Effects of nicotine on cultured rat heart cells

Wenzel, Duane G.; Wheatley, James W.; Byrd, G.Don

doi:10.1016/0041-008x(70)90052-9

Cited by 88 publications

(17 citation statements)

References 15 publications

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“…Muscle cells were separated from endothelioid cells [13] and were plated in 96-well cluster dishes (Costar | at 2.1 x 5 ~ cells/well or 7500 cell/ram 2 cell surface. Cells were grown in Eagles minimum essential medium with 10% heat-inactivated fetal bovine serum and antibiotics.…”

Section: Methodsmentioning

confidence: 99%

Ethanol as an arrhythmogen and an antiarrhythmic agent with reoxygenation arrhythmias of cultured heart cells

Wenzel

Fuh

1981

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Cultures of neonatal rat heart myoblasts exposed to constant ethanol concentrations of 26, 64, 160 or 400 mg% for 3 days were more arrhythmle during this time than control cultures. Although cell growth was not measurably affected, the evidence suggested that arrhythmlas may have developed from impaired eell-to-ceU contact. Exposure of these treated cells to an arrhythmogenle procedure involving hypoxia and reoxygenatlon, demonstrated a modest antiarrhythmie action of ethanol.

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Section: Methodsmentioning

confidence: 99%

Ethanol as an arrhythmogen and an antiarrhythmic agent with reoxygenation arrhythmias of cultured heart cells

Wenzel

Fuh

1981

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“…The cells were maintained at 37°C in a mixture of 5% CO 2 and 95% air (pH of medium: 7.2-7.4). Muscle cells (M) were separated from endothelial cells (E) by the pour-off technique also described by Wenzel et al (1970). This technique is based on the principle that the E cells attach to the bottom of the dish at a faster rate than the M cells.…”

Section: Cell Isolationmentioning

confidence: 99%

“…Myocardial cells were isolated under aseptic conditions by the method of Wenzel et al (1970). Hearts (20-30) were dissected from rat pups euthanized by decapitation and placed immediately into a glass petri dish containing ice-cold BSS (calcium-and magnesium-free Hanks balanced salt solution containing, g/l: 8.0 NaCI; 0.4 KCI; 0.05 Na 2 HPO 4 ; 0.6 KH 2 PO 4 ; 0.35 NaHCO 3 ; 0.01 phenol red; and 1.0 glucose).…”

Section: Cell Isolationmentioning

confidence: 99%

Effects of cocaine and norepinephrine on primary cultures of neonatal rat myocardial cells

Welder

Eselin

Melchert

et al. 1992

Journal of Toxicology and Environmental Health

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Sudden cardiac death associated with cocaine (Coc) abuse in healthy, physically active individuals became a grave concern in the late 1980s. It is well documented that physical activity increases circulating plasma catecholamine levels. Catecholamines as well as Coc are independently capable of inducing toxic cardiac effects. The purpose of this investigation was to evaluate the synergistic or additive toxic effects of norepinephrine (NE) and Coc in primary myocardial cell cultures obtained from 3- to 5-d-old Sprague-Dawley rats. Alterations in lactate dehydrogenase release (LDH), lysosomal neutral red retention (NR), beating activity, and morphology were evaluated after treatment of the cells for 1-24 h with 1 x 10(-3) M Coc alone, 1 x 10(-5) M Coc alone, 1 x 10(-5) M NE alone, 1 x 10(-3) M Coc with 1 x 10(-5) M NE, or 1 x 10(-5) M Coc with 1 x 10(-5) M NE. LDH release was elevated significantly after 24 h only with those cells exposed to 1 x 10(-3) M Coc alone and 1 x 10(-3) M Coc + 1 x 10(-5) M NE. Using NR retention as a score for lysosomal treatment of the cells with 1 x 10(-5) M Coc and 1 x 10(-3) M Coc alone did not decrease dye retention significantly. However, 1 x 10(-5) M NE combined with 1 x 10(-3) M Coc significantly reduced lysosomal dye retention as early as 1 h after treatment. After 24 h, 1 x 10(-5) M NE alone and 1 x 10(-5) M NE combined with 1 x 10(-5) M Coc significantly increased lysosomal fragility. Beating activity was altered in all treatment groups. Contractile activity was slow and irregular or completely absent with 1 x 10(-5) and 1 x 10(-3) M Coc, respectively. When NE (1 x 10(-5) M) was combined with both concentrations of Coc, there was distinct focalization of sharp, rapid contractions within the cells, which were asynchronous and/or arrhythmic in nature. Those cells exposed to 1 x 10(-5) M NE with 1 x 10(-5) M Coc for 24 h appeared hypercontracted with marked pseudopodia and cytoplasmic granule formation distinctly different from that exhibited by the cells exposed to 1 x 10(-5) M Coc alone. These data demonstrate that NE potentiates the adverse effects of Coc on contractile activity and morphology of spontaneously contracting neonatal myocardial cells maintained in culture.

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“…Beating rates were determined as previously described by Wenzel et al (1970). Measurements were made at the end of the desired exposure periods in five randomly selected fields.…”

Section: Beating Ratesmentioning

confidence: 99%

“…Two million cells were plated in 35-mm culture dishes (Falcon). Muscle cells were separated from nonmuscle cells by a pour-off technique based on the rate of attachment of the cells to the culture dishes (Wenzel et al, 1970). Myocyte cultures were maintained in 2 ml Eagle's minimum essential medium (MEM) (Gibco) with 5% newborn calf serum (Gibco).…”

Section: Cell Culture Proceduresmentioning

confidence: 99%

Cardiotoxicity of tricyclic antidepressants in primary cultures of rat myocardial cells

Acosta

Ramos

1984

Journal of Toxicology and Environmental Health

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Primary cultures of myocardial cells were used to evaluate the cardiotoxic potential of various tricyclic antidepressants (TCAs). Lactate dehydrogenase (LDH) leakage, cellular viability, and beating rates were measured to compare the cardiotoxicity of amitriptyline, desipramine, imipramine, and nortriptyline. Tricyclic antidepressants were added to the cultures to give final concentrations of 1 X 10(-5), 1 X 10(-4), and 1 X 10(-3) M. Treatments lasted 1 and 4 h. All TCAs tested caused significant release of LDH and decreased cellular viability when added at 1 X 10(-3) M for 1 and 4 h. Amitriptyline was the only compound that caused significant LDH release 4 h after exposure to lower doses. Decreased viability was observed 4 h after exposure to all TCAs at a concentration of 1 X 10(-4) and 1 X 10(-3) M. Arrhythmias were observed 1 h after exposure to 1 X 10(-5) and 1 X 10(-4) M amitriptyline. All doses of amitriptyline inhibited beating 4 h after exposure. Imipramine, desipramine, and nortriptyline at a concentration of 1 X 10(-5) M decreased the beating rates of cultured myocytes 1 and 4 h after exposure. Arrhythmias and/or total inhibition of beating were observed when the cultures were exposed to higher concentrations of these compounds. Based on these data, the rank order of cardiotoxicity was amitriptyline greater than imipramine = desipramine greater than nortriptyline.

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Effects of nicotine on cultured rat heart cells

Cited by 88 publications

References 15 publications

Ethanol as an arrhythmogen and an antiarrhythmic agent with reoxygenation arrhythmias of cultured heart cells

Ethanol as an arrhythmogen and an antiarrhythmic agent with reoxygenation arrhythmias of cultured heart cells

Effects of cocaine and norepinephrine on primary cultures of neonatal rat myocardial cells

Cardiotoxicity of tricyclic antidepressants in primary cultures of rat myocardial cells

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