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Title: Nickel chloride inhibits metabolic coronary vasodilatation in isolated rat hearts

Conference · · Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
OSTI ID:5499204

Nickel is a potent coronary vasoconstrictor and it is released from ischemic myocardium. To determine whether or not nickel ions cause coronary vasoconstriction when local vasodilator mechanisms are stimulated the authors studied the inter-relation between exogenous nickel chloride (NiCl/sub 2/) and metabolic coronary vasodilatation in isolated rat hearts perfused by a modified Langendorff technique. NiCl/sub 2/ induced dose-dependent (10/sup -7/-10/sup -5/M) increases in coronary vascular resistance in spontaneously beating hearts. Pacing of the hearts (380/min) and infusing adenosine (10/sup -6/M) evoked comparable increases in coronary flow but did not affect the coronary vasoconstriction caused by NiCl/sub 2/. At concentrations (> 10/sup -7/M) which evoked vasoconstriction, NiCl/sub 2/ significantly reduced vasodilator responses evoked by pacing, transient coronary occlusion and adenosine. Lower concentrations, which did not cause vasoconstriction, had no effect on these vasodilator responses. Thus, at relative low concentrations NiCl/sub 2/ inhibits metabolic dilatation of the coronary vessels which may contribute to the increased vascular resistance caused by the trace metal under ischemic/hypoxic conditions.

Research Organization:
Mayo Clinic, Rochester, MN
OSTI ID:
5499204
Report Number(s):
CONF-8604222-
Journal Information:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States), Vol. 45:3; Conference: 70. annual meeting of the Federation of American Society for Experimental Biology, St. Louis, MO, USA, 13 Apr 1986
Country of Publication:
United States
Language:
English