Ischemic and pressure-induced hyperemia: a comparison.

OBJECTIVE

There is reason to question whether hyperemia after pressure occlusion is caused solely by local ischemia. This study quantitatively compared the response to the two forms of occlusion on the finger.

DESIGN

Blood flow was measured by laser Doppler continuously before, during, and for 40 minutes after a 2-minute occlusion of flow at the finger dorsum and at the plantar surface of the finger tip (finger pulp), which has a much higher arteriolar density than the dorsum. Occlusion to the same low level was carried out either with a cuff at the base of the finger or by direct pressure of the laser Doppler probe head. Comparison experiments were performed with the probe head heated to 44 degrees C to elicit maximal local vasodilation.

SETTING

Outpatient clinic.

PARTICIPANTS

Eleven healthy volunteers.

MAIN OUTCOME MEASURES

Magnitude and duration of skin blood flow after occlusion.

RESULTS

Cuff occlusion at the base of the finger produced a typical, short-lived hyperemic response at both finger dorsum and finger pulp. The peak level at finger dorsum was 17.6 +/- 1.4mL/min/100g, approximately a twofold increase over the baseline flow level. The duration of the hyperemic response was 3.6 +/- 0.8 minutes. The baseline flow at the finger pulp was three times greater than at the finger dorsum, and peak flow after occlusion was also three times higher (44.3 +/- 2.6 mL/min/100g). The duration of hyperemia at finger pulp was 4.2 +/- 0.9 minutes. After pressure occlusion at the finger dorsum the hyperemic peak was higher (26.7 +/- 4.2 mL/min/100g; p < .05) and the duration of hyperemia was four times longer (16.9 +/- 2.3 minutes; p < .01) than after cuff occlusion. At the finger pulp, the pressure-induced hyperemic peak was also greater than the peak after cuff occlusion (56.3 +/- 1.7mL/min/100g; p < .05), with a longer duration than after cuff occlusion (11.1 +/- 1.1min; p < .01). Thermal stimulation significantly reduced the differences between cuff- and pressure-induced occlusion. There was a slow increase in flow over the 40-minute monitoring period. The maximal flow reached was approximately 100mL/min/100g at both finger dorsum and finger pulp. At both sites, however, the maximal flow level was attained more rapidly than the control condition without prior occlusion.

CONCLUSIONS

These results confirmed that the pressure-induced hyperemic response is greater and of longer duration than that produced by flow ischemia alone. Thermal stimulation essentially abolishes the differences, suggesting that there is a common mechanism of vasodilatation. The mechanistic differences between pressure-induced and ischemic hyperemia remain to be determined.