Microcirculatory compensation to progressive atherosclerotic disease.

Research paper by P L PL Cisek, A R AR Eze, A J AJ Comerota, R R Kerr, B B Brake, P P Kelly

Indexed on: 01 Jan '97Published on: 01 Jan '97Published in: Annals of Vascular Surgery


The precapillary resistance in the skin of the foot increases with standing. This mechanism, termed the venoarterial reflex (VAR) restricts arterial inflow, and avoids an excessive rise in capillary pressure. This study tests the hypothesis that there is microcirculatory compensation to atherosclerotic disease of increasing severity. Foot skin perfusion (FSP) was measured in 100 limbs with a laser Doppler placed on the plantar aspect of the great toe. Limbs were categorized as normal (n = 31) with an ankle brackial index (ABI) > or = 0.96, claudicants (n = 42) ABI 0.5-0.86, and critical ischemia (n = 27) with an ABI < or = 0.49 or a pulse volume recording consistent with severe peripheral vascular disease and symptoms of rest pain or tissue loss. Segmental Doppler pressures and pulse volume recordings were performed prior to laser Doppler measurements. Subjects with clinical signs or symptoms of chronic venous insufficiency were excluded. The resting foot skin perfusion was measured in the horizontal and dependent position, with the patient supine and sitting. Comparisons within categories were done using Wilcoxon matched pairs signed rank test and between groups with Mann-Whitney U test for unpaired data. Differences were considered significant if they exceeded the 95% confidence level (p value < or = 0.05). Resting supine skin perfusion was similar between nondiabetic normals and claudicants and diabetic normals and claudicants. There was a significant decrease in the foot skin perfusion (mean FSP +/- SEM) in the normal limb with a change from the supine (7.8 +/- 2.2 ml/min/100 g) to the dependent (2.8 +/- 0.6 ml/min/100 g) position indicating an intact VAR. This was absent in 33% of the limbs with claudication. Limbs with critical ischemia demonstrated an increase in FSP with dependency (supine 4.0 +/- 1.0 ml/min/100 g) versus dependent (8.4 +/- 1.8 ml/min/100 g) and was present in both diabetic and nondiabetic limbs. Microcirculatory compensation occurs early in atherosclerotic limbs. Although supine FSP is similar in normals and claudicants, a greater percentage of claudicants demonstrate a loss of the VAR. Critically ischemic limbs have increased FSP in the dependent position. These observations indicate that there are microcirculatory alterations in limbs with claudication and assist in explaining why patients with ischemic rest pain obtain relief and develop edema with dependency.