EFFECTS OF ALUMINUM ON THE MECHANICAL AND ELECTRICAL-ACTIVITY OF THE LANGENDORFF-PERFUSED RAT-HEART

The effect of aluminum (Al3+) chloride (1, 5, 10, 50 and 100 mu M) on myocardial electromechanical activity was studied in 10 Langendorff-perfused hearts from adult female Wistar rats. Al3+ decreased the development of isovolumic systolic pressure from 34.3 +/- 2.95 mmHg under control conditions to 11.8 +/- 1.53 mmHg at 100 mu M AlCl3 (P<0.01) (diastolic pressure = 0 mmHg). The atrial and ventricular rates also decreased, but only with AlCl3 concentrations greater than 1 mu M (from 180 +/- 5 to 94 +/- 11 bpm for atrial rate and from 180 +/- 5 to 78 +/- 7 bpm for ventricular rate). Reduction of coronary flow was also observed, reaching 60% at 100 mu M Al3+. A delay in atrioventricular conduction occurred at 10 mu M Al3+, increasing progressively up to 100 mu M (62.3 +/- 4 ms in the Al3+- free solution to 143 +/- 34 ms in the presence of 100 mu M APC, P<0.01, ANOVA). QRS duration did not change as a function of increasing Al3+ concentrations (37.1 +/- 1.7 ms in the Al3+-free solution vs 32.1 +/- 1.6 ms in the presence of 100 mu M Al3+). No qualitative changes in ECG were observed. These data show that the toxic effects of Al3+ the myocardium are reflected in reduced systolic pressure development and coronary flow and increased PR interval. These effects are discussed in terms of the inhibition of nucleotide hydrolysis by Al3+.