Program in Nursing Science, University of California, Irvine, California, 92697, USA (Dr. Holman); Department of Anatomy and Neurobiology, University of California, Irvine, 3216 A Gillespie Neuroscience Research Facility, Irvine, California, 92697, USA (Drs. Guijarro and Piomelli, Mr. Lim); Drug Discovery and Development, Italian Institute of Technology, via Morego 30, Genoa, Italy 16163 (Drs. Guijarro and Piomelli).
Psychosom Med. 2014 Jan;76(1):20-28. doi: 10.1097/PSY.0000000000000025. Epub 2013 Dec 23.
Trauma exposure can precipitate acute stress (AS) and cardiovascular disorders (CVD). Identifying AS-related physiologic changes that affect CVD risk could inform development of early CVD prevention strategies. The endocannabinoid system (ECS) regulates hypothalamic-pituitary-adrenal axis and stress-related cardiovascular function. We examine stress-related ECS activity and its association with cardiovascular biochemistry/function after AS.
Rodents (n = 8-16/group) were exposed to predator odor or saline; elevated plus maze, blood pressure, serum and cardiac ECS markers, and lipid metabolism were assessed 24 hours and 2 weeks postexposure.
At 24 hours, the predator odor group demonstrated anxiety-like behavior and had a) elevated serum markers of cardiac failure/damage (brain natriuretic peptide: 275.1 versus 234.6, p = .007; troponin I: 1.50 versus 0.78, p = .076), lipogenesis (triacylglycerols: 123.5 versus 85.93, p = .018), and inflammation (stearoyl delta-9 desaturase activity: 0.21 versus 0.07, p < .001); b) decreased cardiac 2-arachidonoyl-sn-glycerol (29.90 versus 65.95, p < .001), oleoylethanolamide (114.3 versus 125.4, p = .047), and palmitoylethanolamide (72.96 versus 82.87, p = .008); and c) increased cardiac inflammation (interleukin [IL]-1β/IL-6 ratio: 19.79 versus 13.57, p = .038; tumor necrosis factor α/IL-6 ratio: 1.73 versus 1.03, p = .019) and oxidative stress (thiobarbituric acid reactive substances: 7.81 versus 7.05, p = .022), which were associated with cardiac steatosis (higher triacylglycerol: 1.09 versus 0.72, p < .001). Cardiac lipogenesis persisted, and elevated blood pressure emerged 2 weeks postexposure.
Acute psychological stress elicits ECS-related cardiac responses associated with persistent, potentially pathological changes in rat cardiovascular biochemistry/function.
创伤暴露可引发急性应激（AS）和心血管疾病（CVD）。确定与 AS 相关的影响 CVD 风险的生理变化可以为早期 CVD 预防策略的制定提供信息。内源性大麻素系统（ECS）调节下丘脑-垂体-肾上腺轴和与应激相关的心血管功能。我们研究了 AS 后与应激相关的 ECS 活性及其与心血管生化/功能的关系。
将啮齿动物（n=8-16/组）暴露于捕食者气味或盐水中；在暴露后 24 小时和 2 周评估高架十字迷宫、血压、血清和心脏 ECS 标志物以及脂质代谢。
在 24 小时时，捕食者气味组表现出焦虑样行为，并且 a）血清心功能/损伤标志物升高（脑钠肽：275.1 比 234.6，p=0.007；肌钙蛋白 I：1.50 比 0.78，p=0.076）、脂肪生成（三酰甘油：123.5 比 85.93，p=0.018）和炎症（硬脂酰 delta-9 去饱和酶活性：0.21 比 0.07，p<.001）；b）心脏 2-花生四烯酰基-sn-甘油（29.90 比 65.95，p<.001）、油酰乙醇酰胺（114.3 比 125.4，p=0.047）和棕榈酰乙醇酰胺（72.96 比 82.87，p=0.008）减少；c）心脏炎症增加（白细胞介素[IL]-1β/IL-6 比值：19.79 比 13.57，p=0.038；肿瘤坏死因子α/IL-6 比值：1.73 比 1.03，p=0.019）和氧化应激（硫代巴比妥酸反应物质：7.81 比 7.05，p=0.022），这与心脏脂肪变性相关（更高的三酰甘油：1.09 比 0.72，p<.001）。心脏脂肪生成持续存在，血压升高在暴露后 2 周出现。
急性心理应激引起与应激相关的心脏反应，与大鼠心血管生化/功能的持续、潜在病理性变化相关。
