Postural vasoregulation and mediators of reperfusion injury in venous ulceration

To test the hypothesis that ischemia and reperfusion injury may contribute to the cause or nonhealing of venous ulcers, the effects of postural change on the microcirculation of ulcers and on levels of known mediators of reperfusion injury in their venous effluent were studied.

A standard protocol of stabilization (20 minutes), limb dependency (1 hour), and reelevation (2 hours) was used in 10 patients with venous leg ulcers as proven by clinical history, examination, ankle-brachial pressure index, and light reflective rheography. Superficial blood flow in and around ulcers was repeatedly examined with a new laser-Doppler scanning technique. Blood samples from the saphenous vein or a tributary adjacent to the ulcer before dependency and at 0, 10, 30, 60, and 120 minutes after reelevation were analyzed for tumor necrosis factor-alpha, interleukin (IL)-1RA, IL-1 beta, IL-6, platelet-activating factor, thromboxane B2, leukotriene B4, and P-selectin.

Scans showed a consistent pattern of high ulcer blood flow, which decreased on dependency (p < 0.05) and then returned to baseline levels on reelevation and (in 7 of 10) eventually exceeded initial values. Mediator assays showed that levels of platelet-activating factor, IL-1RA, and IL-6 were significantly higher in resting ulcer venous effluent than in systemic venous samples; the reverse was true for P-selectin. There was no statistically significant change in effluent concentration of any mediator as a function of posture, ulcer size, or healing.

Postural vasoregulation causes relative ischemia and reperfusion in venous leg ulcers. However, this is not associated with changes in release of mediators known to be related to reperfusion injury in internal organs.