excretion or glomerular function although a normal increase in cyclic guanosine monophosphate was demonstrated in plasma and urine. This lack of sensitivity to atrial natriuretic peptide offers a new pathophysiological concept in this syndrome. Treatment with hydrochlorothiazide was successful in this case.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00849256
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  • 2
    Digitale Medien
    Digitale Medien
    Congenital nephrogenic diabetes insipidus — vasopressin and prostaglandins in response to treatment with hydrochlorothiazide and indomethacin (1987)
    Springer
    Pediatric nephrology 1 (1987), S. 485-490 
    Details
    ISSN: 1432-198X
    Schlagwort(e): Hydrochlorothiazide ; Indomethacin ; Nephrogenic diabetes insipidus ; Prostaglandins ; Vasopressin
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract In four boys with congenital nephrogenic diabetes insipidus, plasma arginine-vasopressin (AVP) and urinary excretion of prostaglandins were studied in response to treatment with hydrochlorothiazide and indomethacin. An abnormal relationship between AVP and urine osmolality was demonstrated in all patients. In the first patient, treatment with indomethacin (3 mg/kg per day) resulted in a drop of the inulin and paraminohippurate clearances. In the other three patients urinary excretion of PGE2 was raised, and fell during treatment with hydrochlorothiazide (2 mg/kg per day) and indomethacin (2 mg/kg per day). Urine flow, free water clearance and osmolar clearance decreased during treatment. A combination of both drugs is more effective than hydrochlorothiazide alone and the effect appears to be additive.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00849258
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  • 3
    Digitale Medien
    Digitale Medien
    Atrial natriuretic peptide and sodium homeostasis in chronic renal failure (1989)
    Springer
    Pediatric nephrology 3 (1989), S. 397-400 
    Details
    ISSN: 1432-198X
    Schlagwort(e): Aldosterone ; Atrial natriuretic peptide ; Chronic renal failure ; Dopamine ; Noradrenaline ; Sodium homeostasis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract In order to evaluate the possible role of vasoactive hormones in the mechanism of exaggerated sodium loss due to reduced renal mass we measured plasma concentration of atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA), plasma noradrenaline, and dopamine, in 12 children with advanced chronic renal failure (mean CIn17.8-2.6,x± SEM, CPAH93.5±17 ml/min per 1.73 m2, FENa7.0±0.95%). No patient had clinical signs of volume overload. Plasma concentrations of ANP were not significantly different from those of healthy agematched controls (29.2±7.2 vs 23.2±3.1 fmol/ml) and did not correlate with urinary sodium excretion. Plasma concentrations of aldosterone, PRA and noradrenaline, were also within the physiological range, while plasma dopamine levels were elevated (260±36 vs 98±11 pg/ml, 〈0.001). Our data do not support the notion that ANP or the renin-aldosterone axis play a major role in the adaptation of remaining nephrons to maintain long-term sodium balance in normotensive children with chronic renal failure.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00850214
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  • 4
    Digitale Medien
    Digitale Medien
    Reversal of renal hypertension: Effects on renin, salt and water balance (1978)
    Springer
    Journal of molecular medicine 56 (1978), S. 23-29 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Renale Hypertonie ; Entfernung einer Nierenarterienstenose ; Renaler Salz- und Flüssigkeitsverlust ; Renin-Angiotensin System ; Renal hypertension ; Removal of one artery stenosis ; Salt and fluid loss ; Renin-angiotensin system
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Beschreibung / Inhaltsverzeichnis: Summary The effect of removal of one renal artery stenosis on renal sodium and fluid excretion and on the activity of the renin-angiotensin system (RAS) has been investigated in three types of renal hypertension of rats. Blood pressure fell in all experimental models after declamping, independently of changes in urinary sodium and water excretion or plasma angiotensin II (ANG II). Plasma concentrations of ANG II did not rise in response to salt and fluid loss induced by declamping when the contralateral kidney had been removed or when it was depleted from renin. A high renin content of the declamped kidney prevented major salt and fluid loss, whereas renin depletion of this kidney was accompanied by an exaggerated natriuresis and diuresis. Besides this tubular modulation of renal salt and water handling by the local RAS, glomerular filtration rate could be reduced by a stimulated activity of this system in plasma, indicated by a close relationship between serum urea and plasma ANG II levels.
