BACKGROUND

Adequate cutaneous microvascular blood flow and tissue oxygen tension are important prerequisites for successful tissue repair. The efficacy of tissue repair decreases with age and is linked to the age-related functional decline of unmyelinated sensory neurons that are important for inflammation and tissue repair. However, available information on the effect of these neuronal changes on microvascular blood flow and tissue oxygen tension is limited, particularly under control and injury conditions. The authors had two aims in this study: (a) to assess age-related changes in the relationship between microvascular blood flow and tissue oxygen perfusion under basal and two different stimulated conditions (sensory dependent and sensory independent), and (b) to clarify the biological meaning of transcutaneous partial pressure of oxygen (tcPO2) measurements.

METHODS

The effects of a sensory-independent vasodilator (acetylcholine) and a sensory-dependent vasodilator (capsaicin) on microvascular blood flow and oxygen perfusion in persons of different ages were measured. Laser Doppler flowmetry and a commercially available transcutaneous oxygen monitor (with sensors set at 39 degrees C and 44 degrees C) were used. Healthy volunteers were recruited: 11 young, 14 middle aged, and 19 older.

RESULTS

Under basal conditions (skin temperature, 37 degrees C to 39 degrees C), both basal blood flow and tcPO2 increased with increasing age. However, with the sensor set at 44 degrees C, tcPO2 showed a significant decrease with age. Acetylcholine increased blood flow approximately equally in the three age groups. Capsaicin increased blood flow and tcPO2 in all age groups, with the young showing a greater increase compared with the older participants.

CONCLUSIONS

The age-associated changes in basal and stimulated microvascular blood flow and tcPO2 could be attributed in part to altered neuronal function. Measuring tcPO2 at 39 degrees C showed a trend toward an increase with age. In contrast, a decrease with age was observed when tcPO2 was measured at 44 degrees C, a temperature sufficient to activate sensory nerve endings. The results may reflect a decline in sensory nerve function with age rather than a decrease in oxygen delivery for vascular reasons. This is supported by the complementary data showing a significant age-related decrease in stimulated blood flow in response to capsaicin, with no change in the response to the sensory-independent vasodilator acetylcholine. Thus, for clinical purposes, data obtained using the tcPO2 monitor should be interpreted with full knowledge of the conditions under which the measurements were made. Furthermore, for scientific purposes, the tcPO2 monitor could be used to assess sensory nerve function when sensors are heated to 44 degrees C.