People with Parkinson’s disease (PD) often suffer from various non-motor symptoms, including manifestations of autonomic dysfunction. The latter encompass cardiovascular, urogenital, gastrointestinal manifestations, sexual dysfunction and thermoregulatory disturbances. Autonomic manifestations can be an intrinsic aspect of PD, resulting from degeneration of parasympathetic and sympathetic pathways, or can be secondary to comorbidity or medication intake. As autonomic dysfunction is prevalent and often troublesome, identification and appropriate treatment are relevant steps in the management of people with Parkinson’s disease. Some manifestations of this autonomic dysfunction may precede the onset of PD motor features by many years, and might be considered biomarkers of this disease. A variety of non-pharmacologic and pharmacologic treatments have been investigated for the treatment of autonomic dysfunction in PD, but a limited evidence base is available so far.

The transition from physiological circulation to cardiopulmonary bypass (CPB) represents a major change to the homeostasis of the body including alterations in the distribution of blood flow and oxygen delivery to organs, which may at least in part account for the organ dysfunction during CPB. Layered on top of disturbances in oxygen delivery is a systemic inflammatory response triggered by contact of leukocytes and other blood components with the artificial surfaces of the extracorporeal circuit. While most of these host responses are appropriate and desirable in the context of a localized injury or infection, they are not desirable systemically and contribute to the morbidity and mortality associated with cardiopulmonary bypass.