Cardiovascular actions of palladium compounds in the unanesthetized rat.

The natural occurrence of palladium (Pd) is rare. It is obtained as a by-product during the extraction of platinum and, until the present time, its uses were small in number--principally in the manufacture of jewelry, dental alloys, chemical catalysts, and electrical contacts. Interest in Pd toxicology has been limited to occupational exposures and even that has been sparse. Recently Pd has been chosen as one of the metals to be incorporated into the automotive catalytic converter material. Palladium chloride has been shown to be extremely toxic when given to rabbits intravenously. Animals rapidly injected quickly died with damage chiefly to the heart. This heart damage was not explained or further defined, and other references addressing this subject have not been found. The objective of our study was to investigate and attempt to characterize toxic actions of soluble Pd compounds on the cardiovascular system of the unanesthetized rat. Surgically prepared rats were monitored for ECG, aortic blood pressure, cardiac contractility (dp/dt), and respiration before, during, and 1 hr following intravenous injections of Pd2+ salt solutions. Our findings indicate that injected Pd2+ profoundly disturbs the electrical integrity of ventricular myocardium. Effective doses induce cardiac arrhythmias with the consequential fall in blood pressure; the extent of the response is dose related. An immediate cardiovascular effect is seen when doses of 0.4 mg/kg or more of Pd ion as PdSO4 is administered over a 40-sec period of time via the femoral vein. Pd(NO3)2 and PdCl2 appear to have similar activity. To achieve and equal response three times as much Pd is necessary as (NH4)2PdCl4 or K2PdCl4.