    Notizen: Zusammenfassung An drei verschiedenen Modellen des renalen Hochdrucks der Ratte wurde der Einfluß der Entfernung einer Nierenarterienstenose auf die renale Salz- und Wasserausscheidung, die Aktivität des Renin-Angiotensin Systems und die Höhe des Blutdrucks untersucht. Der erhöhte Blutdruck fiel nach Entklammerung in allen Modellen auf Normalwerte ab, unabhängig von den ausgeschiedenen Mengen an Salz und Flüssigkeit und den Änderungen der Plasma Angiotensin II Konzentrationen. Dabei wurden stimulierte Werte für Angiotensin II im Plasma als Folge des Salz- und Flüssigkeitsverlustes nach Entklammerung nur dann beobachtet, wenn die kontralaterale Niere nicht zuvor bereits entfernt oder reninverarmt war. Der plötzliche Anstieg des renalen Perfusionsdruckes nach Entfernung der Stenose führte zu starken Salz- und Flüssigkeitsverlusten, wenn der Reningehalt der betreffenden Niere gering war, während ein hoher Nierenreningehalt mit einer verringerten Elektrolyt- und Wasserausscheidung einherging. Neben dieser tubulären Modulation der renalen Salz- und Wasserausscheidung durch das lokale Nierenrenin-Angiotensin System kann die Stimulation dieses Systems im Plasma über Veränderungen der glomerulären Filtrationsrate die Nierenfunktion beeinflussen. Dies wird deutlich in Situationen, die mit renalem Salz- und Wasserverlust einhergehen; dabei finden sich enge Beziehungen zwischen der Höhe der Plasma-Harnstoff- und der Angiotensin II Werte.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01477449
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  • 5
    Digitale Medien
    Digitale Medien
    Inhibition of the renin-angiotensin-system in brattleboro rats with hereditary hypothalamic diabetes insipidus (1978)
    Springer
    Journal of molecular medicine 56 (1978), S. 67-70 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Angiotensin II ; Diabetes insipidus Ratten ; Antidiurese ; SQ 14 225 ; Furosemid ; Angiotensin II ; Diabetes insipidus rats ; Antidiuresis ; SQ 14225 ; Furosemide
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Beschreibung / Inhaltsverzeichnis: Summary Brattleboro rats homozygous for hypothalamic hereditary diabetes insipidus (DI rats) were used to investigate the following questions: a) Do exogenous and endogenous angiotensin II (AII) have an antidiuretic effect in diabetes insipidus? b) Does AII mediate the antidiuresis induced by furosemide? The following results were obtained: 1. AII (5 mg/kg s.c. in oil) and furosemide (50 mg/kg i.p.) decreased urine flow and increased urinary sodium excretion. Furosemide led to a two-fold increase of AII plasma concentrations and a decrease of plasma sodium levels. 2. SQ 14 225 (2×2.5 mg/kg p.o.), an angiotensin I-converting enzyme inhibitor, led to an increase of urine flow and to a slightly elevated urinary sodium excretion. 3. When the formation of AII was blocked by SQ 14 225 (2×2.5 mg/kg p.o.), AII plasma concentrations were 2.5-fold decreased, but furosemide still reduced urine flow. We conclude that plasma AII might have an antidiuretic action in DI rats. However, AII does not mediate the antidiuresis induced by furosemide.
    Notizen: Zusammenfassung Bei Brattleboro-Ratten mit hereditärem hypothalamischen Diabetes insipidus (DI Ratten) wurden folgende Fragen untersucht: a) Wirken exogenes and endogenes Angiotensin II (AII) antidiuretisch bei Diabetes insipidus? b) Vermittelt AII den antidiuretischen Effekt von Furosemid? Ergebnisse: 1. AII (5 mg/kg s.c. in Ö1) und Furosemid (50 mg/kg i.p.) verminderten die Urin- und erhöhten die renale Natriumausscheidung. Furosemid führte zu einem zweifachen Anstieg der AII Plasma Konzentration und zur Verminderung der Plasma-Natrium Konzentration. 2. SQ 14 225 (2×2,5 mg/kg p.o.), ein Hemmer des Angiotensin I Converting Enzym, führte zu einer Zunahme der Urin- und der renalen Natriumausscheidung. 3. Auch wenn die Bildung von AII mit SQ 14 225 (2×2,5 mg/kg p.o.) blockiert wurde, reduzierte Furosemid die Urinausscheidung, obwohl die AII Plasma Konzentration 2,5fach vermindert war. Wir schließen daraus, daß Plasma AII bei DI Ratten antidiuretisch wirken kann. Allerdings vermittelt AII nicht den antidiuretischen Effekt von Furosemid.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01477455
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  • 6
    Digitale Medien
    Digitale Medien
    Effects ofβ-adrenergic blocking agents on peripheral vascular resistance (1978)
    Springer
    Journal of molecular medicine 56 (1978), S. 87-90 
    Details
    ISSN: 1432-1440
    Schlagwort(e): β-Rezeptorenblocker ; peripherer Widerstand ; β 1-Selektivität ; β-adrenergic blocking agents ; Peripheral resistance ; β 1-selectivity
