ABSTRACT
The effect of aluminum (Al3+) chloride (1,5,10,50 and 100 µM) 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 ñ 2.95 mmHg under control conditions to 11.8 ñ 1.53 mmHg at 100µM AlCl3 (P<0.01) (diastolic pressure = 0 mmHg). The atrial and ventricular rates also decreased, but only with AlCl3 concentrations greater than 1µM (from 180 ñ 5 to 94 ñ 11 bpm for atrial rate and from 180 ñ 5 to 78 ñ 7 bpm for ventricular rate). Reduction of coronary flow was also observed, reaching 60 percent at 100 µM Al3+. A delay in atrioventricular conduction occurred at 10µM Al3+, increasing progressively up to 100 µM (62.3 ñ 4 ms in the Al3+ - free solution to 143 ñ 34 ms in the presence of 100 µM Al3+, P<0.01, ANOVA). QRS duration did not change as a function of increasing Al3+ concentrations (37.1 ñ 1.7 ms in the Al3+ -free solution vs 32.1 ñ 1.6 ms in the presence of 100 µM Al3+). No qualitative changes in ECG were observed. These data show that the toxic effects of Al3+ on 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+