Some disease states and physiological stresses have been shown to either increase or decrease endogenous nickel concentrations. As reviewed by Sunderman et al. (1986) and the U.S. Environmental Protection Agency (U.S. EPA, 1986), serum nickel concentrations have been found to be elevated in patients after myocardial infarction, severe myocardial ischemia, or acute stroke. Serum nickel concentrations are often decreased in patients with hepatic cirrhosis, possibly due to hypoalbuminemia (McNeely et al., 1971). Physiological stresses such as acute burn injury have been shown to correspond with increased nickel serum levels in rats. Animal studies also indicate that nickel may be an endogenous vasoactive substance and that low concentrations (0.1 µM) of nickel chloride can induce coronary vasoconstriction in the perfused hearts of rats (Edoute et al., 1992).