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Beschreibung / Inhaltsverzeichnis: Summary The effects of the beta-adrenergic blocking agents propranolol, pindolol, atenolol, bunitrolol, and methypranol on the vascular resistance of isolated perfused hindlimbs of rats were investigated. At concentrations of 0.01 µg/ml in the perfusate dl-propranolol und pindolol significantly increased vascular resistance by blockade ofβ 2-receptor mediated vasodilatation, whereas atenolol, bunitrolol and methypranol had no effect on peripheral resistance at this concentration. With increasing concentrations up to 10 µg/ml all drugs, with the exception of atenolol, caused vasodilatation. We conclude that the specificity of beta-blocking agents can be established in the isolated perfused hindlimb vasculature of rats through its effect on vascular resistance. The lack of inhibition of vascularβ 2-receptors at low concentrations of atenolol and also bunitrolol and methypranol show relative selectivity forβ 1-receptors. The differential effects ofβ-adrenergic agents on vascular resistance may have significance for the clinical use of the drugs.
    Notizen: Zusammenfassung Untersucht wurde der Einfluß derβ-Rezeptorenblocker Propranolol, Pindolol, Atenolol, Bunitrolol und Methypranol auf den Gefäßwiderstand der isoliert perfundierten Hinterextremität der Ratte. Bei einer Konzentration von 0,01 µg/ml im Perfusat erhöhten dl-Propranolol und Pindolol den Widerstand deutlich, da die durchβ 2-Rezeptoren vermittelte Vasodilatation ausgeschaltet wurde. Atenolol, Bunitrolol und Methypranol hatten dagegen bei dieser Konzentration keinen Einfluß auf den peripheren Widerstand. Mit steigenden Konzentrationen bis zu 10 µg/ml wirkten alle Pharmaka mit Ausnahme von Atenolol vasodilatatorisch. Wir folgern, daß die Selektivität derβ-Rezeptorenblocker in der isoliert perfundierten Hinterextremität der Ratte durch ihren Effekt auf den Gefäßwiderstand festgestellt werden kann. Wie Atenolol zeigen auch Bunitrolol und Methypranol relative Selektivität fürβ 1-Rezeptoren, da sie in niedrigen Konzentrationen die vaskulärenβ 2-Rezeptoren nicht beeinflussen. Der unterschiedliche Einfluß derβ-Rezeptorenblocker auf den Gefäßwiderstand könnte für die klinische Anwendung der Medikamente Bedeutung haben.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01477458
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  • 7
    Digitale Medien
    Digitale Medien
    Role of diuretics, hormonal derangements, and clinical setting of hyponatremia in medical patients (1988)
    Springer
    Journal of molecular medicine 66 (1988), S. 662-669 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Hyponatremia ; Vasopressin ; Thirst ; Diuretics ; Cardiac failure ; Cirrhosis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Because hyponatremia is frequently associated with preceding diuretic treatment and unrestricted fluid indake — conditions which have not been addressed sufficiently in published literature — we studied the pathophysiology and the clinical setting of such hyponatremia in a large group of internal medicine patients. We observed: a) Of an initial 310 patients with chemical hyponatremia only 204 (64%) had an associated plasma hypoosmolality. Sience a normal plasma osmolality excludes a disturbance of water metabolism only the 204 patients with hypoosmolar hyponatremia were included in the study. This data shows that plasma osmolality is an essential measurement in any evaluation of hyponatremia. b) In 204 consecutive patients with hypoosmolar hyponatremia the electrolyte disturbance was related to advanced congestive cardiac failure in 25%, decompensated liver cirrhosis in 18%, volume contraction in 28%, syndrome of inappropriate antidiuretic hormone secretion in 19% and renal insufficiency in 4%. c) Plasma vasopressin was measurable in 90% of the 204 patients. It is known that radioimmunoassays to measure vasopressin fail to reliably detect low concentrations of circulating vasopressin (〈0.5 pg/ml). It may therefore be stated that hypoosmolar hyponatremia was generally characterized by a failure of antidiuretic hormone suppression. d) Mean daily fluid intake of hyponatremic patients was 2.35±0.15 l. In the presence of stimulated vasiopressin this large a fluid intake is bound to worsen the severity of hyponatremia. e) Of 204 patients 126 were treated with diuretics at the time of study. In these patients hyponatremia worsened during such treatments and was associated with evidence of prerenal azotemia. However there were no significant differences between diuretic-treated and -untreated patients with respect to plasma vasopressin stimulation and amount of fluid intake. In conclusion, stimulated vasopressin and high fluid intake explain the hyponatremia observed in the present study. This applied similary to diuretictreated and -untreated patients.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01726923
