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G Drevensek

Publications and source records attributed to G Drevensek.

11 recordsLinked to original sources

Nicardipine dose dependently reduces the effect of equinatoxin II on coronary flow in isolated rat heart.

Equinatoxin II (EqT II) decreases coronary flow in guinea-pig and rat heart. It increases cytosolic Ca2+ activity and is supposed to form cation selective membrane pores. In the present study we tried to evaluate the influence of the L-type Ca2+ channel antagonist nicardipine upon the vasoconstrictory effect of EqT II on coronary vessels in isolated heart of the rat. Coronary flow was measured during the experiment. Ten min after bolus injection of EqT II the coronary flow decreased to 17.2 +/- 4.3% in experiments without nicardipine, and to 39.4 +/- 4.5% in the group with 0.1 microM nicardipine (p < 0.05). Our results indicate the possibility that L-type Ca2+ channels could be involved in the effects of EqT II on coronary flow in the rat heart.

Animals↗

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↗

Lacidipine decreases the honeybee venom-induced vasoconstriction of the isolated porcine coronary artery.

The venom of the honeybee Apis mellifera induces cardiovascular dysfunction. As its effects on coronary arteries have not yet been described, we studied the effects of the whole honeybee venom (non-volatile part) in the isolated porcine left anterior descending coronary artery (LAD) and the influence of L-type Ca2+ channel blocker, lacidipine, upon the venom effects in LAD. The venom produced concentration dependent contractions (7-70 microg/ml) of the porcine LAD; maximal effect of the venom was approximately the same as the effect of 30 mM KCl. Lacidipine concentration dependently (0.1-10 microM) and significantly (P < or = 0.05) decreased the venom-induced vasoconstriction. The results indicate the involvement of L-type Ca2+ channels in coronary contraction, induced by bee venom.

Animals↗

Thermal conductivity of the porcine heart tissue.

The porcine heart was used as a model for studying the thermal changes in myocardium at cooling and re-warming during open heart surgery. A section of the heart septum was excised and tissue was cut into two similar square slices. The same shape of the tissue, cut from the surface from the upper lateral wall of the left ventricle, covered with epicardium and fat, was taken for another measurement. A thin (<0.5 mm) square thermal source of the same length of the side as the tissue samples was put between the two slices of tissue. This set was placed in the middle of two identical copper cylinders (2r=50 mm, height=55 mm) used to keep the outer side of the specimen at controlled room temperature. Thermal conductivity of the heart tissue was determined at controlled thermal power, and known difference of the temperature at the edge of the tissue and at the middle of the heater, when steady state was reached. Thermal conductivity calculated from the temperature difference and the geometry of heater and samples was 0.75 W/m.K for septal heart tissue, and 0.60 W/m.K for the lateral wall ventricle tissue with epicardium and fat.

Adipose Tissue↗

Nicardipine dose-dependently reduces the effect of equinatoxin II on coronary flow in isolated porcine heart.

Death after i.v. administration of equinatoxin II (EqT II) has been attributed to the circulatory failure resulting from cardiotoxic effects. The mechanism of action is unknown. The aim of the present work was to study the effects of the toxin on vascular tone in the isolated porcine coronary artery and on coronary flow in the isolated pig heart. EqT II caused concentration-dependent contractions of rings of the isolated epicardial porcine coronary artery with an EC50 value of 89+/-5 nM (n=5-6) and maximal effect of about 140% of the contraction induced by 20 nM KCl. On Langendorffs porcine heart preparation EqT II caused a dose-dependent decrease of coronary flow. At EqT II doses lower than 0.05 micromol/100 g of heart weight there were no measurable effects of the toxin. At dose 0.5 micromol/100 g the toxin decreased coronary flow to less than 9.8+/-2.5% of the control value. The constrictory effect of the toxin on isolated porcine coronary arteries was diminished by the L-type calcium channel antagonist nicardipine (NC). NC in 1 microM concentration almost completely abolished the effect of EqT II on coronary flow. Our results confirmed involvement of L-type calcium channels in the vasoconstrictory effects of EqT II on epicardial coronary arteries.

Animals↗

Action of mibefradil and lacidipine on the isolated human anterior tibial artery.

In isolated human anterior tibial artery the effects of two different types of calcium channel antagonists, mibefradil (a selective T-type Ca2+ channel antagonist) and lacidipine (a 1,4 dihydropyridine Ca2+ channel antagonist, acting at L- and T-type, but binds preferentially at L-type Ca2+ channels) were compared. Both drugs reduced the contractions of isolated arteries induced by 60 mM KCl. The potency (IC50) of mibefradil was 6.5 microM and of lacidipine 82.4 nM. The potencies of both Ca2+ channel antagonists differed significantly (p<0.001 at 0.1 and 1 microM; p<0.01 at 10 microM). Lacidipine was 79-times more effective than mibefradil in reducing the vasoconstriction in isolated human anterior tibial artery. One of the reasons for higher potency of lacidipine could be a higher density of L-type than of T-type Ca2+ channels in tissue of the human anterior tibial artery.

Calcium Channel Blockers↗

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↗

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↗

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↗