Gomes M G, Moreira C A, Mill J G, Massaroni L, Oliveira E M, Stefanon I, Vassallo D V
Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, Brasil.
Braz J Med Biol Res. 1994 Jan;27(1):95-100.
The effect of aluminum (Al3+) chloride (1, 5, 10, 50 and 100 microM) 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 microM AlCl3 (P < 0.01) (diastolic pressure = 0 mmHg). The atrial and ventricular rates also decreased, but only with AlCl3 concentrations greater than 1 microM (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 microM Al3+. A delay in atrioventricular conduction occurred at 10 microM Al3+, increasing progressively up to 100 microM (62.3 +/- 4 ms in the Al(3+)-free solution to 143 +/- 34 ms in the presence of 100 microM Al3+, 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 microM 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+.
在10只成年雌性Wistar大鼠的Langendorff灌流心脏中，研究了氯化铝（Al3+）（1、5、10、50和100微摩尔）对心肌机电活动的影响。Al3+使等容收缩压从对照条件下的34.3±2.95 mmHg降至100微摩尔AlCl3时的11.8±1.53 mmHg（P<0.01）（舒张压=0 mmHg）。心房率和心室率也降低，但仅在AlCl3浓度大于1微摩尔时出现（心房率从180±5次/分钟降至94±11次/分钟，心室率从180±5次/分钟降至78±7次/分钟）。还观察到冠状动脉血流量减少，在100微摩尔Al3+时达到60%。在10微摩尔Al3+时发生房室传导延迟，并逐渐增加至100微摩尔（在无Al(3+)溶液中为62.3±4毫秒，在存在100微摩尔Al3+时为143±34毫秒，P<0.01，方差分析）。QRS时限并未随Al3+浓度增加而改变（在无Al(3+)溶液中为37.1±1.7毫秒，在存在100微摩尔Al3+时为32.1±1.6毫秒）。未观察到心电图的定性变化。这些数据表明，Al3+对心肌的毒性作用表现为收缩压发展和冠状动脉血流量降低以及PR间期延长。根据Al3+对核苷酸水解的抑制作用对这些效应进行了讨论。