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  • 8
    Digitale Medien
    Digitale Medien
    Sympathetic vascular tone in spontaneous hypertension of rats (1978)
    Springer
    Journal of molecular medicine 56 (1978), S. 131-138 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Sympathische Aktivität ; Plasma Noradrenalin ; Adrenalin ; Dopamin ; Gefäßreaktivität ; Uptake Aktivität ; Genetische Hypertonie ; Sympathetic activity ; Plasma noradrenaline ; Adrenaline ; Dopamine ; Vascular reactivity ; Uptake activity ; Spontaneous hypertension
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Beschreibung / Inhaltsverzeichnis: Summary Differences in sympathetic vascular tone between Wistar Kyoto rats (WKR) and stroke prone spontaneously hypertensive rats (spSHR) were determined by comparing the following parameters: sympathetic activity was evaluated by determinations of plasma catecholamines (noradrenaline, adrenaline, dopamine) combined with the measurement of the neuronal and extraneuronal uptake of noradrenaline using an isolated rat heart preparation. The responsiveness of vascular smooth muscle to vasopressor agents was tested in the isolated perfused hindlimb preparation. At the age of 5, 12, 15, and 28 weeks sympathetic nervous activity was significantly higher in spSHR than in WKR since plasma noradrenaline was elevated by almost 50% in the presence of an unaltered activity of the uptake mechanisms. The responsiveness of vascular smooth muscle to noradrenaline was markedly enhanced in spSHR. Besides increased maximal vasoconstriction in response to BaCl2 (20 mmol/l) after potassium chloride depolarization or supramaximal doses of noradrenaline (10−3 mol/l), a supersensitivity of vascular smooth muscle to noradrenaline could also be detected in spSHR (age 5 weeks). The threshold dose and the ED50 were reduced by 25% in spSHR in response to noradrenaline infusions. No changes in threshold or ED50 were found in response to potassium chloride depolarization. The stimulated sympathetic activity in spSHR and the increased responsiveness of resistance vessels to noradrenaline, both contribute to the rise in sympathetic vascular tone. The finding of an increased sympathetic vascular tone in very early stages of hypertension suggest that this factor, producing a primary increase in total peripheral resistance underlies the development of high blood pressure in spSHR.
    Notizen: Zusammenfassung Unterschiede des sympathischen Gefäßtonus zwischen spontan hypertonen Ratten (spSHR) und Wistar Kyoto Ratten (WKR) wurden an Hand folgender Größen erfaßt: Die sympathische Aktivität wurde ermittelt durch die Bestimmung der Plasmakatecholamine (Noradrenalin, Adrenalin und Dopamin) bei gleichzeitiger Messung der neuronalen und extraneuronalen Wiederaufnahme von Noradrenalin im isolierten Präparat (Langendorff Herz). Die Ansprechbarkeit glatter Gefäßmuskulatur auf vasopressorische Substanzen wurde in der isoliert perfundierten Hinterextremität der Ratte gemessen. Die sympathische Aktivität war bei spSHR im Alter von 5, 12, 15 und 28 Wochen gesteigert, da die Konzentration von Noradrenalin im Plasma um 50% bei unveränderter neuronaler und extraneuronaler Wiederaufnahme erhöht war. Die Ansprechbarkeit der glatten Gefäßmuskulatur gegenüber Noradrenalin war bei spSHR verstärkt. Neben einer stärkeren maximalen Vasokonstriktion nach supramaximalen Dosen von Noradrenalin (10−3 mol/l) oder BaCl2 (20 mmol/l) fand sich eine spezifische Überempfindlichkeit der einzelnen glatten Muskelzelle gegenüber Noradrenalin bei 5 Wochen alten spontan hypertonen Ratten. Während nach Kaliumdepolarisation keine Unterschiede in der Schwellendosis oder der ED50 auftraten, waren diese bei spSHR für die Noradrenalin-induzierten Widerstandserhöhungen um 25% vermindert. Die stimulierte sympathische Aktivität sowie die erhöhte Ansprechbarkeit der Widerstandsgefäße gegenüber Noradrenalin bei spSHR sind Ursache des gesteigerten sympathischen Gefäßtonus, der über eine Erhöhung des peripheren Widerstandes die Entwicklung des hohen Blutdrucks bei der genetischen Hypertonie der Ratte verursacht.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01477464
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  • 9
    Digitale Medien
