Zhu B, Sun Y, Sievers R E, Shuman J L, Glantz S A, Chatterjee K, Parmley W W, Wolfe C L
Cardiovascular Division, Department of Medicine, University of California, San Francisco, 94143-0124, USA.
Am Heart J. 1996 Jul;132(1 Pt 1):91-100. doi: 10.1016/s0002-8703(96)90395-6.
This study examined the effects of L-arginine on myocardial infarct size, hemodynamics, and vascular reactivity in environmental tobacco smoke (ETS)-exposed and non-ETS-exposed rats. We previously demonstrated that exposure to ETS increased myocardial infarct size in a rat model of ischemia and reperfusion. If reduced reperfusion was caused by endothelial cell damage and increased vascular tone, L-arginine (ARG) would increase nitric oxide and better protect the heart. Sixty Sprague-Dawley rats were randomly divided into four groups: ETS or non-ETS (control) with and without ARG (2.25% ARG in drinking water). The ETS groups were exposed to passive smoking (4 Marlboro cigarettes per 15 minutes, 6 hours a day) for 6 weeks. After 6 weeks, all rats were subjected to 35 minutes of left coronary artery occlusion and 120 minutes of reperfusion, with hemodynamic monitoring. Aortic rings were harvested to evaluate vascular reactivity. Average air nicotine, carbon monoxide, and total particulate concentrations were 1304 +/- 215 microgram/m3, 78 +/- 2.0 ppm, and 31 +/- .7 mg/m3 (mean +/- SEM) for the ETS-exposed rats. Infarct size (infarct mass/risk area x 100%) increased with ETS exposure but decreased significantly in the ETS-with-ARG group compared with the ETS-without-ARG group (42% +/- 6% vs 64% +/- 6%, mean +/- SEM; p = 0.043). The benefit of ARG was dependent on ETS exposure (ETS x ARG interaction, p = 0.043). There were no significant differences between groups in heart rate, systolic pressure, and rate-pressure product. ARG significantly decreased myocardial infarct size after ischemia and reperfusion in ETS-exposed rats. Neither the adverse effects of ETS on infarct size nor the blockage of this effect by ARG appears to be the result of ETS-induced alterations in hemodynamics.
本研究考察了L-精氨酸对暴露于环境烟草烟雾（ETS）和未暴露于ETS的大鼠的心肌梗死面积、血流动力学及血管反应性的影响。我们之前证明，在缺血再灌注大鼠模型中，暴露于ETS会增加心肌梗死面积。如果再灌注减少是由内皮细胞损伤和血管张力增加所致，那么L-精氨酸（ARG）会增加一氧化氮并更好地保护心脏。60只Sprague-Dawley大鼠被随机分为四组：暴露于ETS或未暴露于ETS（对照组），且分别给予或不给予ARG（饮用水中含2.25% ARG）。ETS组大鼠接受被动吸烟（每15分钟4支万宝路香烟，每天6小时），持续6周。6周后，所有大鼠均接受35分钟的左冠状动脉阻塞和120分钟的再灌注，并进行血流动力学监测。采集主动脉环以评估血管反应性。暴露于ETS的大鼠的平均空气尼古丁、一氧化碳和总颗粒物浓度分别为1304±215微克/立方米、78±2.0 ppm和31±0.7毫克/立方米（平均值±标准误）。梗死面积（梗死质量/危险区域×100%）随ETS暴露而增加，但与未给予ARG的ETS组相比，给予ARG的ETS组显著减小（42%±6% 对64%±6%，平均值±标准误；p = 0.043）。ARG的益处依赖于ETS暴露（ETS×ARG交互作用，p = 0.043）。各组在心率、收缩压和心率-压力乘积方面无显著差异。在暴露于ETS的大鼠中，ARG显著减小了缺血再灌注后的心肌梗死面积。ETS对梗死面积的不利影响以及ARG对该影响的阻断似乎均不是由ETS诱导的血流动力学改变所致。
