Pathophysiology of Raynauds Phenomenon
In the normal physiologic state, cutaneous blood flow to acral sites such as the fingers, toes, and tips of the nose and ears serve as an important part of the body’s mechanism of thermoregulation. Cutaneous blood flow can exceed 6 L/minute in periods of hyperthermia when the body attempts to “vent” heat through such sites; in contrast, cold environments can drop cutaneous blood flow to nearly undetectable levels. RP represents an exaggerated vascular response to cold and stress, most commonly at acral sites responsible for thermoregulation.
Neural signals, circulating hormones and mediators from immunomodulatory and endothelial cells all may affect blood vessel reactivity. Subsequent changes in blood vessel radius play a prominent role in RP, as a given reduction in radius results in a four-fold decrease in the blood flow (law of Poiseuille). Neural signals that modulate vascular reactivity include epinephrine, norepinephrine, vasopressin, bradykinin, histamine, and leukotrienes among others. Additional mediators from circulating cells include serotonin and ATP/ADP. Mediators from endothelial cells include prostacyclin, nitric oxide, endothelin, and other contractile factors. Patients with RP, therefore, suffer from diminished cutaneous blood flow due to alterations in the neural input (primary and secondary RP) as well as mediators from endothelial and immunomodulatory cells (secondary RP).
