title: Postischemic hyperemia in subjects with lower limbs obstructive arteriopathy: role of PGI2 and endothelin.
abstract: The physiological basis of postischemic hyperemia is not yet fully understood. The present study investigated the effects of pharmacologic manipulation of the prostaglandin system on local hemodynamics. Strain-gauge plethysmography was used to study 8 normal subjects and 9 patients with obliterating arterial disease of the lower limbs. Hemodynamic evaluations were performed before treatment, after seven days of low-dose acetylsalicylic acid (100 mg/day) to inhibit platelet thromboxane synthesis, and after acute infusion of 1 g of acetylsalicylic acid to inhibit endothelial prostacyclin synthesis. In patients with arterial disease, the hemodynamic study was also carried out after infusion of iloprost, a synthetic prostacyclin analogue. Acute infusion of acetylsalicylic acid significantly reduced basal blood flow in normal subjects, but not in patients with arterial disease. In the latter group, iloprost affected neither basal nor maximal postischemic flow. The study also evaluated the role of endothelin in musculocutaneous hemodynamic regulation, both in physiological conditions and in atherosclerosis. This part of the study addressed the possibility that the hemodynamic effects of vasodilator prostanoids like prostacyclin might affect endothelin release in vivo. During reactive hyperemia, plasma endothelin was reduced in normal subjects (-1.02 pg/mL, 95% CI: -2.23, 0.08), but not in patients with atherosclerosis (-0.35 pg/mL, 95% CI: -1.45, 0.75). In both groups, plasma endothelin was not affected by aspirin. These findings confirm the role of prostacyclin in local hemodynamic regulation. In the normal subject, musculocutaneous blood flow seems to depend at least in part on the action of vasodilator prostanoids and endothelin. This is not the case in patients with arterial disease, in whom plasma endothelin does not seem to be affected by postischemic changes in blood flow. A possible explanation for this difference could be alteration of the endothelial function in patients with arterial disease, related to the functional and structural characteristics of the artery wall in atherosclerosis.
authors.affiliation: Chair of Internal Medicine, University of Verona, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Pancera
authors.forename: P
authors.initials: P
authors.lastname: Minuz
authors.forename: L
authors.initials: L
authors.lastname: Rossi
authors.forename: M
authors.initials: M
authors.lastname: Ribul
authors.forename: E
authors.initials: E
authors.lastname: Arosio
authors.forename: A
authors.initials: A
authors.lastname: Lechi
mesh_terms: D000368:Aged; D001161:Arteriosclerosis / Q000503:physiopathology*; D001241:Aspirin / Q000494:pharmacology; D016232:Endothelins / Q000097:blood / Q000502:physiology*; D011464:Epoprostenol / Q000502:physiology*; D006439:Hemodynamics; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology*; D016285:Iloprost / Q000494:pharmacology; D007511:Ischemia / Q000503:physiopathology*; D007866:Leg / Q000098:blood supply*; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D010991:Plethysmography; D012039:Regional Blood Flow / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D016232:Endothelins; D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents; D011464:Epoprostenol; D016285:Iloprost; D001241:Aspirin