Inhibition of PAF-acether effects on isolated guinea pig hearts by zinc ions (Zn2+) |
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Authors: | Angelos Evangelou Vicky Kalfakakou Jaques Benveniste Bernard Arnoux |
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Institution: | (1) Laboratory of Experimental Physiology, Faculty of Medicine, University of Ioannina, 45110 Ioannina, Greece;(2) INSERM U 200, University of Paris-sud, 92140 Clamart, France |
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Abstract: | PAF-acether is a phospholipid synthesized by most animal tissues and exerting a strong decrease on the heart’s contractile
force and coronary flow. PAF-acether (10−9 and 10−10
M) was administered to isolated guinea pig hearts perfused via the Langendorff apparatus with Chenoweth solution. Zinc (1.5
μM) is known to benefit heart function thus, Zn2+ (1.5, 7.5, and 30 μM) was added in the perfusing solution before or after PAF-acether administration. Contractile force, coronary flow, and heart
rate were recorded by means of a Narco MK-IV Physiograph throughout all modes of perfusion. Calcium inhibitor (Verapamil 10−10
M) and Pb2+ Co2+ (1.5×10−6
M) were used subsequently in the perfusing solutions in order to elucidate some of the Zn and PAF interactions observed. All
hearts were analyzed for their Zn and Ca content by means of an Atomic Absorption Spectrophotometry (AAS). Our data suggest
that low concentrations of zinc (1.5 μM) can strongly inhibit PAF-induced decrease of contractile force and coronary flow. Zinc-inhibiting effects on PAF's negative
inotropic action (myocytic level) is not exerted through Zn−Ca antagonism. Nevertheless, a Zn−Ca antagonism in the arteriolar
level cannot be excluded. Zinc inhibits PAF selectively only if it is administered before PAF injection and this strongly
suggests a receptor interaction between the metal and the phospholipid at the heart level. |
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Keywords: | Zinc PAF heart contractile force coronary flow |
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