E Alison Holman1, Ana Guijarro1, James Lim1, Daniele Piomelli1. 1. 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).
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: Acute psychological stress elicits ECS-related cardiac responses associated with persistent, potentially pathological changes in rat cardiovascular biochemistry/function.
OBJECTIVE: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. METHODS: 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. RESULTS: 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. CONCLUSIONS: Acute psychological stress elicits ECS-related cardiac responses associated with persistent, potentially pathological changes in rat cardiovascular biochemistry/function.
Authors: E Alison Holman; Roxane Cohen Silver; Michael Poulin; Judith Andersen; Virginia Gil-Rivas; Daniel N McIntosh Journal: Arch Gen Psychiatry Date: 2008-01
Authors: Catherine M Stoney; Sheila G West; Joel W Hughes; Lisa M Lentino; Montenique L Finney; James Falko; Linda Bausserman Journal: Psychophysiology Date: 2002-01 Impact factor: 4.016