Mgs. Gomes et al., EFFECTS OF ALUMINUM ON THE MECHANICAL AND ELECTRICAL-ACTIVITY OF THE LANGENDORFF-PERFUSED RAT-HEART, Brazilian journal of medical and biological research, 27(1), 1994, pp. 95-100
The effect of aluminum (Al3+) chloride (1, 5, 10, 50 and 100 mu M) on
myocardial electromechanical activity was studied in 10 Langendorff-pe
rfused hearts from adult female Wistar rats. Al3+ decreased the develo
pment of isovolumic systolic pressure from 34.3 +/- 2.95 mmHg under co
ntrol conditions to 11.8 +/- 1.53 mmHg at 100 mu M AlCl3 (P<0.01) (dia
stolic pressure = 0 mmHg). The atrial and ventricular rates also decre
ased, 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 observ
ed, reaching 60% at 100 mu M Al3+. A delay in atrioventricular conduct
ion 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 pres
ence 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 Al
3+-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 systoli
c pressure development and coronary flow and increased PR interval. Th
ese effects are discussed in terms of the inhibition of nucleotide hyd
rolysis by Al3+.