Acute exposure to lead increases myocardial contractility independent of hypertension development.

Acute exposure to lead increases myocardial contractility independent of hypertension development.
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与高血压发育无关,急性暴露于铅增加心肌收缩力。

DOI:
10.1590/1414-431x20122190
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发表时间:
2013-02
期刊:
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
影响因子:
--
通讯作者:
Vassallo DV
Vassallo DV
中科院分区:
其他
文献类型:
--
作者:
Fioresi M;Furieri LB;Simões MR;Ribeiro RF Jr;Meira EF;Fernandes AA;Stefanon I;Vassallo DV

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我们研究了急性给药小剂量铅随时间对麻醉大鼠血流动力学参数的影响,以确定心肌收缩力的变化是否依赖于高血压的发展。雄性Wistar大鼠静脉注射醋酸铅320 μg/kg,连续2 h。  用离体左心室乳头肌评价心肌收缩力,同时测定Na+,K+-ATP酶和肌球蛋白Ca ~(2+)-ATP酶活性。电极导线显著增加了左心室收缩压(对照:112 ± 3.7 mmHg vs电极导线:129 ± 3.2 mmHg)和右心室收缩压(对照:28 ± 1.2 mmHg vs电极导线:34 ± 1.2 mmHg),而没有改变心率。  乳头肌暴露于8 µM醋酸铅,60分钟后进行评价。  等长收缩增加(对照:0.546 ± 0.07 vs电极导线:0.608 ± 0.06 g/mg),张力峰值时间缩短(对照:268 ± 13 vs电极导线:227 ± 5.58 ms),但松弛时间不变。  暂停后增强组间相似(n = 6/组),表明肌浆网活性无变化,通过本方案间接评价。暴露于醋酸铅1小时后,乳头肌对β-肾上腺素能激动剂(10 µM异丙肾上腺素)反应过度。 此外,休息后收缩减少,表明肌膜钙内流减少。用8 µM醋酸铅处理的心脏样本显示Na+,K+-ATP酶(对照组与铅组相比约增加140%,P < 0.05)和肌球蛋白ATP酶(对照组与铅组相比约增加30%,P < 0.05)活性增加。 我们的研究结果表明,急性暴露于低浓度的铅产生直接的正性肌力和lustropic对心肌收缩力的影响,并增加右心室和左心室收缩压,从而可能有助于高血压的早期发展。
We studied the effects of the acute administration of small doses of lead over time on hemodynamic parameters in anesthetized rats to determine if myocardial contractility changes are dependent or not on the development of hypertension. Male Wistar rats received 320 µg/kg lead acetate iv once, and their hemodynamic parameters were measured for 2 h. Cardiac contractility was evaluated in vitro using left ventricular papillary muscles as were Na+,K+-ATPase and myosin Ca2+-ATPase activities. Lead increased left- (control: 112 ± 3.7 vs lead: 129 ± 3.2 mmHg) and right-ventricular systolic pressures (control: 28 ± 1.2 vs lead: 34 ± 1.2 mmHg) significantly without modifying heart rate. Papillary muscles were exposed to 8 µM lead acetate and evaluated 60 min later. Isometric contractions increased (control: 0.546 ± 0.07 vs lead: 0.608 ± 0.06 g/mg) and time to peak tension decreased (control: 268 ± 13 vs lead: 227 ± 5.58 ms), but relaxation time was unchanged. Post-pause potentiation was similar between groups (n = 6 per group), suggesting no change in sarcoplasmic reticulum activity, evaluated indirectly by this protocol. After 1-h exposure to lead acetate, the papillary muscles became hyperactive in response to a β-adrenergic agonist (10 µM isoproterenol). In addition, post-rest contractions decreased, suggesting a reduction in sarcolemmal calcium influx. The heart samples treated with 8 µM lead acetate presented increased Na+,K+-ATPase (approximately 140%, P < 0.05 for control vs lead) and myosin ATPase (approximately 30%, P < 0.05 for control vs lead) activity. Our results indicated that acute exposure to low lead concentrations produces direct positive inotropic and lusitropic effects on myocardial contractility and increases the right and left ventricular systolic pressure, thus potentially contributing to the early development of hypertension.
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期刊: CIRCULATION
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期刊: HYPERTENSION
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