Acute administration of nicotine induces transient elevation of blood pressure and increases myocardial infarct size in rats.
Acute administration of nicotine induces transient elevation of blood pressure and increases myocardial infarct size in rats.
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尼古丁的急性给药会诱导血压的短暂升高，并增加大鼠的心肌梗塞大小。
DOI：
10.1016/j.heliyon.2020.e05450
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发表时间：
2020-11
期刊：
影响因子：
4
通讯作者：
Kloner RA
中科院分区：
文献类型：
--
作者：
Zhao L;Dai W;Carreno J;Shi J;Kleinman MT;Kloner RA
我们在急性心肌缺血和再灌注梗塞大鼠模型中研究了尼古丁对心肌梗塞面积、无复流、血流动力学和心功能的急性影响。雌性 Sprague-Dawley 大鼠（n = 23/组）在开始冠状动脉闭塞之前接受 2.0 μg/kg/min 的静脉内负荷剂量的尼古丁或盐水对照 30 分钟，然后在 30 分钟闭塞和 3 小时再灌注结束时接受维持剂量 0.35 μg/kg/min 的尼古丁。基线时，各组之间的收缩压（血压，mmHg）（尼古丁，69.0 ± 2.7；对照，69.3 ± 4.4；p = NS）或舒张压（尼古丁，45.7 ± 3.2；对照，48.2 ± 4.2；p = NS）没有差异。开始注射负荷剂量后 10 分钟，给予尼古丁最初会增加收缩压（尼古丁，97.0 ± 8.6；对照，69.2 ± 3.3，p < 0.0001）和舒张压（尼古丁，65.6 ± 6.4；对照，47.4 ± 3.1，p = 0.0003）； 30 分钟后，两组血压均降至对照水平。在闭塞和再灌注期间，尼古丁不会改变血压和心率。与对照组相比，尼古丁显着增加了心肌梗塞面积占缺血风险区的百分比（尼古丁，54.9±1.9；对照，48.6±2.7，p<0.05），但尼古丁不影响无复流面积和心脏功能。虽然急性尼古丁只会短暂升高血压，但它不会影响冠状动脉闭塞期间的血流动力学参数。尼古丁会增加心肌梗塞面积，这表明梗塞面积的增加不仅仅是由于后负荷、心率或收缩力改变导致需氧量增加，还可能是由于对心肌有更直接的影响。尼古丁;心肌梗塞;缺血和再灌注损伤；血流动力学；细胞生物学；病理生理学；健康科学；心脏病学；病理;毒理学
We investigated the acute effects of nicotine on myocardial infarct size, no reflow, hemodynamics and cardiac function in an acute myocardial ischemia and reperfusion infarction rat model. Female Sprague-Dawley rats (n = 23/group) received an intravenous loading dose of nicotine at 2.0 μg/kg/min or saline control for 30 min before starting coronary artery occlusion, then followed by a maintenance dose 0.35 μg/kg/min of nicotine to the end of 30 min occlusion and 3 h reperfusion. At baseline, there was no difference in systolic blood pressure (BP in mmHg) (nicotine, 69.0 ± 2.7; control, 69.3 ± 4.4; p = NS) or diastolic BP (nicotine, 45.7 ± 3.2; control, 48.2 ± 4.2; p = NS) between groups. Nicotine administration initially increased systolic BP (nicotine, 97.0 ± 8.6; control, 69.2 ± 3.3, p < 0.0001) and diastolic BP (nicotine, 65.6 ± 6.4; control, 47.4 ± 3.1, p = 0.0003) at 10 min after starting injection of the loading dose; BP dropped to control levels in both groups at 30 min. During occlusion and reperfusion, the BP and heart rate were not altered by nicotine. Nicotine significantly increased myocardial infarct size as a percentage of the ischemic risk zone compared to the controls (nicotine, 54.9 ± 1.9; control, 48.6 ± 2.7, p < 0.05), but nicotine did not affect the no-reflow size and heart function. While acute nicotine only transiently elevated blood pressure, it did not affect hemodynamic parameters during coronary artery occlusion. Nicotine increased myocardial infarct size, suggesting that the increase in infarct size was not simply due to an increase in oxygen demand due to altered afterload, heart rate, or contractility, but may have been due to a more direct effect on the myocardium. Nicotine; myocardial infarction; Ischemia and reperfusion injury; Hemodynamic; Cell biology; Pathophysiology; Health Sciences; Cardiology; Pathology; Toxicology
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影响因子：
--
作者：
Dow JS;Bhandari A;Hale SL;Kloner RA
通讯作者：
Kloner RA
影响因子：
2.8
作者：
Brunetti, Ryan;Hicklin, Harry;Soliman, Elsayed Z.
通讯作者：
Soliman, Elsayed Z.
影响因子：
4.6
作者：
Chaumont, Martin;de Becker, Benjamin;van de Borne, Philippe
通讯作者：
van de Borne, Philippe
影响因子：
5.4
作者：
Dai W;Herring MJ;Hale SL;Kloner RA
通讯作者：
Kloner RA
DOI：
10.1038/nrcardio.2017.36
发表时间：
2017-08
期刊：
Nature reviews. Cardiology
影响因子：
--
作者：
Benowitz NL;Fraiman JB
通讯作者：
Fraiman JB