Biomedical subjects

G Drevensek

Publications and source records attributed to G Drevensek.

4 recordsLinked to original sources

PubMed2000

Lowering of the coronary flow in isolated rat heart by equinatoxin II depends upon extracellular Ca2+ concentration.

Equinatoxin II (EqT II) is a basic polypeptide toxin from the sea anemone Actinia equina (L.). Its LD50 in mice is 33 g/kg. The cause of death after intravenous application has been attributed to the circulatory failure resulting in the cardiotoxic effects. In Langendorff's rat and guinea-pig heart preparations EqT II caused dose dependent decrease in the coronary flow (CF). Morphologic changes of different cell cultures incubated with EqT II are the result of Ca2+ entry through the newly formed discrete pores. Pores in the cell membranes are composed of the toxin oligomeres. In the present study we tried to evaluate the dependence of vasoconstrictor effects of EqT II on isolated rat hearts upon the Ca2+ concentration in the perfusion solution. EqT II did not affect the CF in the group without Ca2+. The strongest effect was observed in the group with 1.5 mM Ca2+ where the CF decreased to 7.7+/-7%. The results of our experiments indicate that the effects of EqT II on CF depend on Ca2+ concentration in the extracellular solution.

Animals↗

PubMed1999

Effects of equinatoxin II from Actinia equina (L.) on isolated rat heart: the role of direct cardiotoxic effects in equinatoxin II lethality.

Equinatoxin II is a lethal basic protein isolated from the sea anemone Actinia equina (L.) with LD50 in mice 35 microg/kg. The putative cause of death is cardiorespiratory arrest, but the mechanism of cardiotoxicity is poorly understood. It is not clear whether the toxin injected intravenously into an experimental animal reaches the heart in a concentration sufficient to cause direct effects on the heart. Therefore experiments were performed on rats and on isolated rat hearts in order to investigate the possible direct cardiotoxic effects of the toxin. For this reason the hearts were perfused with different concentrations of the toxin and with the effluent from the lungs collected during perfusion of the lungs with equinatoxin II. The results revealed the clear dose-dependent, direct cardiotoxic effects of the toxin and of the effluent from the lungs on Langendorff's heart preparations. The threshold concentration of equinatoxin II causing a drop in the perfusion rate, decreased left ventricular pressure, arrhythmia and increased LDH release, was found to be around 0.1 to 1 nM. With 10 nM equinatoxin II the left ventricular pressure dropped to 14+/-11% of the control, and the coronary flow to 9+/-3%. These effects were followed by arrhythmia and cardiac arrest. The concentration of equinatoxin recovered from the lungs after the perfusion with 100 nM equinatoxin II ranged between 0.8 and 5 nM. The results indicate that direct cardiotoxic effects of equinatoxin II play an important role in the lethal effects of the toxin.

Animals↗

PubMed1996

Effects of chloropyramine and famotidine on postischaemic and posthypoxic myocardial damage in isolated rat hearts.

In isolated rat hearts effects of chloropyramine (CP), histamine H1 antagonist, and famotidine (FA), H2 antagonist, upon two different myocardial injuries, ischaemia-reperfusion and hypoxia-reoxygenation were studied. In both types of injury the effects of drugs were seen mainly during reperfusion and reoxygenation, respectively. During reperfusion neither CP nor FA influenced amplitude of contractions, but CP lowered heart rate, +dp/dtmax and coronary flow. During reoxygenation CP and FA lowered early posthypoxic contractions, whereas CP decreased and FA increased heart rate. CP and FA did not significantly influence the post-ischaemic and posthypoxic lactate dehydrogenase (LDH) release. Present results indicate the existence of H1 and H2 receptors in rat heart as well as their involvement in both types of studied injuries.

Animals↗

PubMed1996

Computer support for experiments on isolated hearts.

The left ventricular pressure (LVP) and ECG signals that appear during and after ischaemia tend to be very irregular (fibrillation, arrhythmia). Computer based data acquisition system, that we developed to support experiments on isolated Langendorff's rat heart, enabled the usage of methods derived from non-linear dynamics. To classify the irregularity of heart action, ECG and LVP time series have been used to calculate correlation dimension (D2) and largest Lyapunov exponent. We compared the results of signals derived from isolated heart at standard conditions and hearts rendered ischaemic for 60 minutes. Our results show that the level of irregularity can be classified efficiently using the quoted approach.

Animals↗