PROSTAGLANDINS HAVE LIMITED ACTIONS ON ABNORMALITIES OF BEATING INDUCED IN CULTURED HEART-CELLS

Prostaglandins [PG] are antiarrhythmic in a variety of situations including ischemic arrhythmias, but the mechanisms involved are not known. The protective actions of PGA2, PGE2, PGF1.alpha., PGF2.beta. and PGI2 against abnormalities of beating induced in cultured rat heart cells were studied. Abnormalities of beating were included in single cells by a variety of agents including ouabain, Ca2+, K+, dinitrophenol (DNP) and toxic material from the jellyfish Cyanea capillata. Abnormalities were assessed in terms of rate, rate range, subjective arrhythmic behavior and percent cells beating. The PG (at 10-7-10-5 M) were added with the arrhythmogenic agent to test for their ability to modify agent-induced beating abnormalities and were compared with lidocaine and quinidine. PG alone had minimal direct effects on the cells and only minimally reduced responses to arrhythmogenic agents. The most protective PG, PGE2 and PGF1.alpha., tended to normalize beating behavior most noticeably in DNP-treated cells. Lidocaine and quinidine were effective against Ca2+-induced changes while worsening those of K+. A general ability to protect disturbed cardiac cells is not seen with high concentrations of PG.