The effects of inflammation on the vascular responses to acute mental stress

Evidence exists for the role of acute mental stress as a trigger for myocardial infarction. Despite the fact that the underlying mechanisms are not fully understood, inflammation and the vascular responses to stress are two mechanisms which have been implicated. After a critical analysis of the methods used to measure the vascular responses to acute mental stress (Chapter 2), this thesis examined the effects of acute inflammation on resting cardiac and mood measures (Chapter 3), and on the vascular responses to stress in a healthy population (Chapters 4 - 6). Two different protocols (vaccination and eccentric exercise) induced inflammation. Inflammation did not alter resting cardiac function or mood (Chapter 3). Despite no alteration in resting vascular function, acute inflammation did attenuate stress-induced vasodilation (Chapter 4 and 6). The effects of inflammation on stress-induced vasodilation were more prominent at the site of inflammation, indicating a localised impact of inflammation on stress-induced vasodilation. These findings suggest a possible interaction between inflammation and the vascular responses to mental stress, which could be a mechanism for the triggering of a myocardial infarction through mental stress. Further work is needed to identify the exact mechanisms through which this attenuation occurs, with a view to enhancing the vascular responses to stress in chronically inflamed populations