Additive positive inotropic effects of milrinone, ouabain and calcium in diseased human ventricular myocardium

1986 ◽  
Vol 64 (15) ◽  
pp. 708-712 ◽  
Author(s):  
L. Brown ◽  
M. Näbauer ◽  
E. Erdmann
Keyword(s):  
Ventricular Myocardium ◽  
Inotropic Effects ◽  
Positive Inotropic Effects ◽  
Human Ventricular Myocardium

scholarly journals P4482Anticancer drug istaroxime exerts strong positive inotropic effects in failing human ventricular myocardium

2017 ◽  
Vol 38 (suppl_1) ◽  
Author(s):  
E. Kolesnik ◽  
M. Wallner ◽  
M. Khafaga ◽  
D.M. Eaton ◽  
G. Schwantzer ◽  
...  
Keyword(s):  
Ventricular Myocardium ◽  
Inotropic Effects ◽  
Positive Inotropic Effects ◽  
Human Ventricular Myocardium

Small concentrations of mercury enhances positive inotropic effects in the rat ventricular myocardium

2005 ◽  
Vol 20 (1) ◽  
pp. 22-25
Author(s):  
Diego Falcochio ◽  
Gabriela Poltronieri Souza de Assis ◽  
Ivanita Stefanon ◽  
Dalton Valentim Vassallo
Keyword(s):  
Ventricular Myocardium ◽  
Inotropic Effects ◽  
Positive Inotropic Effects

Mechanism of the Negative Inotropic Effect of Thiopental in Isolated Ferret Ventricular Myocardium 

1995 ◽  
Vol 82 (2) ◽  
pp. 436-450 ◽  
Author(s):  
Philippe R. Housmans ◽  
Turkan S. Kudsioglu ◽  
Jonathan Bingham
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Negative Inotropic Effect ◽  
Ventricular Myocardium ◽  
Underlying Mechanism ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Force Peak ◽  
Human Ventricular Myocardium ◽  
Negative Inotropic Effects

Background Thiopental's myocardial depressant effects are well known and most likely involve some alteration in intracellular Ca2+ homeostasis. The aim of this study was to investigate the mechanisms of thiopental's negative inotropic effects and its underlying mechanism in isolated ferret ventricular myocardium (which shows physiologic characteristics similar to human ventricular myocardium), and in frog ventricular myocardium, in which Ca2+ ions for myofibrillar activation are derived almost entirely from transsarcolemmal influx. Methods The authors analyzed the effects of thiopental after beta-adrenoceptor blockade on variables of contractility and relaxation, and on the free intracellular Ca2+ transient detected with the Ca(2+)-regulated photoprotein aequorin. Thiopental's effects also were evaluated in ferret right ventricular papillary muscles in which the sarcoplasmic reticulum (SR) function was impaired by ryanodine and in frog ventricular strips with little or no SR function. Results At concentration > or = 10(-4) M, which is in the high range of the clinically encountered free plasma thiopental concentrations, thiopental decreased contractility and the amplitude of the intracellular Ca2+ transient. At equal peak force, peak aequorin luminescence in 10(-4) M thiopental and [Ca2+]0 > 2.25 mM was slightly smaller than that in control conditions at [Ca2+]o = 2.25 mM. This indicates that thiopental causes a small increase in myofibrillar Ca2+ sensitivity. After inactivation of sarcoplasmic reticulum Ca2+ release with 10(-6) M ryanodine, a condition in which myofibrillar activation depends almost exclusively on transsarcolemmal Ca2+ influx, thiopental caused a further decrease in contractility and in the amplitude of the intracellular Ca2+ transient, and thiopental's relative negative inotropic effect was not different from that in control muscles not exposed to ryanodine. Thiopental, > or = 10(-4) M, decreased contractility in frog ventricular myocardium. Conclusions These findings indicate that the direct negative inotropic effect of thiopental results from a decrease in intracellular Ca2+ availability. At least part of thiopental's action is caused by inhibition of transsarcolemmal Ca2+ influx. These effects become apparent at concentrations routinely present during intravenous induction with thiopental.

Atrial myocardium is the predominant inotropic target of adrenomedullin in the human heart

2007 ◽  
Vol 293 (5) ◽  
pp. H3001-H3007 ◽  
Author(s):  
Egbert Bisping ◽  
Gero Tenderich ◽  
Paul Barckhausen ◽  
Burkhard Stumme ◽  
Sebastian Bruns ◽  
...  
Keyword(s):  
Light Emission ◽  
Ventricular Myocardium ◽  
Right Atrial ◽  
Dependent Manner ◽  
Atrial Myocardium ◽  
Concentration Dependent Manner ◽  
Maximal Increase ◽  
Inotropic Effects ◽  
Positive Inotropic Effects ◽  
Camp Levels

Adrenomedullin (ADM) is an endogenous peptide with favorable hemodynamic effects in vivo. In this study, we characterized the direct functional effects of ADM in isolated preparations from human atria and ventricles. In electrically stimulated human nonfailing right atrial trabeculae, ADM (0.0001–1 μmol/l) increased force of contraction in a concentration-dependent manner, with a maximal increase by 35 ± 8% (at 1 μmol/l; P < 0.05). The positive inotropic effect was accompanied by a disproportionate increase in calcium transients assessed by aequorin light emission [by 76 ± 20%; force/light ratio (ΔF/ΔL) 0.58 ± 0.15]. In contrast, elevation of extracellular calcium (from 2.5 to 3.2 mmol/l) proportionally increased force and aequorin light emission (ΔF/ΔL 1.0 ± 0.1; P < 0.05 vs. ADM). Consistent with a cAMP-dependent mechanism, ADM (1 μmol/l) increased atrial cAMP levels by 90 ± 12%, and its inotropic effects could be blocked by the protein kinase A (PKA) inhibitor H-89. ADM also exerted positive inotropic effects in failing atrial myocardium and in nonfailing and failing ventricular myocardium. The inotropic response was significantly weaker in ventricular vs. atrial myocardium and in failing vs. nonfailing myocardium. In conclusion, ADM exerts Ca2+-dependent positive inotropic effects in human atrial and less-pronounced effects in ventricular myocardium. The inotropic effects are related to increased cAMP levels and stimulation of PKA. In heart failure, the responsiveness to ADM is reduced in atria and ventricles.

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