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Role of prostaglandin E2 in contractile abnormality induced by calcium ionophore, A23187

From the Department of Neurology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, Japan.

We evaluated the possible role of prostaglandin E2 (PGE2) in the calcium(Ca⁺⁺)-mediated damage of skeletal muscle by a calcium ionophore (A23187) that induces excessive Ca⁺⁺ influx. Twitch and tetanus of rat diaphragms were depressed with either PGE2 or A23187. A23187-induced depression was reduced by PG synthesis inhibitors, aspirin, or indomethacin, though less than that by a protease inhibitor, leupeptin. PGE2-induced depression was also inhibited by leupeptin. Damage of the muscle cell by excessive intracellular free Ca⁺⁺ may thus be mediated via a PGE2 pathway besides other mechanisms including nonlysosomal, Ca⁺⁺ -activated proteases.

Address correspondence and reprint requests to Dr. Takamori, Department of Neurology, Kanazawa University School of Medicine, 13-1, Takaramachi, Kanazawa, Ishikawa, Japan 920.

This investigation was supported by research grants funded by the Ministries of Education (56480173) and Health and Welfare (82.04, NCNMMD), Japan.

Accepted for publication April 13, 1983.