Toscano Cindy Medici, Filetti Filipe Martinuzo, Almenara Camila Cruz Pereira, Fioresi Mirian, Vassallo Dalton Valentim
Dept. of Physiological Sciences, Federal University of Espiríto Santo, Vitória, ES CEP 29043-900, Brazil; Nursing Course, University Center FAESA, Vitória, ES CEP 29053-360, Brazil.
Dept. of Physiological Sciences, Federal University of Espiríto Santo, Vitória, ES CEP 29043-900, Brazil; Nursing Course, FAVENI College, Venda Nova do Imigrante, ES CEP 29375-000, Brazil.
Life Sci. 2022 Jul 1;300:120579. doi: 10.1016/j.lfs.2022.120579. Epub 2022 Apr 27.
Copper is an essential factor for the body's homeostasis. However, excess copper compromises organic functions.
We investigated the effects of copper exposure for 30 days on blood pressure (BP) and cardiac contractility and the putative involvement of nitric oxide (NO) and reactive oxygen species.
Wistar rats (12 weeks old, 280 g) were randomized to the treated group that was exposed for 30 days to copper (2000 μg/kg/day CuCl) and the control (Ct) group that received intraperitoneal saline (0.9%).
The blood concentration of copper was ~1.26 μg/mL in the copper-exposed group and ~0.024 μg/mL in the Ct group. The main metal accumulations occurred in the liver and kidneys. Copper exposure increased systolic BP (Cu: 141 ± 3 mmHg; Ct: 133 ± 3 mmHg) (tail cuff method), left ventricular systolic pressure and papillary muscle force. Calcium release from the sarcoplasmic reticulum was reduced. The contractile response to Ca was increased by copper, and the effect was not altered by L-NAME. Copper increased contractions dependent on sarcolemmal Ca influx, and this effect was not altered by L-NAME. The percentage response to isoproterenol decreased in the copper-exposed group, but L-NAME did not alter this reduction. Papillary force development at the peak and plateau of tetanic contractions also increased after copper exposure, but this effect was not altered by L-NAME. In situ detection of OH local production increased.
Copper increased BP and cardiac force, increased Ca inflow, reduced Ca reuptake by the sarcoplasmic reticulum, and increased OH local production. Copper exposure at doses considered tolerable affects cardiac contractility.
铜是人体稳态的必需因素。然而，过量的铜会损害机体功能。
我们研究了30天铜暴露对血压（BP）和心脏收缩力的影响以及一氧化氮（NO）和活性氧的可能参与情况。
将12周龄、体重280克的Wistar大鼠随机分为处理组，该组大鼠接受30天的铜暴露（2000μg/kg/天CuCl），以及对照组（Ct），该组大鼠接受腹腔注射生理盐水（0.9%）。
铜暴露组的血液铜浓度约为1.26μg/mL，Ct组约为0.024μg/mL。主要的金属蓄积发生在肝脏和肾脏。铜暴露增加了收缩压（铜暴露组：141±3mmHg；Ct组：133±3mmHg）（尾袖法）、左心室收缩压和乳头肌张力。肌浆网的钙释放减少。铜增加了对钙的收缩反应，且L-NAME未改变该效应。铜增加了依赖肌膜钙内流的收缩，且L-NAME未改变该效应。铜暴露组对异丙肾上腺素的反应百分比降低，但L-NAME未改变这种降低。铜暴露后，强直收缩峰值和平台期的乳头肌张力也增加，但L-NAME未改变该效应。原位检测发现局部OH生成增加。
铜增加了血压和心脏力量，增加了钙内流，减少了肌浆网对钙的再摄取，并增加了局部OH生成。在可耐受剂量下的铜暴露会影响心脏收缩力。
