Intracellular Ca(2+) overload induced by extracellular Ca(2+) entry plays an important role in acute heart dysfunction by tentacle extract from the jellyfish Cyanea capillata.

The exact mechanism of acute heart dysfunction caused by jellyfish venom remains unclear for the moment. In the present study, we examined the problem caused by the tentacle extract (TE) from the jellyfish Cyanea capillata at the levels of whole animal, isolated heart, primarily cultured cardiomyocytes, and intracellular Ca(2+). The heart indexes, including HR, APs, LVPs, and MMLs, were all decreased significantly by TE in both whole animal and Langendorff-perfused isolated heart model. Imbalance of cardiac oxygen supply and demand also took place. In both Ca(2+)-containing and Ca(2+)-free bathing solutions, TE could cause obvious cytoplasmic Ca(2+) overload in NRVMs, but the cytoplasmic Ca(2+) increased faster, Ca(2+) overload peaks arrived earlier, and the morphological changes were more severe under the extracellular Ca(2+)-containing condition. L-type Ca(2+) channel blockers, as well as the inhibitor of ryanodine receptor (ryanodine), could improve the viability of NRVMs. Moreover, diltiazem significantly inhibited the acute heart dysfunction caused by TE in both Langendorff isolated heart model and whole animal. These results suggested that intracellular Ca(2+) overload induced by extracellular Ca(2+) entry plays an important role in acute heart failure by TE from the jellyfish C. capillata. Inhibition of extracellular Ca(2+) influx is a promising antagonistic alternative for heart damage by jellyfish venom.