    Digitale Medien
    Kardiovaskuläre Wirkung des antidiuretischen Hormons Arginin-Vasopressin (1985)
    Springer
    Journal of molecular medicine 63 (1985), S. 989-999 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Dehydration ; Hemodynamics ; Hypertension ; Vasopressin ; Vasopressin antagonists
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The two major biological actions of vasopressin are antidiuresis and vasoconstriction. The antidiuretic action of low concentrations of vasopressin is well established and concentrations 10 to 100 times above those required for antidiuresis elevate arterial blood pressure. Antidiuresis is mediated by V2-receptors at the kidney, whereas vasopressin constricts arterioles by binding at V1-receptors. Pharmacological effects of specific antagonists of the vasoconstrictor activity of vasopressin (vascular or V1-receptor antagonists) are presented. Low concentrations of vasopressin do have significant hemodynamic effects. Physiological concentrations of vasopressin cause vasoconstriction and elevate systemic vascular resistance. In subjects with intact cardiovascular reflex activity, however, cardiac output falls concomitantly and blood pressure therefore does not change. In animals with baroreceptor deafferentation or in patients with blunted baroreceptor reflexes (autonomic insufficiency) a rise in plasma vasopressin causes vasoconstriction and an increase in blood pressure, because cardiac output does not fall under these conditions. Vasopressin contributes substantially via increase in systemic vascular resistance to maintain blood pressure during water deprivation. During hemorrhage and hypotension vasopressin has a major role to restore blood pressure. In experimental hypertension vasopressin contributes to the development and maintenance of high blood pressure in DOCA, but not in genetic hypertensive rats. The role of vasopressin in human hypertension is not yet clear. Vasopressin in extrahypothalamic areas of the brain affects circulatory regulation by interaction with central cardiovascular control centers. The exact mechanism of how vasopressin is involved in central regulation of blood pressure remains to be established. In contrast to our previous opinion vasopressin is a vasoactive hormone also at low plasma concentrations. Its cardiovascular action is more complex than previously assumed.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01737635
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  • 10
    Digitale Medien
    Digitale Medien
    Recovery from withdrawal of inhaled nitric oxide and kinetics of nitric oxide-induced inhibition of nitric oxide synthase activity in vitro (2000)
    Springer
    Intensive care medicine 26 (2000), S. 330-335 
    Details
    ISSN: 1432-1238
    Schlagwort(e): Key words Intensive care ; Critical care ; Acute respiratory distress syndrome ; Persistent pulmonary hypertension of the newborn ; Feedback inhibition
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Objective: To examine the kinetics of successful nitric oxide (NO) withdrawal in vivo and in vitro.¶Design and setting: Prospective study in a university pediatric intensive care ward and research laboratory.¶Patients and materials: Nineteen patients with acute respiratory distress syndrome (ARDS) or persistent pulmonary hypertension of the newborn (PPHN). Primary porcine pulmonary artery cells in vitro.¶Interventions: NO inhalation and withdrawal in patients; exposure to NO donor sodium nitroprusside (SNP) and gaseous NO in vitro.¶Measurements and results: In patients: a slight, but significant, increase of oxygenation index (OI) from 4.57 ± 0.24 cmH2O/torr (mean ± SEM) to 4.90 ± 0.26 cmH2O/torr after withdrawal of NO (p 〈 0.001). Recovery of OI (4.43 ± 0.23 cmH2O/torr) 30 min after weaning, a significant drop after 4 h (3.72 ± 0.17 cmH2O/torr; p 〈 0.001), values restored after 12 h.¶In vitro: NO synthase (NOS) activity was significantly lower in SNP-incubated cells (20.0 ± 4.0 μm/min) than in control cells (37.6 ± 7.0 μm/min; p 〈 0.05). Thirty minutes after SNP withdrawal there was NOS activity of 35.8 ± 10.0 μm/min with a significant increase by 4 h (p 〈 0.05). No alteration of endothelial NOS (ENOS) mRNA expression by NO (Northern Blot).¶Conclusion: In patients there is a slight, but significant, reversible increase of OI after successful weaning from NO. In vitro, NO leads to a reversible decrease of ENOS activity on a post mRNA level, resembling clinical observations.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s001340051158
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