Hatcher Jeffrey, Gu He, Cheng Zixi Jack
Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816, USA.
Department of Anesthesia, University of Iowa Hospital and Clinics, Iowa City, IA 52242, USA.
Oxid Med Cell Longev. 2016;2016:3686829. doi: 10.1155/2016/3686829. Epub 2015 Dec 28.
Overproduction of reactive oxygen species (ROS), such as the superoxide radical (O2 (∙-)), is associated with diseases which compromise cardiac autonomic function. Overexpression of SOD1 may offer protection against ROS damage to the cardiac autonomic nervous system, but reductions of O2 (∙-) may interfere with normal cellular functions. We have selected the C57B6SJL-Tg (SOD1)2 Gur/J mouse as a model to determine whether SOD1 overexpression alters cardiac autonomic function, as measured by baroreflex sensitivity (BRS) and aortic depressor nerve (ADN) recordings, as well as evaluation of baseline heart rate (HR) and mean arterial pressure (MAP). Under isoflurane anesthesia, C57 wild-type and SOD1 mice were catheterized with an arterial pressure transducer and measurements of HR and MAP were taken. After establishing a baseline, hypotension and hypertension were induced by injection of sodium nitroprusside (SNP) and phenylephrine (PE), respectively, and ΔHR versus ΔMAP were recorded as a measure of baroreflex sensitivity (BRS). SNP and PE treatment were administered sequentially after a recovery period to measure arterial baroreceptor activation by recording aortic depressor nerve activity. Our findings show that overexpression of SOD1 in C57B6SJL-Tg (SOD1)2 Gur/J mouse preserved the normal HR, MAP, and BRS but enhanced aortic depressor nerve function.
活性氧（ROS）如超氧阴离子自由基（O2(∙-)）的过度产生与损害心脏自主神经功能的疾病有关。超氧化物歧化酶1（SOD1）的过表达可能提供保护，防止ROS对心脏自主神经系统的损伤，但O2(∙-)的减少可能会干扰正常细胞功能。我们选择C57B6SJL-Tg (SOD1)2 Gur/J小鼠作为模型，以确定SOD1过表达是否会改变心脏自主神经功能，通过压力反射敏感性（BRS）和主动脉减压神经（ADN）记录进行测量，并评估基线心率（HR）和平均动脉压（MAP）。在异氟烷麻醉下，将动脉压力传感器插入C57野生型和SOD1小鼠体内，测量HR和MAP。在建立基线后，分别注射硝普钠（SNP）和去氧肾上腺素（PE）诱导低血压和高血压，并记录ΔHR与ΔMAP作为压力反射敏感性（BRS）的指标。在恢复期后依次给予SNP和PE治疗，通过记录主动脉减压神经活动来测量动脉压力感受器激活。我们的研究结果表明，C57B6SJL-Tg (SOD1)2 Gur/J小鼠中SOD1的过表达维持了正常的HR、MAP和BRS，但增强了主动脉减压神经功能。
