Thermal provocation to evaluate microvascular reactivity in human skin

Abstract

With increased interest in predictive medicine, development of a relatively noninvasive technique that can improve prediction of major clinical outcomes has gained considerable attention. Current tests that are the target of critical evaluation, such as flow-mediated vasodilation of the brachial artery and pulse-wave velocity, are specific to the larger conduit vessels. However, evidence is mounting that functional changes in the microcirculation may be an early sign of globalized microvascular dysfunction. Thus development of a test of microvascular reactivity that could be used to evaluate cardiovascular risk or response to treatment is an exciting area of innovation. This mini-review is focused on tests of microvascular reactivity to thermal stimuli in the cutaneous circulation. The skin may prove to be an ideal site for evaluation of microvascular dysfunction due to its ease of access and growing evidence that changes in skin vascular reactivity may precede overt clinical signs of disease. Evaluation of the skin blood flow response to locally applied heat has already demonstrated prognostic utility, and the response to local cooling holds promise in patients in whom cutaneous disorders are present. Whether either of these tests can be used to predict cardiovascular morbidity or mortality in a clinical setting requires further evaluation.

Fig. 1.

Photograph of the arm spray device in which maximal skin blood flow (SkBF) can be measured. A: the device is attached to a temperature-controlled water bath that circulates water into the cylindrical device. Water is applied to the forearm via numerous spray nozzles. B: the upper cuff for venous occlusion plethysmography. C: the distal cuff to occlude blood flow to the hand. D: temperature gauge within the water spray.

Fig. 2.

Representative tracing of the SkBF response to local heating to 42°C, followed by maximal heating to 43.5°C. The initial rapid rise relies predominantly on the local sensory nerves and nitric oxide. The second rise leads to a plateau that predominantly dependent on nitric oxide.

Fig. 3.

Representative tracing of the SkBF response to local cooling to 24°C. Data are redrawn from Ref. . The initial decrease in SkBF with cooling is followed by a transient vasodilation. This is then followed by a progressive decrease in SkBF with sustained cooling.