Titlebook: Inotropic Stimulation and Myocardial Energetics; Hj. Just,Ch. Holubarsch,H. Scholz Conference proceedings 1989 Springer-Verlag Berlin Heid

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Norman R. Alpert,E. M. Blanchard,L. A. Mulieri,R. Nagai,A. Zarain-Herberg,M. Periasamyraktischen Arzt und Dermatologen, sondern auch für die Industrie [15, 22, 30, 34, 39, 42]. Letztere bietet als Reaktion auf die hohe Prävalenz zahlreiche Produkte speziell für empfindliche Haut an (Abb. 4.1), obschon nicht klar definiert und allgemein bekannt ist, was genau die häufig verwendeten Be

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Adrenoceptors in myocardial regulation: concomitant contribution from both alpha- and beta-adrenoception or by concomitant stimulation of α.- and ß-adrenoceptors in myocardium. The pure ß-adrenergic effects of noradrenaline were also quantified. Interactions between the two receptor systems were studied. The pure α.- and ß-adrenergic effects of noradrenaline, respectively, were achieved separately

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On the mechanism of positive inotropic effects of alpha-adrenoceptor agonistsl 1,4,5-trisphosphate (1,4,5-IP.) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP.). Both 1,4,5-IP. and 1,3,4,5-IP. sensitize myocardial contractile proteins in chemically skinned fibers. In addition to the Ca . releasing effect of 1,4,5-IP. from the sarcoplasmic reticulum the Ca.-sensitizing eff

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Energy requirements of contraction and relaxation: implications for inotropic stimulation of the fairements. If this interpretation is correct, inotropic stimulation, by increasing energy utilization, could contribute to the progressive myocardial cell death that characterizes end-stage cardiac hypertrophy. This deterioration could be delayed by the depressed myocardial contractility in the chroni

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Genetic and non-genetic control of myocardial calciumright ventricular rabbit myocardium are presented. Genetic reorganization of the intracellular structure of the myocardium is achieved by producing right ventricular pressure overload and thyrotoxic hypertrophy. The mechanical performance of the pressure overload heart is slowed while time to peak t

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Studies on the mechanism of action of the bipyridine milrinone on the heartved that milrinone acts by inhibiting phosphodiesterase IV, thus increasing cyclic AMP, [Ca .]. and cardiac contractile force and relaxation..Maximal force produced by milrinone is greater when single-dose response curves are compared to cumulative dose-response curves. In vitro, milrinone produces