BACKGROUND: Thromboangiitis obliterans (TAO) is an occlusive arterial disease and a separate disease entity from atherosclerosis. It occurs mainly in the small and medium-sized vessels. Although the cause of TAO is unknown, systemic factors (immunological or humoral) may be involved in addition to abnormal peripheral microcirculation. Endothelium is now recognized as an important factor in the maintenance of microvascular circulation and the inhibition of platelet aggregation. This study examines the possible impairment of endothelium-dependent vasodilation in the peripheral vasculature of patients with TAO. METHODS AND RESULTS: Forearm blood flow (FBF) changes induced by the endothelium-dependent vasodilator acetylcholine, the endothelium-independent vasodilator sodium nitroprusside, and occlusion-induced reactive hyperemia were measured plethysmographically in eight patients with TAO and in eight healthy control subjects matched for age and smoking status. The increase in FBF response to intra-arterial acetylcholine infusion was lower in patients with TAO than in healthy control subjects (peak FBF, 22.9 +/- 2.9 versus 14.1 +/- 2.8 mL/min per dL of tissue volume; P < .01). In contrast, there was no significant difference in the increase in FBF response to sodium nitroprusside infusion between the two groups (peak FBF 13.1 +/- 4.0 versus 16.3 +/- 2.5 mL/min per dL of tissue volume; P = NS). In the case of reactive hyperemia, there were no significant differences between the two groups at any time points of hyperemia (peak FBF, 32.9 +/- 4.0 versus 31.4 +/- 3.3 mL/min per dL of tissue volume; P = NS). CONCLUSIONS: These results indicate that peripheral endothelium-dependent vasodilation is impaired in the nondiseased limb of patients with TAO. This type of vascular dysfunction may contribute to such characteristics as segmental proliferative lesion and thrombus formation in the peripheral vessels of patients with TAO.
BACKGROUND:Thromboangiitis obliterans (TAO) is an occlusive arterial disease and a separate disease entity from atherosclerosis. It occurs mainly in the small and medium-sized vessels. Although the cause of TAO is unknown, systemic factors (immunological or humoral) may be involved in addition to abnormal peripheral microcirculation. Endothelium is now recognized as an important factor in the maintenance of microvascular circulation and the inhibition of platelet aggregation. This study examines the possible impairment of endothelium-dependent vasodilation in the peripheral vasculature of patients with TAO. METHODS AND RESULTS: Forearm blood flow (FBF) changes induced by the endothelium-dependent vasodilator acetylcholine, the endothelium-independent vasodilator sodium nitroprusside, and occlusion-induced reactive hyperemia were measured plethysmographically in eight patients with TAO and in eight healthy control subjects matched for age and smoking status. The increase in FBF response to intra-arterial acetylcholine infusion was lower in patients with TAO than in healthy control subjects (peak FBF, 22.9 +/- 2.9 versus 14.1 +/- 2.8 mL/min per dL of tissue volume; P < .01). In contrast, there was no significant difference in the increase in FBF response to sodium nitroprusside infusion between the two groups (peak FBF 13.1 +/- 4.0 versus 16.3 +/- 2.5 mL/min per dL of tissue volume; P = NS). In the case of reactive hyperemia, there were no significant differences between the two groups at any time points of hyperemia (peak FBF, 32.9 +/- 4.0 versus 31.4 +/- 3.3 mL/min per dL of tissue volume; P = NS). CONCLUSIONS: These results indicate that peripheral endothelium-dependent vasodilation is impaired in the nondiseased limb of patients with TAO. This type of vascular dysfunction may contribute to such characteristics as segmental proliferative lesion and thrombus formation in the peripheral vessels of patients with TAO.