Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice

作者：Batchu Sri N; Smolock Elaine M; Dyachenko Igor A; Murashev Arkady N; Korshunov Vyacheslav A^*

来源：Journal of the American Heart Association, 2015, 4(5): e001952.

DOI：10.1161/JAHA.115.001952

• carotid arteries
• heart rate variability
• inflammation
• mouse

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.
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 (approximate to 2-fold) in SJL compared with C3HeB mice. Circulating proinflammatory monocytes (CD11b(+) Ly6C(Hi)) 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.

• 出版日期2015-5