title: Autonomic dysfunction determines stress-induced cardiovascular and immune complications in mice.
abstract: BACKGROUND
  Clinical studies suggest that acute inflammation in patients with elevated heart rate (HR) increases morbidity and mortality. The SJL/J (SJL) inbred mouse strain is a unique genetic model that has higher HR and systemic and vascular inflammation compared with C3HeB/FeJ (C3HeB) mice. The goal of this study was to investigate the role of stress on cardiac and vascular complications between 2 strains.
  
  
  RESULTS
  Radiotelemetry was used for continuous recordings of HR and blood pressure in mice. Hemodynamic differences between mouse strains were very small without stress; however, tail-cuff training generated mild stress and significantly increased HR (≈2-fold) in SJL compared with C3HeB mice. Circulating proinflammatory monocytes (CD11b(+)Ly6C(H) (i)) significantly increased in SJL mice but not in C3HeB mice after stress. Presence of Ly6C(+) cells in injured carotids was elevated only in SJL mice after stress; however, a transfer of bone marrow cells from SJL/C3HeB to C3HeB/SJL chimeras had no effect on HR or vascular inflammation following stress. Arterial inflammation (VCAM-1(+)) was greater in SJL inbred mice or SJL recipient chimeras, even without stress or injury. HR variability was reduced in SJL mice compared with C3HeB mice.
  
  
  CONCLUSIONS
  We found that impaired parasympathetic activity is central for stress-induced elevation of HR and systemic and vascular inflammation; however, immune cells from stress-susceptible mice had no effect on HR or vascular inflammation in stress-protected mice.
authors.affiliation: Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY (S.N.B., E.M.S., V.A.K.).
authors.forename: Sri N
authors.initials: SN
authors.lastname: Batchu
authors.affiliation: Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY (S.N.B., E.M.S., V.A.K.).
authors.forename: Elaine M
authors.initials: EM
authors.lastname: Smolock
authors.affiliation: Pushchino State Natural-Science Institute, Pushchino, Russia (I.A.D., A.N.M.) Pushchino Branch, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Pushchino, Russia (I.A.D., A.N.M.).
authors.forename: Igor A
authors.initials: IA
authors.lastname: Dyachenko
authors.affiliation: Pushchino State Natural-Science Institute, Pushchino, Russia (I.A.D., A.N.M.) Pushchino Branch, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Pushchino, Russia (I.A.D., A.N.M.).
authors.forename: Arkady N
authors.initials: AN
authors.lastname: Murashev
authors.affiliation: Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY (S.N.B., E.M.S., V.A.K.) Biomedical Genetics, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY (V.A.K.).
authors.forename: Vyacheslav A
authors.initials: VA
authors.lastname: Korshunov
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002339:Carotid Arteries / Q000276:immunology / Q000473:pathology; D006339:Heart Rate; D006706:Homeostasis; D007249:Inflammation / Q000097:blood / Q000473:pathology; D051379:Mice; D008809:Mice, Inbred C3H; D008815:Mice, Inbred Strains; D009000:Monocytes / Q000276:immunology; D010276:Parasympatholytics; D013045:Species Specificity; D013312:Stress, Physiological / Q000276:immunology*; D013686:Telemetry / Q000379:methods
chemical_list: D010276:Parasympatholytics
keywords: carotid arteries; heart rate variability; inflammation; mouse