TaiCatoxin (TCX), a complex toxin isolated from Taipan snake venom, is believed to have a specific blocking activity on voltage-dependent cardiac calcium channels. The aim of this study was to investigate the effects of TCX on a broad range of heart muscle cell functions, i.e. electrophysiology, contractility, automaticity and the related biochemical modifications. Myocyte-enriched cultures were prepared from newborn rat heart ventricles. The transmembrane potentials were recorded with glass microelectrodes. The contractions were monitored photometrically. TCX decreased the action potential amplitudes, mainly by lowering the plateau. The action potential duration and the contraction parameters were decreased. Although TCX has a minor overall negative chronotropic effect, it evoked transient but severe arrhythmias and prolonged changes in the intercellular electrical coupling. Moreover, the action of TCX appeared to be dose-dependent. These effects are consistent with a specific blockade of the L-type, voltage-dependent calcium channels, but effects of other components of the toxin complex cannot be excluded. TCX also exhibits phospholipase A2 activity leading to the release of Iysophospholipids and FFA (acyl CoA and acyl carnitine), which have detrimental effects on cellular integrity and function.

Action Potentials↗

PubMedDate not supplied

Reversible and irreversible damage in reoxygenated 'ischemic' ventricular myocytes in culture.

The LDH release pattern from cardiomyocytes under 'ischemia-like' conditions shows two phases. In the initial slow phase, reoxygenation immediately stops further enzyme release. Accelerated LDH release, which occurs concomitantly with Iysosomal enzyme release, characterizes the second phase of 'ischemia.' Reoxygenation at this stage does not put a stop to further enzyme release. Reoxygenation during the first phase of 'ischemia' rapidly restored ATP level, while in the second phase, ATP levels remained low even after 6 h of reoxygenation. This study as well as previous data seem to suggest that irreversible cellular damage leading to cell death, occurs by synergistic action of many effectors, each of which does not necessarily cause irreversible damage.

Adenosine Triphosphate↗

PubMedDate not supplied

Palmitate oxidation by beating heart cells in culture.

Palmitic acid oxidation has been studied in cultures of beating heart cells. The data reported suggest: 1. The main source of fatty acids for oxidation in cell cultures is provided by lypolysis of preexisting intracellular fatty acids. Most fatty acids that have just entered the cell are not oxidized immediately. Thus, aged heart cells in culture seem to retain their ability to utilize fatty acids as their main energy source. 2. In cultured heart cells, the amount of CO2 obtained from the carboxyl group was much higher than that obtained from the methyl group. On the other hand, beta-hydroxybutrate has been shown to be formed mainly from the methyl group. This may indicate that beta-oxidation terminates at the beta-hydroxybutyrate stage because of premature dissociation of this last intermediate from the enzyme complex.

Animals↗