Autonomic dysfunction determines stress-induced cardiovascular and immune complications in mice

Methods and 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.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. © 2015 the authors. published on behalf of the american heart association,inc.,by wiley blackwell.