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1.
Braz. j. med. biol. res ; 27(1): 95-100, jan. 1994. ilus
Article in English | LILACS | ID: lil-136498

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+


Subject(s)
Animals , Female , Rats , Aluminum/pharmacology , Heart , Electrocardiography/drug effects , In Vitro Techniques , Coronary Circulation , Heart/physiology , Osmolar Concentration , Perfusion , Arterial Pressure , Rats, Inbred Strains
2.
Braz. j. med. biol. res ; 25(8): 861-4, 1992. ilus
Article in English | LILACS | ID: lil-113584

ABSTRACT

The effects of increasing concentrations of mercury (Hg2+) chloride (0.5, 1, 2 and 10 uM) on the myocardial electromechanical activity were studied on 10 Langendorff-perfused rat hearts. Hg2+ decreased the development of isovolumic systolic pressure from 20.3 ñ 2.13 mmHg under control conditions to 6.25 ñ 1.32 mmHg at 10 uM HgCl2 (P<0.01) (diastolic pressure = 0 mm Hg). The atrial and ventricular rates also decreased at uM, 1 uM and 2 uM HgCl2 when compared to the Hg2+ - free solution (from 201 ñ 4 to 126 ñ 15 bpm). However, at 10 uM Hg2+ the atrial rate increased (155 ñ 19 bpm) whereas the ventricular rate did not change significantly (119 ñ 13 bpm). A delay in atrioventricular conduction occured at 0.5 uM Hg2+ (64 ñ 4 ms in the Hg2+ free solution to 91 ñ 14 ms in the presence of 0.5 uM Hg2+, P<0.05) with no further changes at higher Hg2+ concentrations. The QRS-T duration also increased as a function of increasing Hf2+ concentrations (58 ñ 5.5 ms in the Hg2+ -free solution to 123 ñ 15 ms in the presence of 10 uM Hg2+ , P<0.01). Qualitative changes of ECG such as extrasystoles , atrial or ventricular arrhythmias and A-V blocks were also observed. The inhibitory action of Hg2+ on ATP hydrolysis and on Ca2+ and Na+-K+ ATPases suggested to occur in other tissues could be the mechanism responsible for the observations reported here


Subject(s)
Rats , Blood Volume , Mercuric Chloride/adverse effects , Electrocardiography , Heart , Myocardium , Perfusion , Mercuric Chloride/toxicity
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