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Brazilian Journal Of Medical And Biological Research • January 1994<br />

Effects of aluminum<br />

on the mechanical and electrical activity<br />

of the Langendorff-perfused rat heart<br />

Author information<br />

Gomes MG1, Moreira CA, Mill JG,<br />

Massaroni L, Oliveira EM, Stefanon I, Vassallo DV.<br />

Departamento de Ciências Fisiológicas<br />

Universidade Federal do Espírito Santo<br />

Vitória, Brasil<br />

Abstract<br />

The effect of aluminum (Al3+) chloride (1, 5, 10, 50 and 100 microM) on myocardial electromechanical<br />

activity was studied in 10 Langendorff-perfused hearts from adult female<br />

Wistar rats. Al3+ decreased the development of isovolumic systolic pressure from 34.3<br />

+/- 2.95 mmHg under control conditions to 11.8 +/- 1.53 mmHg at 100 microM AlCl3 (P<br />

< 0.01) (diastolic pressure = 0 mmHg). The atrial and ventricular rates also decreased, but<br />

only with AlCl3 concentrations greater than 1 microM (from 180 +/- 5 to 94 +/- 11 bpm for<br />

atrial rate and from 180 +/- 5 to 78 +/- 7 bpm for ventricular rate). Reduction of coronary<br />

flow was also observed, reaching 60% at 100 microM Al3+. A delay in atrioventricular<br />

conduction occurred at 10 microM Al3+, increasing progressively up to 100 microM (62.3<br />

+/- 4 ms in the Al(3+)-free solution to 143 +/- 34 ms in the presence of 100 microM Al3+, P<br />

< 0.01, ANOVA). QRS duration did not change as a function of increasing Al3+ concentrations<br />

(37.1 +/- 1.7 ms in the Al(3+)-free solution vs 32.1 +/- 1.6 ms in the presence of 100<br />

microM Al3+). No qualitative changes in ECG were observed. These data show that the<br />

toxic effects of Al3+ on the myocardium are reflected in reduced systolic pressure development<br />

and coronary flow and increased PR interval. These effects are discussed in terms of<br />

the inhibition of nucleotide hydrolysis by Al3+.<br />

“These data show that<br />

the toxic effects of aluminum chloride<br />

on the myocardium are reflected in reduced<br />

systolic pressure development and<br />

coronary flow and increased PR interval.”<br />

http://www.ncbi.nlm.nih.gov/pubmed/8173535

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