Stabilizing effect of antioxidants and inhibitors of prostaglandin synthesis on after-contractions in Ca2+-overloaded myocardium.
Ca2+ overload followed by after-contractions was induced by perfusion of mammalian papillary muscles with O-K0+, high Ca2+ solution. The effect of lipotrophic agents (dexamethasone, indomethacin) or free radical scavengers (alpha-tocopherol, reduced glutathione, synthetic antioxidant) was tested at different stages of Ca2+ overloading processes. All the agents tested proved to be effective in attenuating the after-contractions. Activation of lipid peroxidation has been suggested as one of the possible molecular events underlying mechanical destabilization of Ca2+-overloaded myocardium.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002415:Cats; D066298:In Vitro Techniques; D008054:Lipid Peroxides / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects*; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000502:physiology; D011453:Prostaglandins / Q000096:biosynthesis*; D011817:Rabbits; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D008054:Lipid Peroxides; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011451:Prostaglandin-Endoperoxide Synthases; D002118:Calcium