Possible role of nickel ions in the pathogenesis of ischemic coronary vasoconstriction in the dog heart.
To test the hypothesis that nickel ions released from the ischemic dog myocardium [18] play a role in the pathogenesis of ischemic coronary vasoconstriction, the present experiments on the in situ heart of the anesthetized open-chest dog were designed to analyze coronary vascular action of intravenous (i.v.) and intracoronary (i.c.) injection of exogenous NiCl2 under the influence of ischemia, arterial hypoxemia and adenosine. The experimental results showed that (1) exogenous NiCl2 induced coronary vasoconstriction by a direct action on coronary vessels in low doses (0.02 mg X kg-1 i.v. bolus injection, or 0.04 mg X min-1 X kg-1 i.c. infusion) comparable to the Ni amount released endogenously, (2) NiCl2 significantly inhibited postocclusion reactive hyperemia and coronary vasorelaxation in response to arterial hypoxemia or intracoronary infusion of adenosine, (3) NiCl2 is capable of inducing coronary vasoconstriction when the coronary arteries are dilated by low flow ischemia, arterial hypoxemia and adenosine infusion, and (4) the Ni-sensitivity of coronary arteries increases significantly under these conditions. A hypothetical model is proposed summarizing the possible positive feedback loops triggered by endogenous Ni-release, which may cause coronary vasoconstriction in the ischemic dog myocardium.
D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D000860:Hypoxia / Q000378:metabolism; D009532:Nickel / Q000378:metabolism* / Q000494:pharmacology; D010477:Perfusion; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects
C022838:nickel chloride; D009532:Nickel; D000241:Adenosine