The inotropic effects of dopamine and its precursor levodopa on isolated human ventricular myocardium

1985 ◽  
Vol 63 (21) ◽  
pp. 1117-1123 ◽  
Author(s):  
L. Brown ◽  
B. Lorenz ◽  
E. Erdmann
Keyword(s):  
Ventricular Myocardium ◽  
Inotropic Effects ◽  
Human Ventricular Myocardium

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.

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

Abstract 69: Diminished T-Tubule Density in Newborn Human Ventricular Cells Is Associated with Heterogeneity of Calcium Transients

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Talib Saafir ◽  
Brian Crawford ◽  
Ming Shen ◽  
Guoliang Ding ◽  
Paul M Kirshbom ◽  
...  
Keyword(s):  
Age Groups ◽  
Ventricular Myocardium ◽  
Outer Edge ◽  
Calcium Transients ◽  
Calcium Handling ◽  
Live Cells ◽  
Ventricular Cells ◽  
T Tubules ◽  
Human Ventricular Myocardium ◽  
First Year Of Life

For children with congenital heart disease (CHD), therapies developed for adults may have different effects on immature myocardium. Thus, it is critical to understand calcium handling in the young human ventricle. Methods: Human ventricular cells were isolated from tissue removed as part of the surgical repair for CHDs from two age groups: newborns (<1 week old) and infants (2-12 months old). Developmental changes in t-tubules were examined in live cells with Di-8 ANEPPS which highlights the cell membrane. We measured the T-index (percent of cell interior occupied by t-tubules), averaged for at least 3 confocal z-sections per cell. Changes in calcium transients were measured by confocal line scans in cells loaded with Fluo-4 and field stimulated (37°C). Results: Newborn human myocytes have very few t-tubules whereas infant myocytes have a range of t-tubule densities. The T-index in newborn myocytes was significantly less than in infant myocytes (4.4±0.2%, n=8 cells, 3 newborns vs. 9.1±0.9%, n=55 cells, 7 infants). Furthermore, there was sizable heterogeneity in the T-index for each patient in the infant group, in which some cells had few t-tubules and others had many t-tubules. We calculated the coefficient of variation (CV=SD/mean*100) for each patient and compared CV values for newborns vs. infants. CV was significantly greater in infants compared to newborns (46.5±7.4%, n=7, vs. 9.4±1.9%, n=3, p<0.02). In addition, calcium transients from newborn cells had a ‘U’ shaped wavefront with calcium first increasing at the outer edge of the cell then propagating toward the center. In contrast, infant cells had a homogenous calcium wavefront. The delay of peak calcium from the edge to center was significantly longer in newborns compared to infants (61.7±8.9 ms, n=8 cells, 3 newborns vs. 10.6±1.6 ms, n=6 cells, 4 infants, p<0.001). Conclusions: There are heterogeneous calcium transients in newborn human myocytes that correspond to a lack of t-tubules. Furthermore, t-tubule development occurs in a heterogeneous manner throughout the first year of life with cells from the same patient exhibiting different degrees of t-tubule development. This is the first study to examine t-tubule development and calcium transients in the very young human ventricular myocardium.

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