When human fingers are exposed to cold, the blood vessels in the skin contract. Thus less blood goes to the periphery for heat transfer with the environment. This, however, can lead to problems in the fingers: the cold reduces the mobility and sensitivity of the fingers, thus increasing the risk for cold injuries and decreasing the manual dexterity. Fortunately, the fingers are equipped with arterio-venous anastomoses (AVA). These are shortcuts between the arterial and venous system. The AVA open and close periodically and thus allow warm blood to enter the finger tips. The opening of the vessels in the cold is called Cold Induced Vasodilation (CIVD). A competition exists between mechanisms under central control (closure of blood vessels to retain body heat) and local mechanisms (opening of blood vessels to avoid local cold injuries). This competition is the topic of this thesis.
In a series of experiments the relation between finger blood flow and body temperature is investigated. Heat is easily transferred to the environment by the fingers when the body is relatively warm. A distinction can be made between body core temperature and mean skin temperature of the body in relation to their effect on the CIVD response. A relatively high skin temperature leads to a quick onset of CIVD; a relatively high core temperature leads to a large amplitude of CIVD. CIVD is minimal in a cold body and consequently the risk for local cold injuries is higher than with a warm body. The temperature of the hand also plays a role: CIVD is enhanced when the hand is cold.
The CIVD-reaction of neighbouring fingers shows much similarity in shape and timing. This similarity is probably not related to nerve supply, but more likely to blood supply. No relation was found in CIVD between fingers of different hands. This suggests that finger blood flow is controlled by different mechanisms for the left and right hand.
The mechanism of the CIVD-reaction is not well known. For a long time it was assumed that the cold/pain sensors in the skin trigger nerves that release vasodilating substances (axon-reflex). In an experiment, however, it appeared to be impossible to evoke an axon-reflex in a cold hand. This makes another hypothesis more likely that states that a paralysis of the muscle wall of the AVA occurs in the cold.