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  • 1990-1994  (2)
  • 1965-1969
  • 1940-1944
  • 68,35.Fx  (1)
  • Nifedipine  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Applied physics 53 (1991), S. 369-376 
    ISSN: 1432-0630
    Keywords: 68.55.−a ; 68,35.Fx ; 61.16.Fk
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: Abstract The growth of Pt(111) by Pt vapour deposition is studied by He diffraction as a function of substrate temperature and deposition rate. At a deposition rate of about 2.5×10−2 monolayers/second several growth modes are observed: layer-by-layer (2D-) growth at 450 K≲T s≲800 K, multilayer (3D-) growth at 340 K≲T s≲450 K and reentrant layer-by-layer (2D-) growth at T s≲340 K. The observed growth modes and in particular the reentrant 2D-growth are shown to be characteristic of growing Pt(111) under clean conditions, i.e. not influenced by contaminants. The influence of the intra- and interlayer mass transport on the growth mode is discussed in the light of experimental and simulation results. The 3D-growth mode is attributed to the existence of an activation barrier which suppresses the descent of adatoms from the top of the growing adatom islands onto the lower terraces. The barrier can be overcome by thermal adatoms at T s≳450 K enabling interlayer mass transport which leads to 2D-growth. The reentrant 2D-growth occurs due to a break down of this barrier for small, irregularly shaped islands.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 44 (1993), S. S57 
    ISSN: 1432-1041
    Keywords: Renal haemodynamics ; Captopril ; Nifedipine ; Metoprolol ; protein restriction ; celiprolol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Glomerular hyperfiltration and hypertension may contribute to the progression of chronic renal insufficiency regardless of the underlying disease. Protein restriction and antihypertensive treatment are used to slow the decline in renal function. However, little is known about the interaction of protein loading and antihypertensive treatment on glomerular haemodynamics in humans. This paper compares the renal haemodynamic effects ofβ-adrenoceptor blockers with those of the calcium channel antagonist nifedipine and the ACE inhibitor captopril on resting glomerular filtration and during glomerular hyperfiltration. In two separate studies the effects of nifedipine, captopril, metoprolol, and celiprolol on renal haemodynamics have been investigated. In two groups of healthy volunteers (n =13) inulin and PAH clearances were measured, first under fasting conditions and afterwards during aminoacid infusion. In fasting subjects nifedipine and metoprolol induced glomerular hyperfiltration, while celiprolol and captopril did not significantly affect GFR. Without premedication, and also after nifedipine, metoprolol and celiprolol, the aminoacid infusion significantly increased the GFR. After premedication with captopril, however, aminoacid-induced hyperfiltration was prevented. In fasting subjects captopril, celiprolol and metoprolol elevated PAH clearance. With our without premedication aminoacid infusion increased renal plasma flow compared to baseline on the control day. We conclude that in healthy subjects, acute administration of antihypertensive drugs results in different renal haemodynamic responses. In contrast to captopril and celiprolol, nifedipine and metoprolol induce glomerular hyperfiltration like protein loading. Thus, they may counteract the renal haemodynamic effects of protein restriction. Celiprolol behaves similarly to captopril, since it increases renal perfusion without inducing glomerular hyperfiltration, a pattern which might reflect lower glomerular pressure. Only captopril, however, was able to prevent glomerular hyperfiltration induced by aminoacids. If these observations are confirmed during chronic treatment of patients with impaired renal function, they may suggest that certain antihypertensive drugs reverse, while others seem more likely to support the effect of protein restriction on renal haemodynamics and on the progression of renal disease.
    Type of Medium: Electronic Resource
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