• M S Krishnamoorthy, P Muthu, and N Parthiban.
• Department of Pharmacology and Environmental Toxicology, Dr. ALM P.G. Institute of Basic Medical Sciences, University of Madras, India.
• Toxicol. Lett. 1992 Sep 1; 62 (2-3): 155-62.

AbstractThe present work investigated the effect of preperfusion of ascending concentrations of lead acetate (LA) (10(-9), 10(-7) and 10(-5) M) on digoxin (DGN) cardiotoxicity in isolated frog heart, in order to look for any consequent variations in its lead-induced potentiation. The DGN perfusion time(s) and DGN exposure (micrograms DGN/10 mg heart weight) for, and myocardial DGN level (ng DGN/g wet tissue) at, cardiac arrest were the parameters evaluated so as to assess cardiotoxicity. Both sodium acetate and LA (10(-7) M) preperfusion led to a diminution in cardiac rate at 10 min of DGN perfusion without altering the contractility compared to the DGN alone group. With regard to DGN perfusion time for cardiac arrest, preperfusion of ascending concentrations of LA induced a corresponding decrease which was statistically significant (P < 0.05). On the other hand, in the experimental group that received preperfusion of 10(-9) M LA, the DGN exposure for cardiac arrest was not significantly different from that of the control, whereas in the 10(-7) and 10(-5) M groups, it was significantly lower (P < 0.05). In the experimental group that received preperfusion of 10(-7) M LA, the significant reduction in DGN perfusion time and DGN exposure was well corroborated by a diminution in the myocardial DGN level (4.01 +/- 0.17 ng/g wet tissue in comparison with the control value of 5.72 +/- 0.4 ng/g wet tissue, P < 0.05) at cardiac arrest. Taken together, these data reveal that with the preperfusion of LA in ascending concentrations, there is a relative increase in LA-induced potentiation of DGN cardiotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

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